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class="js-profile-view-count"></span></p></div></span></div><div class="ri-section"><div class="ri-section-header"><span>Interests</span></div><div class="ri-tags-container"><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="39643530" href="https://www.academia.edu/Documents/in/Quebec"><div id="js-react-on-rails-context" style="display:none" data-rails-context="{"inMailer":false,"i18nLocale":"en","i18nDefaultLocale":"en","href":"https://independent.academia.edu/CaroleGarofalo","location":"/CaroleGarofalo","scheme":"https","host":"independent.academia.edu","port":null,"pathname":"/CaroleGarofalo","search":null,"httpAcceptLanguage":null,"serverSide":false}"></div> <div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Quebec"]}" data-trace="false" data-dom-id="Pill-react-component-474990c9-9e6c-4d33-8b98-73dacf66c60f"></div> <div 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id="Pill-react-component-79b473b7-3589-494f-ac5a-7bd17d6d60c4"></div> </a><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="39643530" href="https://www.academia.edu/Documents/in/European"><div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["European"]}" data-trace="false" data-dom-id="Pill-react-component-1a1e5a1e-44c1-4a9a-bbb5-f040e6e2ed03"></div> <div id="Pill-react-component-1a1e5a1e-44c1-4a9a-bbb5-f040e6e2ed03"></div> </a><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="39643530" href="https://www.academia.edu/Documents/in/Consensus"><div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Consensus"]}" data-trace="false" data-dom-id="Pill-react-component-4a8acf25-cc91-4db3-a8f4-4277fdf77841"></div> <div id="Pill-react-component-4a8acf25-cc91-4db3-a8f4-4277fdf77841"></div> </a></div></div></div></div><div class="right-panel-container"><div class="user-content-wrapper"><div class="uploads-container" id="social-redesign-work-container"><div class="upload-header"><h2 class="ds2-5-heading-sans-serif-xs">Uploads</h2></div><div class="documents-container backbone-social-profile-documents" style="width: 100%;"><div class="u-taCenter"></div><div class="profile--tab_content_container js-tab-pane tab-pane active" id="all"><div class="profile--tab_heading_container js-section-heading" data-section="Papers" id="Papers"><h3 class="profile--tab_heading_container">Papers by Carole Garofalo</h3></div><div class="js-work-strip profile--work_container" data-work-id="19380187"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380187/Localization_Structure_and_Regulation_of_AMP_Activated_Protein_Kinase_in_the_Small_Intestine"><img alt="Research paper thumbnail of Localization, Structure and Regulation of AMP-Activated Protein Kinase in the Small Intestine" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380187/Localization_Structure_and_Regulation_of_AMP_Activated_Protein_Kinase_in_the_Small_Intestine">Localization, Structure and Regulation of AMP-Activated Protein Kinase in the Small Intestine</a></div><div class="wp-workCard_item"><span>Gastroenterology</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380187"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380187"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380187; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380187]").text(description); $(".js-view-count[data-work-id=19380187]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget 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class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380186/Biochemical_and_Molecular_Actions_of_Nutrients_Research_Communication">Biochemical and Molecular Actions of Nutrients Research Communication</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Recently, the idea was advanced that short- chain fatty acids (SCFA) may potentially regulate int...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Recently, the idea was advanced that short- chain fatty acids (SCFA) may potentially regulate intestinal fat absorption. The aim of this investigation was to examine the effects of butyrate on the intracellular events governing the assembly of triglyceride-lipoproteins in enterocytes. To this end, differentiated human Caco-2 cells were exposed to 10 or 20 mmol/L butyrate for 20 h. The incubation</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="5e6eb4944c1b5f3b513060daa83c9d6f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":40587803,"asset_id":19380186,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/40587803/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380186"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380186"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380186; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380186]").text(description); $(".js-view-count[data-work-id=19380186]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19380186; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19380186']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19380186, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "5e6eb4944c1b5f3b513060daa83c9d6f" } } $('.js-work-strip[data-work-id=19380186]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380186,"title":"Biochemical and Molecular Actions of Nutrients Research Communication","translated_title":"","metadata":{"abstract":"Recently, the idea was advanced that short- chain fatty acids (SCFA) may potentially regulate intestinal fat absorption. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19380185"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380185/Combined_n_3_and_n_6_essential_fatty_deficiency_is_a_potent_modulator_of_plasma_lipids_lipoprotein_composition_and_lipolytic_enzymes"><img alt="Research paper thumbnail of Combined (n-3 and n-6) essential fatty deficiency is a potent modulator of plasma lipids, lipoprotein composition, and lipolytic enzymes" class="work-thumbnail" src="https://attachments.academia-assets.com/40587781/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380185/Combined_n_3_and_n_6_essential_fatty_deficiency_is_a_potent_modulator_of_plasma_lipids_lipoprotein_composition_and_lipolytic_enzymes">Combined (n-3 and n-6) essential fatty deficiency is a potent modulator of plasma lipids, lipoprotein composition, and lipolytic enzymes</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Essential fatty acids (EFA) are important structural and functional components of cell membranes....</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Essential fatty acids (EFA) are important structural and functional components of cell membranes. Their deficiency has been associated with several clinical and biochemical abnor- malities. In the present study, the lipid profile as well as the concentration, composition, and metabolism of lipoproteins were examined in rats rendered EFA-deficient over a period of 12 weeks. Changes in plasma fatty acids mainly</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="15852a2843bb491bb9396e06626c916d" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":40587781,"asset_id":19380185,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/40587781/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380185"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380185"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380185; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380185]").text(description); $(".js-view-count[data-work-id=19380185]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19380185; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19380185']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19380185, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "15852a2843bb491bb9396e06626c916d" } } $('.js-work-strip[data-work-id=19380185]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380185,"title":"Combined (n-3 and n-6) essential fatty deficiency is a potent modulator of plasma lipids, lipoprotein composition, and lipolytic enzymes","translated_title":"","metadata":{"abstract":"Essential fatty acids (EFA) are important structural and functional components of cell membranes. 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Changes in plasma fatty acids mainly","internal_url":"https://www.academia.edu/19380185/Combined_n_3_and_n_6_essential_fatty_deficiency_is_a_potent_modulator_of_plasma_lipids_lipoprotein_composition_and_lipolytic_enzymes","translated_internal_url":"","created_at":"2015-12-02T14:00:35.822-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":39643530,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":11545766,"work_id":19380185,"tagging_user_id":39643530,"tagged_user_id":31248312,"co_author_invite_id":null,"email":"e***y@recherche-ste-justine.qc.ca","affiliation":"Universit茅 de Montr茅al","display_order":0,"name":"Emile Levy","title":"Combined (n-3 and n-6) essential fatty deficiency is a potent modulator of plasma lipids, lipoprotein composition, and lipolytic 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/></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/12440530/An_Intervention_to_Promote_Breast_Milk_Production_in_Mothers_of_Preterm_Infants">An Intervention to Promote Breast Milk Production in Mothers of Preterm Infants</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/CaroleGarofalo">Carole Garofalo</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://umontreal.academia.edu/EmileLevy">Emile Levy</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/AnnemoniqueNuyt">Anne-monique Nuyt</a></span></div><div class="wp-workCard_item"><span>Western journal of nursing research</span><span>, Jan 13, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">A pilot study was conducted to estimate the effects of a breast milk expression education and sup...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">A pilot study was conducted to estimate the effects of a breast milk expression education and support intervention on breast milk production outcomes in mothers of very and extremely preterm infants. Forty mothers of hospitalized preterm infants (&lt;30 weeks of gestation) were randomized to the experimental intervention or standard care for 6 weeks. Duration and frequency of breast milk expressions and volume of expressed breast milk were measured daily. Samples of breast milk were collected thrice during the study and analyzed for their lipid concentration. Mothers in the experimental group had a statistically significant higher duration of breast milk expression in min/day (p = .043). Differences observed between the two groups regarding the frequency of breast milk expression, volume of breast milk, and lipid concentration were not statistically significant. Results suggest that the experimental intervention may promote breast milk production in mothers of very and extremely pre...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="12440530"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="12440530"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12440530; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12440530]").text(description); $(".js-view-count[data-work-id=12440530]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12440530; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12440530']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12440530, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=12440530]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12440530,"title":"An Intervention to Promote Breast Milk Production in Mothers of Preterm Infants","translated_title":"","metadata":{"abstract":"A pilot study was conducted to estimate the effects of a breast milk expression education and support intervention on breast milk production outcomes in mothers of very and extremely preterm infants. Forty mothers of hospitalized preterm infants (\u0026lt;30 weeks of gestation) were randomized to the experimental intervention or standard care for 6 weeks. Duration and frequency of breast milk expressions and volume of expressed breast milk were measured daily. Samples of breast milk were collected thrice during the study and analyzed for their lipid concentration. Mothers in the experimental group had a statistically significant higher duration of breast milk expression in min/day (p = .043). Differences observed between the two groups regarding the frequency of breast milk expression, volume of breast milk, and lipid concentration were not statistically significant. Results suggest that the experimental intervention may promote breast milk production in mothers of very and extremely pre...","publication_date":{"day":13,"month":1,"year":2014,"errors":{}},"publication_name":"Western journal of nursing research"},"translated_abstract":"A pilot study was conducted to estimate the effects of a breast milk expression education and support intervention on breast milk production outcomes in mothers of very and extremely preterm infants. Forty mothers of hospitalized preterm infants (\u0026lt;30 weeks of gestation) were randomized to the experimental intervention or standard care for 6 weeks. Duration and frequency of breast milk expressions and volume of expressed breast milk were measured daily. Samples of breast milk were collected thrice during the study and analyzed for their lipid concentration. Mothers in the experimental group had a statistically significant higher duration of breast milk expression in min/day (p = .043). Differences observed between the two groups regarding the frequency of breast milk expression, volume of breast milk, and lipid concentration were not statistically significant. Results suggest that the experimental intervention may promote breast milk production in mothers of very and extremely pre...","internal_url":"https://www.academia.edu/12440530/An_Intervention_to_Promote_Breast_Milk_Production_in_Mothers_of_Preterm_Infants","translated_internal_url":"","created_at":"2015-05-18T05:12:43.667-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31248312,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":564462,"work_id":12440530,"tagging_user_id":31248312,"tagged_user_id":39643530,"co_author_invite_id":217969,"email":"c***o@recherche-ste-justine.qc.ca","display_order":0,"name":"Carole Garofalo","title":"An Intervention to Promote Breast Milk Production in Mothers of Preterm Infants"},{"id":564424,"work_id":12440530,"tagging_user_id":31248312,"tagged_user_id":31459997,"co_author_invite_id":217964,"email":"a***t@recherche-ste-justine.qc.ca","display_order":null,"name":"Anne-monique Nuyt","title":"An Intervention to Promote Breast Milk Production in Mothers of Preterm Infants"}],"downloadable_attachments":[],"slug":"An_Intervention_to_Promote_Breast_Milk_Production_in_Mothers_of_Preterm_Infants","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":31248312,"first_name":"Emile","middle_initials":null,"last_name":"Levy","page_name":"EmileLevy","domain_name":"umontreal","created_at":"2015-05-18T05:12:19.584-07:00","display_name":"Emile Levy","url":"https://umontreal.academia.edu/EmileLevy"},"attachments":[],"research_interests":[{"id":588,"name":"Nursing","url":"https://www.academia.edu/Documents/in/Nursing"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19380184"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380184/Modulatory_role_of_PYY_in_transport_and_metabolism_of_cholesterol_in_intestinal_epithelial_cells"><img alt="Research paper thumbnail of Modulatory role of PYY in transport and metabolism of cholesterol in intestinal epithelial cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380184/Modulatory_role_of_PYY_in_transport_and_metabolism_of_cholesterol_in_intestinal_epithelial_cells">Modulatory role of PYY in transport and metabolism of cholesterol in intestinal epithelial cells</a></div><div class="wp-workCard_item"><span>PloS one</span><span>, 2012</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Gastrointestinal peptides are involved in modulating appetite. Other biological functions attribu...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Gastrointestinal peptides are involved in modulating appetite. Other biological functions attributed to them include the regulation of lipid homeostasis. However, data concerning PYY remain fragmentary. The objectives of the study were: (i) To determine the effect of PYY on intestinal transport and synthesis of cholesterol, the biogenesis of apolipoproteins (apos) and assembly of lipoproteins and (ii) To analyze whether the effects of PYY are similar according to whether cells are exposed to PYY on apical or basolateral surface. Caco-2/15 cells were incubated with PYY (1-36) administered either to the apical or basolateral medium, at concentrations of 50 or 200 nM for 24 hours. De novo synthesis of cholesterol, cholesterol uptake, and assembly of lipoproteins were evaluated through the incorporation of [(14)C]-acetate, [(14)C]-cholesterol, and [(14)C]-oleate, respectively. Biogenesis of apos (A-I, A-IV, E, B-48 and B-100) was examined by the incorporation of [(35)S]-methionine. The ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380184"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380184"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380184; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380184]").text(description); $(".js-view-count[data-work-id=19380184]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19380184; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19380184']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19380184, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=19380184]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380184,"title":"Modulatory role of PYY in transport and metabolism of cholesterol in intestinal epithelial cells","translated_title":"","metadata":{"abstract":"Gastrointestinal peptides are involved in modulating appetite. Other biological functions attributed to them include the regulation of lipid homeostasis. However, data concerning PYY remain fragmentary. The objectives of the study were: (i) To determine the effect of PYY on intestinal transport and synthesis of cholesterol, the biogenesis of apolipoproteins (apos) and assembly of lipoproteins and (ii) To analyze whether the effects of PYY are similar according to whether cells are exposed to PYY on apical or basolateral surface. Caco-2/15 cells were incubated with PYY (1-36) administered either to the apical or basolateral medium, at concentrations of 50 or 200 nM for 24 hours. De novo synthesis of cholesterol, cholesterol uptake, and assembly of lipoproteins were evaluated through the incorporation of [(14)C]-acetate, [(14)C]-cholesterol, and [(14)C]-oleate, respectively. Biogenesis of apos (A-I, A-IV, E, B-48 and B-100) was examined by the incorporation of [(35)S]-methionine. The ...","publication_date":{"day":null,"month":null,"year":2012,"errors":{}},"publication_name":"PloS one"},"translated_abstract":"Gastrointestinal peptides are involved in modulating appetite. Other biological functions attributed to them include the regulation of lipid homeostasis. However, data concerning PYY remain fragmentary. The objectives of the study were: (i) To determine the effect of PYY on intestinal transport and synthesis of cholesterol, the biogenesis of apolipoproteins (apos) and assembly of lipoproteins and (ii) To analyze whether the effects of PYY are similar according to whether cells are exposed to PYY on apical or basolateral surface. Caco-2/15 cells were incubated with PYY (1-36) administered either to the apical or basolateral medium, at concentrations of 50 or 200 nM for 24 hours. De novo synthesis of cholesterol, cholesterol uptake, and assembly of lipoproteins were evaluated through the incorporation of [(14)C]-acetate, [(14)C]-cholesterol, and [(14)C]-oleate, respectively. Biogenesis of apos (A-I, A-IV, E, B-48 and B-100) was examined by the incorporation of [(35)S]-methionine. 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We investigated in vitro some of the mechanisms of this transport. Caco-2/15 cells internalize leptin from the apical medium and release it through transcytosis in the basal medium in a time- temperature-dependent and saturable fashion. Leptin receptors are revealed on the apical brush-border membrane of the Caco-2 cells. RNA-mediated silencing of the receptor led to decreases in the uptake and basolateral release. Leptin in the basal medium was found bound to the soluble form of its receptor. An inhibitor of clathrin-dependent endocytosis (chlorpromazine) decreased leptin uptake. Confocal immunocytochemistry and the use of brefeldin A and okadaic acid revealed the passage of leptin through the Golgi apparatus. We propose that leptin transcytosis by intestinal cells depends on its receptor, on clathrin-coated vesicles and transits through the Golgi apparatus.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="49eec4b9e24dda6aa9bc3511cc7c0614" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":40587796,"asset_id":19380183,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/40587796/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380183"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380183"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380183; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380183]").text(description); $(".js-view-count[data-work-id=19380183]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19380183; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19380183']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19380183, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "49eec4b9e24dda6aa9bc3511cc7c0614" } } $('.js-work-strip[data-work-id=19380183]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380183,"title":"Receptor-Mediated Transcytosis of Leptin through Human Intestinal Cells In Vitro","translated_title":"","metadata":{"abstract":"Gastric Leptin is absorbed by duodenal enterocytes and released on the basolateral side towards the bloodstream. 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An inhibitor of clathrin-dependent endocytosis (chlorpromazine) decreased leptin uptake. Confocal immunocytochemistry and the use of brefeldin A and okadaic acid revealed the passage of leptin through the Golgi apparatus. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19380181"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380181/Sar1b_transgenic_male_mice_are_more_susceptible_to_high_fat_diet_induced_obesity_insulin_insensitivity_and_intestinal_chylomicron_overproduction"><img alt="Research paper thumbnail of Sar1b transgenic male mice are more susceptible to high-fat diet-induced obesity, insulin insensitivity and intestinal chylomicron overproduction" class="work-thumbnail" src="https://attachments.academia-assets.com/42094697/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380181/Sar1b_transgenic_male_mice_are_more_susceptible_to_high_fat_diet_induced_obesity_insulin_insensitivity_and_intestinal_chylomicron_overproduction">Sar1b transgenic male mice are more susceptible to high-fat diet-induced obesity, insulin insensitivity and intestinal chylomicron overproduction</a></div><div class="wp-workCard_item"><span>The Journal of nutritional biochemistry</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In the intracellular secretory network, nascent proteins are shuttled from the endoplasmic reticu...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">In the intracellular secretory network, nascent proteins are shuttled from the endoplasmic reticulum to the Golgi by transport vesicles requiring Sar1b, a small GTPase. Mutations in this key enzyme impair intestinal lipid transport and cause chylomicron retention disease. The main aim of this study was to assess whether Sar1b overexpression under a hypercaloric diet accelerated lipid production and chylomicron (CM) secretion, thereby inducing cardiometabolic abnormalities. To this end, we generated transgenic mice overexpressing human Sar1b (Sar1b(+/+)) using pBROAD3-mcs that features the ubiquitous mouse ROSA26 promoter. In response to a high-fat diet (HFD), Sar1b(+/+) mice displayed significantly increased body weight and adiposity compared with Sar1b(+/+) mice under the same regimen or with wild-type (WT) mice exposed to chow diet or HFD. Furthermore, Sar1b(+/+) mice were prone to liver steatosis as revealed by significantly elevated hepatic triglycerides (TG) and cholesterol in ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b9f0c58be08cd3a8d6074a7d93bb50cf" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":42094697,"asset_id":19380181,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/42094697/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380181"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380181"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380181; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380181]").text(description); $(".js-view-count[data-work-id=19380181]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19380181; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19380181']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19380181, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "b9f0c58be08cd3a8d6074a7d93bb50cf" } } $('.js-work-strip[data-work-id=19380181]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380181,"title":"Sar1b transgenic male mice are more susceptible to high-fat diet-induced obesity, insulin insensitivity and intestinal chylomicron overproduction","translated_title":"","metadata":{"abstract":"In the intracellular secretory network, nascent proteins are shuttled from the endoplasmic reticulum to the Golgi by transport vesicles requiring Sar1b, a small GTPase. 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href="https://www.academia.edu/12440523/A_polyphenol_rich_cranberry_extract_protects_from_diet_induced_obesity_insulin_resistance_and_intestinal_inflammation_in_association_with_increased_Akkermansia_spp_population_in_the_gut_microbiota_of_mice"><img alt="Research paper thumbnail of A polyphenol-rich cranberry extract protects from diet-induced obesity, insulin resistance and intestinal inflammation in association with increased Akkermansia spp. population in the gut microbiota of mice" class="work-thumbnail" src="https://attachments.academia-assets.com/46182959/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/12440523/A_polyphenol_rich_cranberry_extract_protects_from_diet_induced_obesity_insulin_resistance_and_intestinal_inflammation_in_association_with_increased_Akkermansia_spp_population_in_the_gut_microbiota_of_mice">A polyphenol-rich cranberry extract protects from diet-induced obesity, insulin resistance and intestinal inflammation in association with increased Akkermansia spp. population in the gut microbiota of mice</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/CaroleGarofalo">Carole Garofalo</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://umontreal.academia.edu/EmileLevy">Emile Levy</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/Genevi%C3%A8vePilon">Genevi猫ve Pilon</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://ulaval.academia.edu/DenisRoy">Denis Roy</a></span></div><div class="wp-workCard_item"><span>Gut</span><span>, Jan 30, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The increasing prevalence of obesity and type 2 diabetes (T2D) demonstrates the failure of conven...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The increasing prevalence of obesity and type 2 diabetes (T2D) demonstrates the failure of conventional treatments to curb these diseases. The gut microbiota has been put forward as a key player in the pathophysiology of diet-induced T2D. Importantly, cranberry (Vaccinium macrocarpon Aiton) is associated with a number of beneficial health effects. We aimed to investigate the metabolic impact of a cranberry extract (CE) on high fat/high sucrose (HFHS)-fed mice and to determine whether its consequent antidiabetic effects are related to modulations in the gut microbiota. C57BL/6J mice were fed either a chow or a HFHS diet. HFHS-fed mice were gavaged daily either with vehicle (water) or CE (200鈥卪g/kg) for 8鈥厀eeks. The composition of the gut microbiota was assessed by analysing 16S rRNA gene sequences with 454 pyrosequencing. CE treatment was found to reduce HFHS-induced weight gain and visceral obesity. CE treatment also decreased liver weight and triglyceride accumulation in associatio...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="10523ea6e051192f1bcf2d3ebf701e8e" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":46182959,"asset_id":12440523,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/46182959/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="12440523"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="12440523"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12440523; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12440523]").text(description); $(".js-view-count[data-work-id=12440523]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12440523; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12440523']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12440523, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "10523ea6e051192f1bcf2d3ebf701e8e" } } $('.js-work-strip[data-work-id=12440523]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12440523,"title":"A polyphenol-rich cranberry extract protects from diet-induced obesity, insulin resistance and intestinal inflammation in association with increased Akkermansia spp. population in the gut microbiota of mice","translated_title":"","metadata":{"abstract":"The increasing prevalence of obesity and type 2 diabetes (T2D) demonstrates the failure of conventional treatments to curb these diseases. The gut microbiota has been put forward as a key player in the pathophysiology of diet-induced T2D. Importantly, cranberry (Vaccinium macrocarpon Aiton) is associated with a number of beneficial health effects. We aimed to investigate the metabolic impact of a cranberry extract (CE) on high fat/high sucrose (HFHS)-fed mice and to determine whether its consequent antidiabetic effects are related to modulations in the gut microbiota. C57BL/6J mice were fed either a chow or a HFHS diet. HFHS-fed mice were gavaged daily either with vehicle (water) or CE (200鈥卪g/kg) for 8鈥厀eeks. The composition of the gut microbiota was assessed by analysing 16S rRNA gene sequences with 454 pyrosequencing. CE treatment was found to reduce HFHS-induced weight gain and visceral obesity. 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}); </script> <div class="js-work-strip profile--work_container" data-work-id="19380180"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380180/Effect_of_retinoic_acid_on_cell_proliferation_and_differentiation_as_well_as_on_lipid_synthesis_lipoprotein_secretion_and_apolipoprotein_biogenesis"><img alt="Research paper thumbnail of Effect of retinoic acid on cell proliferation and differentiation as well as on lipid synthesis, lipoprotein secretion, and apolipoprotein biogenesis" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380180/Effect_of_retinoic_acid_on_cell_proliferation_and_differentiation_as_well_as_on_lipid_synthesis_lipoprotein_secretion_and_apolipoprotein_biogenesis">Effect of retinoic acid on cell proliferation and differentiation as well as on lipid synthesis, lipoprotein secretion, and apolipoprotein biogenesis</a></div><div class="wp-workCard_item"><span>American Journal of Physiology-gastrointestinal and Liver Physiology</span><span>, 2007</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Dietary vitamin A and its active metabolites are essential nutrients for many functions as well a...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Dietary vitamin A and its active metabolites are essential nutrients for many functions as well as potent regulators of gene transcription and growth. Although the epithelium of the small intestine is characterized by rapid and constant renewal and enterocytes play a central role in the absorption and metabolism of alimentary retinol, very little is known about the function of retinoids in the human gastrointestinal epithelium and mechanisms by which programs engage the cell cycle are poorly understood. We have assessed the effects of 10 microM 9- and 13-cis-retinoic acid (RA) on proliferation and differentiation processes, lipid esterification, apolipoprotein (apo) biogenesis and lipoprotein secretion along with nuclear factor gene transcription. Treatment of Caco-2 cells with RA at different concentrations and incubation periods revealed the reduction of thymidine incorporation in 60% preconfluent or 100% confluent cells. Concomitantly, RA 1) modulated D-type cyclins by reducing the mitogen-sensitive cyclin D1 and upregulating cyclin D3 expressions and 2) caused a trend of increase in p38 MAPK, which triggers CDX2, a central protein in cell differentiation. RA remained without effect on lipoprotein output and apo synthesis, even for apo A-I that possesses RARE in its promoter. RA, in combination with 22-hydroxycholesterol, could induce apo A-I gene expression without any impact on apo A-I mass. Only the gene expression of peroxisome proliferator-activated receptor (PPAR)beta, retinoic receptor (RAR)beta, and RARgamma was augmented and no alteration was noted in PPARalpha, PPARgamma, liver X receptor (LXR)alpha, LXRbeta, and retinoid X receptors. Taken together, these data highlight RA-induced cell differentiation via specific signaling without a significant impact on apo A-I synthesis.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380180"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380180"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380180; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380180]").text(description); $(".js-view-count[data-work-id=19380180]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19380180; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19380180']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19380180, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=19380180]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380180,"title":"Effect of retinoic acid on cell proliferation and differentiation as well as on lipid synthesis, lipoprotein secretion, and apolipoprotein biogenesis","translated_title":"","metadata":{"abstract":"Dietary vitamin A and its active metabolites are essential nutrients for many functions as well as potent regulators of gene transcription and growth. 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Concomitantly, RA 1) modulated D-type cyclins by reducing the mitogen-sensitive cyclin D1 and upregulating cyclin D3 expressions and 2) caused a trend of increase in p38 MAPK, which triggers CDX2, a central protein in cell differentiation. RA remained without effect on lipoprotein output and apo synthesis, even for apo A-I that possesses RARE in its promoter. RA, in combination with 22-hydroxycholesterol, could induce apo A-I gene expression without any impact on apo A-I mass. Only the gene expression of peroxisome proliferator-activated receptor (PPAR)beta, retinoic receptor (RAR)beta, and RARgamma was augmented and no alteration was noted in PPARalpha, PPARgamma, liver X receptor (LXR)alpha, LXRbeta, and retinoid X receptors. 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We have assessed the effects of 10 microM 9- and 13-cis-retinoic acid (RA) on proliferation and differentiation processes, lipid esterification, apolipoprotein (apo) biogenesis and lipoprotein secretion along with nuclear factor gene transcription. Treatment of Caco-2 cells with RA at different concentrations and incubation periods revealed the reduction of thymidine incorporation in 60% preconfluent or 100% confluent cells. Concomitantly, RA 1) modulated D-type cyclins by reducing the mitogen-sensitive cyclin D1 and upregulating cyclin D3 expressions and 2) caused a trend of increase in p38 MAPK, which triggers CDX2, a central protein in cell differentiation. RA remained without effect on lipoprotein output and apo synthesis, even for apo A-I that possesses RARE in its promoter. RA, in combination with 22-hydroxycholesterol, could induce apo A-I gene expression without any impact on apo A-I mass. Only the gene expression of peroxisome proliferator-activated receptor (PPAR)beta, retinoic receptor (RAR)beta, and RARgamma was augmented and no alteration was noted in PPARalpha, PPARgamma, liver X receptor (LXR)alpha, LXRbeta, and retinoid X receptors. Taken together, these data highlight RA-induced cell differentiation via specific signaling without a significant impact on apo A-I synthesis.","internal_url":"https://www.academia.edu/19380180/Effect_of_retinoic_acid_on_cell_proliferation_and_differentiation_as_well_as_on_lipid_synthesis_lipoprotein_secretion_and_apolipoprotein_biogenesis","translated_internal_url":"","created_at":"2015-12-02T14:00:35.139-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":39643530,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":11545765,"work_id":19380180,"tagging_user_id":39643530,"tagged_user_id":31248312,"co_author_invite_id":null,"email":"e***y@recherche-ste-justine.qc.ca","affiliation":"Universit茅 de Montr茅al","display_order":0,"name":"Emile Levy","title":"Effect of retinoic acid on cell proliferation and differentiation as well as on lipid synthesis, lipoprotein secretion, and apolipoprotein biogenesis"},{"id":11545775,"work_id":19380180,"tagging_user_id":39643530,"tagged_user_id":31223745,"co_author_invite_id":null,"email":"e***n@recherche-ste-justine.qc.ca","display_order":4194304,"name":"Edgard Delvin","title":"Effect of retinoic acid on cell proliferation and differentiation as well as on lipid synthesis, lipoprotein secretion, and apolipoprotein biogenesis"},{"id":11545796,"work_id":19380180,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":217951,"email":"a***e@gmail.com","display_order":6291456,"name":"Alain San茅","title":"Effect of retinoic acid on cell proliferation and differentiation as well as on lipid synthesis, lipoprotein secretion, and apolipoprotein biogenesis"},{"id":11545800,"work_id":19380180,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":2711272,"email":"e***y@umontreal.ca","display_order":7340032,"name":"E. Tremblay","title":"Effect of retinoic acid on cell proliferation and differentiation as well as on lipid synthesis, lipoprotein secretion, and apolipoprotein biogenesis"}],"downloadable_attachments":[],"slug":"Effect_of_retinoic_acid_on_cell_proliferation_and_differentiation_as_well_as_on_lipid_synthesis_lipoprotein_secretion_and_apolipoprotein_biogenesis","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":39643530,"first_name":"Carole","middle_initials":null,"last_name":"Garofalo","page_name":"CaroleGarofalo","domain_name":"independent","created_at":"2015-12-02T13:59:52.848-08:00","display_name":"Carole Garofalo","url":"https://independent.academia.edu/CaroleGarofalo"},"attachments":[],"research_interests":[{"id":167,"name":"Physiology","url":"https://www.academia.edu/Documents/in/Physiology"},{"id":57201,"name":"Apolipoproteins","url":"https://www.academia.edu/Documents/in/Apolipoproteins"},{"id":60436,"name":"Cell Differentiation","url":"https://www.academia.edu/Documents/in/Cell_Differentiation"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":151448,"name":"American","url":"https://www.academia.edu/Documents/in/American"},{"id":184609,"name":"Lipid metabolism","url":"https://www.academia.edu/Documents/in/Lipid_metabolism"},{"id":186234,"name":"Medical Physiology","url":"https://www.academia.edu/Documents/in/Medical_Physiology"},{"id":227285,"name":"Lipoprotein(a)","url":"https://www.academia.edu/Documents/in/Lipoprotein_a_-1"},{"id":314125,"name":"Caco-2 cells","url":"https://www.academia.edu/Documents/in/Caco-2_cells"},{"id":458879,"name":"Lipoproteins","url":"https://www.academia.edu/Documents/in/Lipoproteins"},{"id":469643,"name":"Retinoic Acid","url":"https://www.academia.edu/Documents/in/Retinoic_Acid"},{"id":591594,"name":"Tretinoin","url":"https://www.academia.edu/Documents/in/Tretinoin"},{"id":782251,"name":"Cell Proliferation","url":"https://www.academia.edu/Documents/in/Cell_Proliferation"}],"urls":[{"id":6101557,"url":"http://ajpgi.physiology.org/cgi/doi/10.1152/ajpgi.00295.2007"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19380179"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380179/Dried_Apple_Peel_Extract_Prevents_Oxidative_Stress_and_Inflammation_in_Intestinal_Cells"><img alt="Research paper thumbnail of Dried Apple Peel Extract Prevents Oxidative Stress and Inflammation in Intestinal Cells" class="work-thumbnail" src="https://attachments.academia-assets.com/40587799/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380179/Dried_Apple_Peel_Extract_Prevents_Oxidative_Stress_and_Inflammation_in_Intestinal_Cells">Dried Apple Peel Extract Prevents Oxidative Stress and Inflammation in Intestinal Cells</a></div><div class="wp-workCard_item"><span>Free Radical Biology and Medicine</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="30249a268bcee7a3bb58e59eb57aa71a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":40587799,"asset_id":19380179,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/40587799/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380179"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380179"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380179; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "30249a268bcee7a3bb58e59eb57aa71a" } } $('.js-work-strip[data-work-id=19380179]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380179,"title":"Dried Apple Peel Extract Prevents Oxidative Stress and Inflammation in Intestinal Cells","translated_title":"","metadata":{"grobid_abstract":"Vitamin E, also called tocopherol (TOH), belongs to a class of vitamins referred to as lipid-soluble vitamins and well known for its antioxidant effects in living cells. Vitamin E is not produced in the body; it can only be obtained by mean of food from plant sources or through natural and synthetic supplements. Vitamin E is commercially extracted primarily from vegetable oils such as palm, canola, corn, cotton or soybean oils. Studies have shown that during industrial production a significant loss of tocopherols occurs in the range of 25% to 35% due to either thermal breakdown or chemical reactions. the majority of the tocopherol loss during oil processing is due to oxidation which renders the molecule ineffective with respect to its vitamin's function. Tocopherolquinone is one of the major oxidation products of vitamin E. The present study is the first to demonstrate that stannous chloride (SnCl 2 .2H 2 O) ion is capable of reducing 伪tocopherolquinone (TQ) back to 伪-tocopherol. Experiments conducted by reacting pure commercial standard 伪-TQ with stannous chloride (II) in organic solvent (methanol) yield promising results by reducing 95% of the 伪-TQ and producing vitamin E. These results led us to the isolation by HPLC of a fraction of TQ that was successfully reduced back to TOH. the TQ was obtained by oxidation reaction in vitro of a small quantity of commercial standard 伪-TOH and copper chloride (CuCl 2 ). in this study, stannous chloride has also proven to provide an important antioxidation effect by preventing the oxidation of TOH when exposed to a powerful oxidation catalyst such as CuCl 2 . the present study has shown as well for the first time the reaction of chromium (III) hexahydrate CrCl 3 .6 (H 2 O) with 伪tocopherolquinone resulting in the formation of 伪-tocopherol. This discovery presents a double advantage with regard to its applications: on one hand it can help reduce significantly the loss of vitamin E during industrial processing and on the other hand it could explain the still unanswered question on the potential antioxidant properties of chromium (III) reported in several publications. Background: It has been shown that dietary supplementation with Malaysian red palm oil improves functional recovery and reduces infarct size, following ischaemia/reperfusion (IR) in rat hearts. We subsequently investigated the composition of several other palm oils. These palm oils are consumed as a regular part of the diet in many parts of Africa and South-America. Materials and Methods: Oils were analyzed for fatty acid composition, antioxidant and trace metal content. Results: Fatty acid and antioxidant composition of palm oils from Africa yielded similar results to that of the Malaysian product. South-American palm oil however showed some differences in fatty acid composition, as well as significant differences in antioxidant content, especially with respect to vitamin E content. Trace metal analysis of oils are under way. Conclusion: Malaysian red palm oil supplementation reduces myocardial ischaemia/reperfusion injury and infarct size, through its natural antioxidant and fatty acid content. We hypothesize that African palm oil will have similar effects than the Malaysian counterpart with regards to cardiovascular protection. Further studies need to be done with the South-American palm oil to determine its effects on cardiovascular protection in the rat model. a (BPA), an important occupational and environmental chemical, causes toxicity to several organ systems including the liver. However, very little is known regarding the precise molecular mechanisms and cellular targets responsible for BPA toxicity. Studies in experimental animal models report that mitochondrial damage could be involved in BPA-induced liver injury. Given that BPA adversely affects the liver, and considering the central role of the liver in whole body energy metabolism and homeostasis, it is critical to understand the mechanisms behind BPA-induced hepatotoxicity. the aim of the present study was to evaluate the effects of BPA on metabolism and mitochondrial function by measuring the oxygen consumption rate (OCR) in primary rat hepatocytes using an XF24 analyzer (Seahorse Bioscience). Primary rat hepatocytes were plated in collagencoated Seahorse 24-well plates, allowed to attach for 5 h, and then exposed to various concentrations of BPA (0, 1,10, and 100 碌M) for 12 h before measuring OCR. Basal and maximal respiration, as well as the proton leak, were significantly increased following exposure to 100 碌M BPA compared to untreated control hepatocytes. Cell viability was unaffected in rat hepatocytes exposed to 1 碌M BPA, and decreased by only 22% and 30% with 10 碌M and 100 碌M BPA concentrations, respectively. Importantly, these results are in agreement with previous studies showing BPA-mediated increases in the rate of state 4 oxygen consumption in isolated mitochondria. These findings suggest that BPA may cause bioenergetic stress in cells by uncoupling. in summary, our results show that BPA negatively impacts mitochondrial function leading to critical alterations in the metabolic profile of hepatocytes.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Free Radical Biology and Medicine","grobid_abstract_attachment_id":40587799},"translated_abstract":null,"internal_url":"https://www.academia.edu/19380179/Dried_Apple_Peel_Extract_Prevents_Oxidative_Stress_and_Inflammation_in_Intestinal_Cells","translated_internal_url":"","created_at":"2015-12-02T14:00:35.014-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":39643530,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":11545764,"work_id":19380179,"tagging_user_id":39643530,"tagged_user_id":31248312,"co_author_invite_id":null,"email":"e***y@recherche-ste-justine.qc.ca","affiliation":"Universit茅 de Montr茅al","display_order":0,"name":"Emile Levy","title":"Dried Apple Peel Extract Prevents Oxidative Stress and Inflammation in Intestinal Cells"},{"id":11545774,"work_id":19380179,"tagging_user_id":39643530,"tagged_user_id":31223745,"co_author_invite_id":null,"email":"e***n@recherche-ste-justine.qc.ca","display_order":4194304,"name":"Edgard Delvin","title":"Dried Apple Peel Extract Prevents Oxidative Stress and Inflammation in Intestinal Cells"}],"downloadable_attachments":[{"id":40587799,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/40587799/thumbnails/1.jpg","file_name":"j.freeradbiomed.2011.10.143.pdf20151202-22750-1ar7eso","download_url":"https://www.academia.edu/attachments/40587799/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Dried_Apple_Peel_Extract_Prevents_Oxidat.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/40587799/j.freeradbiomed.2011.10.143-libre.pdf20151202-22750-1ar7eso?1449093975=\u0026response-content-disposition=attachment%3B+filename%3DDried_Apple_Peel_Extract_Prevents_Oxidat.pdf\u0026Expires=1732020033\u0026Signature=HcNjqE6lfPoDNMXfBY8f3Z9whavewHNLEyQjZR3MaZk0XjTKoS~~pLQD8i8CPTXwbHvLAisJWvxsNSO4lcVk0tI-5u08W5aGmp2sCsKC-e9-v5wC994wR2xzyEdCJrgcnTKCgRE11Ha-c2FbeLS52fbAcO3QkbFy6ANpcqri3kuVnZSGz6pLl~iNCbPyUMpOahMO-edNkdwRrWoktrBwBKtRqjvPvtu7EpIccjUFneyhrHt9XMh-K6OWzwoLib8~b-Ln6hUEN-HxD8C2nnCV-Hp1vOAIgIfi3VNtqYCDhlzADquE-NBVmxvpx9CSRb5q5toF8uUT7E6D9fTNL2HB9Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Dried_Apple_Peel_Extract_Prevents_Oxidative_Stress_and_Inflammation_in_Intestinal_Cells","translated_slug":"","page_count":2,"language":"en","content_type":"Work","owner":{"id":39643530,"first_name":"Carole","middle_initials":null,"last_name":"Garofalo","page_name":"CaroleGarofalo","domain_name":"independent","created_at":"2015-12-02T13:59:52.848-08:00","display_name":"Carole Garofalo","url":"https://independent.academia.edu/CaroleGarofalo"},"attachments":[{"id":40587799,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/40587799/thumbnails/1.jpg","file_name":"j.freeradbiomed.2011.10.143.pdf20151202-22750-1ar7eso","download_url":"https://www.academia.edu/attachments/40587799/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Dried_Apple_Peel_Extract_Prevents_Oxidat.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/40587799/j.freeradbiomed.2011.10.143-libre.pdf20151202-22750-1ar7eso?1449093975=\u0026response-content-disposition=attachment%3B+filename%3DDried_Apple_Peel_Extract_Prevents_Oxidat.pdf\u0026Expires=1732020033\u0026Signature=HcNjqE6lfPoDNMXfBY8f3Z9whavewHNLEyQjZR3MaZk0XjTKoS~~pLQD8i8CPTXwbHvLAisJWvxsNSO4lcVk0tI-5u08W5aGmp2sCsKC-e9-v5wC994wR2xzyEdCJrgcnTKCgRE11Ha-c2FbeLS52fbAcO3QkbFy6ANpcqri3kuVnZSGz6pLl~iNCbPyUMpOahMO-edNkdwRrWoktrBwBKtRqjvPvtu7EpIccjUFneyhrHt9XMh-K6OWzwoLib8~b-Ln6hUEN-HxD8C2nnCV-Hp1vOAIgIfi3VNtqYCDhlzADquE-NBVmxvpx9CSRb5q5toF8uUT7E6D9fTNL2HB9Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"urls":[{"id":6101556,"url":"http://www.sciencedirect.com/science/article/pii/S0891584911007726"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19380178"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380178/Prevention_of_oxidative_stress_inflammation_and_mitochondrial_dysfunction_in_the_intestine_by_different_cranberry_phenolic_fractions"><img alt="Research paper thumbnail of Prevention of oxidative stress, inflammation and mitochondrial dysfunction in the intestine by different cranberry phenolic fractions" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380178/Prevention_of_oxidative_stress_inflammation_and_mitochondrial_dysfunction_in_the_intestine_by_different_cranberry_phenolic_fractions">Prevention of oxidative stress, inflammation and mitochondrial dysfunction in the intestine by different cranberry phenolic fractions</a></div><div class="wp-workCard_item"><span>Clinical Science</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Cranberry fruit has been reported to have high antioxidant effectiveness that is potentially link...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Cranberry fruit has been reported to have high antioxidant effectiveness that is potentially linked to its richness in diversified polyphenolic content. The aim of the present study was to determine the role of cranberry polyphenolic fractions in oxidative stress (OxS), inflammation and mitochondrial functions using intestinal Caco-2/15 cells. The combination of HPLC and UltraPerformance LC庐-tandem quadrupole (UPLC-TQD) techniques allowed us to characterize the profile of low, medium and high molecular mass polyphenolic compounds in cranberry extracts. The medium molecular mass fraction was enriched with flavonoids and procyanidin dimers whereas procyanidin oligomers (DP &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt; 4) were the dominant class of polyphenols in the high molecular mass fraction. Pre-incubation of Caco-2/15 cells with these cranberry extracts prevented iron/ascorbate-mediated lipid peroxidation and counteracted lipopolysaccharide-mediated inflammation as evidenced by the decrease in pro-inflammatory cytokines (TNF-伪 and interleukin-6), cyclo-oxygenase-2 and prostaglandin E2. Cranberry polyphenols (CP) fractions limited both nuclear factor 魏B activation and Nrf2 down-regulation. Consistently, cranberry procyanidins alleviated OxS-dependent mitochondrial dysfunctions as shown by the rise in ATP production and the up-regulation of Bcl-2, as well as the decline of protein expression of cytochrome c and apoptotic-inducing factor. These mitochondrial effects were associated with a significant stimulation of peroxisome-proliferator-activated receptor 纬 co-activator-1-伪, a central inducing factor of mitochondrial biogenesis and transcriptional co-activator of numerous downstream mediators. Finally, cranberry procyanidins forestalled the effect of iron/ascorbate on the protein expression of mitochondrial transcription factors (mtTFA, mtTFB1, mtTFB2). Our findings provide evidence for the capacity of CP to reduce intestinal OxS and inflammation while improving mitochondrial dysfunction.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380178"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380178"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380178; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380178]").text(description); $(".js-view-count[data-work-id=19380178]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19380178; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19380178']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19380178, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=19380178]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380178,"title":"Prevention of oxidative stress, inflammation and mitochondrial dysfunction in the intestine by different cranberry phenolic fractions","translated_title":"","metadata":{"abstract":"Cranberry fruit has been reported to have high antioxidant effectiveness that is potentially linked to its richness in diversified polyphenolic content. The aim of the present study was to determine the role of cranberry polyphenolic fractions in oxidative stress (OxS), inflammation and mitochondrial functions using intestinal Caco-2/15 cells. The combination of HPLC and UltraPerformance LC庐-tandem quadrupole (UPLC-TQD) techniques allowed us to characterize the profile of low, medium and high molecular mass polyphenolic compounds in cranberry extracts. The medium molecular mass fraction was enriched with flavonoids and procyanidin dimers whereas procyanidin oligomers (DP \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt; 4) were the dominant class of polyphenols in the high molecular mass fraction. Pre-incubation of Caco-2/15 cells with these cranberry extracts prevented iron/ascorbate-mediated lipid peroxidation and counteracted lipopolysaccharide-mediated inflammation as evidenced by the decrease in pro-inflammatory cytokines (TNF-伪 and interleukin-6), cyclo-oxygenase-2 and prostaglandin E2. Cranberry polyphenols (CP) fractions limited both nuclear factor 魏B activation and Nrf2 down-regulation. Consistently, cranberry procyanidins alleviated OxS-dependent mitochondrial dysfunctions as shown by the rise in ATP production and the up-regulation of Bcl-2, as well as the decline of protein expression of cytochrome c and apoptotic-inducing factor. These mitochondrial effects were associated with a significant stimulation of peroxisome-proliferator-activated receptor 纬 co-activator-1-伪, a central inducing factor of mitochondrial biogenesis and transcriptional co-activator of numerous downstream mediators. Finally, cranberry procyanidins forestalled the effect of iron/ascorbate on the protein expression of mitochondrial transcription factors (mtTFA, mtTFB1, mtTFB2). Our findings provide evidence for the capacity of CP to reduce intestinal OxS and inflammation while improving mitochondrial dysfunction.","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Clinical Science"},"translated_abstract":"Cranberry fruit has been reported to have high antioxidant effectiveness that is potentially linked to its richness in diversified polyphenolic content. The aim of the present study was to determine the role of cranberry polyphenolic fractions in oxidative stress (OxS), inflammation and mitochondrial functions using intestinal Caco-2/15 cells. The combination of HPLC and UltraPerformance LC庐-tandem quadrupole (UPLC-TQD) techniques allowed us to characterize the profile of low, medium and high molecular mass polyphenolic compounds in cranberry extracts. The medium molecular mass fraction was enriched with flavonoids and procyanidin dimers whereas procyanidin oligomers (DP \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt; 4) were the dominant class of polyphenols in the high molecular mass fraction. Pre-incubation of Caco-2/15 cells with these cranberry extracts prevented iron/ascorbate-mediated lipid peroxidation and counteracted lipopolysaccharide-mediated inflammation as evidenced by the decrease in pro-inflammatory cytokines (TNF-伪 and interleukin-6), cyclo-oxygenase-2 and prostaglandin E2. Cranberry polyphenols (CP) fractions limited both nuclear factor 魏B activation and Nrf2 down-regulation. Consistently, cranberry procyanidins alleviated OxS-dependent mitochondrial dysfunctions as shown by the rise in ATP production and the up-regulation of Bcl-2, as well as the decline of protein expression of cytochrome c and apoptotic-inducing factor. These mitochondrial effects were associated with a significant stimulation of peroxisome-proliferator-activated receptor 纬 co-activator-1-伪, a central inducing factor of mitochondrial biogenesis and transcriptional co-activator of numerous downstream mediators. Finally, cranberry procyanidins forestalled the effect of iron/ascorbate on the protein expression of mitochondrial transcription factors (mtTFA, mtTFB1, mtTFB2). Our findings provide evidence for the capacity of CP to reduce intestinal OxS and inflammation while improving mitochondrial dysfunction.","internal_url":"https://www.academia.edu/19380178/Prevention_of_oxidative_stress_inflammation_and_mitochondrial_dysfunction_in_the_intestine_by_different_cranberry_phenolic_fractions","translated_internal_url":"","created_at":"2015-12-02T14:00:34.930-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":39643530,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":11545760,"work_id":19380178,"tagging_user_id":39643530,"tagged_user_id":31248312,"co_author_invite_id":null,"email":"e***y@recherche-ste-justine.qc.ca","affiliation":"Universit茅 de Montr茅al","display_order":0,"name":"Emile Levy","title":"Prevention of oxidative stress, inflammation and mitochondrial dysfunction in the intestine by different cranberry phenolic fractions"},{"id":11545772,"work_id":19380178,"tagging_user_id":39643530,"tagged_user_id":31223745,"co_author_invite_id":null,"email":"e***n@recherche-ste-justine.qc.ca","display_order":4194304,"name":"Edgard Delvin","title":"Prevention of oxidative stress, inflammation and mitochondrial dysfunction in the intestine by different cranberry phenolic fractions"},{"id":11545782,"work_id":19380178,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":217950,"email":"a***e@criucpq.ulaval.ca","display_order":7340032,"name":"Andr茅 Marette","title":"Prevention of oxidative stress, inflammation and mitochondrial dysfunction in the intestine by different cranberry phenolic fractions"},{"id":11545787,"work_id":19380178,"tagging_user_id":39643530,"tagged_user_id":31309978,"co_author_invite_id":2711269,"email":"m***n@gmail.com","display_order":7864320,"name":"Alain Montoudis","title":"Prevention of oxidative stress, inflammation and mitochondrial dysfunction in the intestine by different cranberry phenolic fractions"}],"downloadable_attachments":[],"slug":"Prevention_of_oxidative_stress_inflammation_and_mitochondrial_dysfunction_in_the_intestine_by_different_cranberry_phenolic_fractions","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":39643530,"first_name":"Carole","middle_initials":null,"last_name":"Garofalo","page_name":"CaroleGarofalo","domain_name":"independent","created_at":"2015-12-02T13:59:52.848-08:00","display_name":"Carole Garofalo","url":"https://independent.academia.edu/CaroleGarofalo"},"attachments":[],"research_interests":[{"id":9334,"name":"Inflammation","url":"https://www.academia.edu/Documents/in/Inflammation"},{"id":14292,"name":"Oxidative Stress","url":"https://www.academia.edu/Documents/in/Oxidative_Stress"},{"id":15719,"name":"Mitochondria","url":"https://www.academia.edu/Documents/in/Mitochondria"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":51711,"name":"Antioxidants","url":"https://www.academia.edu/Documents/in/Antioxidants"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":72314,"name":"Fatty acids","url":"https://www.academia.edu/Documents/in/Fatty_acids"},{"id":233372,"name":"Lipid peroxidation","url":"https://www.academia.edu/Documents/in/Lipid_peroxidation"},{"id":291136,"name":"Intestines","url":"https://www.academia.edu/Documents/in/Intestines"},{"id":314125,"name":"Caco-2 cells","url":"https://www.academia.edu/Documents/in/Caco-2_cells"},{"id":354056,"name":"Plant extracts","url":"https://www.academia.edu/Documents/in/Plant_extracts"},{"id":434453,"name":"Oxidative phosphorylation","url":"https://www.academia.edu/Documents/in/Oxidative_phosphorylation"},{"id":690437,"name":"Vaccinium Macrocarpon","url":"https://www.academia.edu/Documents/in/Vaccinium_Macrocarpon"},{"id":948028,"name":"Proanthocyanidins","url":"https://www.academia.edu/Documents/in/Proanthocyanidins"},{"id":1223957,"name":"Catechin","url":"https://www.academia.edu/Documents/in/Catechin"},{"id":1816594,"name":"Adenosine Triphosphate","url":"https://www.academia.edu/Documents/in/Adenosine_Triphosphate"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19380177"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380177/Effect_of_clentiazem_on_lipid_profile_lipoprotein_composition_and_aortic_fatty_streaks_in_cholesterol_fed_rabbits"><img alt="Research paper thumbnail of Effect of clentiazem on lipid profile, lipoprotein composition and aortic fatty streaks in cholesterol-fed rabbits" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380177/Effect_of_clentiazem_on_lipid_profile_lipoprotein_composition_and_aortic_fatty_streaks_in_cholesterol_fed_rabbits">Effect of clentiazem on lipid profile, lipoprotein composition and aortic fatty streaks in cholesterol-fed rabbits</a></div><div class="wp-workCard_item"><span>Atherosclerosis</span><span>, 1991</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Numerous experimental studies have reported that common antihypertensive drugs such as diuretics,...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Numerous experimental studies have reported that common antihypertensive drugs such as diuretics, beta-blockers, and methyldopa have adverse effects on plasma lipids and lipoproteins. The present study was designed to define the effect of clentiazem (10 mg/kg/day) an antihypertensive drug, on hyperlipidemia in rabbits on a cholesterol-rich diet (1%) for 12 weeks. Compared with controls, clentiazem treated rabbits had lower plasma concentrations of triglycerides (55%), total cholesterol (24%), free cholesterol (27%), esterified cholesterol (23%) and phospholipids (24%). The decrease in cholesterol was accounted for by a reduction of VLDL-cholesterol (13%), IDL-cholesterol (24%) and primarily LDL-cholesterol (45%). Neither HDL-cholesterol nor chemical composition of VLDL, IDL, LDL and HDL was altered. When the aortic atherosclerotic involvement was evaluated by computerized planimetry, a 24% reduction of lesions was noted in clentiazem treated animals (P less than 0.05). Similarly, cholesterol content extracted from aortic wall was decreased. Our data therefore demonstrated that clentiazem is a potential antiatherosclerotic agent capable of decreasing plasma lipids and atherogenic lipoproteins as well as aortic fatty streaks.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380177"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380177"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380177; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380177]").text(description); $(".js-view-count[data-work-id=19380177]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19380177; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19380177']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19380177, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=19380177]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380177,"title":"Effect of clentiazem on lipid profile, lipoprotein composition and aortic fatty streaks in cholesterol-fed rabbits","translated_title":"","metadata":{"abstract":"Numerous experimental studies have reported that common antihypertensive drugs such as diuretics, beta-blockers, and methyldopa have adverse effects on plasma lipids and lipoproteins. The present study was designed to define the effect of clentiazem (10 mg/kg/day) an antihypertensive drug, on hyperlipidemia in rabbits on a cholesterol-rich diet (1%) for 12 weeks. Compared with controls, clentiazem treated rabbits had lower plasma concentrations of triglycerides (55%), total cholesterol (24%), free cholesterol (27%), esterified cholesterol (23%) and phospholipids (24%). The decrease in cholesterol was accounted for by a reduction of VLDL-cholesterol (13%), IDL-cholesterol (24%) and primarily LDL-cholesterol (45%). Neither HDL-cholesterol nor chemical composition of VLDL, IDL, LDL and HDL was altered. When the aortic atherosclerotic involvement was evaluated by computerized planimetry, a 24% reduction of lesions was noted in clentiazem treated animals (P less than 0.05). Similarly, cholesterol content extracted from aortic wall was decreased. Our data therefore demonstrated that clentiazem is a potential antiatherosclerotic agent capable of decreasing plasma lipids and atherogenic lipoproteins as well as aortic fatty streaks.","publication_date":{"day":null,"month":null,"year":1991,"errors":{}},"publication_name":"Atherosclerosis"},"translated_abstract":"Numerous experimental studies have reported that common antihypertensive drugs such as diuretics, beta-blockers, and methyldopa have adverse effects on plasma lipids and lipoproteins. The present study was designed to define the effect of clentiazem (10 mg/kg/day) an antihypertensive drug, on hyperlipidemia in rabbits on a cholesterol-rich diet (1%) for 12 weeks. Compared with controls, clentiazem treated rabbits had lower plasma concentrations of triglycerides (55%), total cholesterol (24%), free cholesterol (27%), esterified cholesterol (23%) and phospholipids (24%). The decrease in cholesterol was accounted for by a reduction of VLDL-cholesterol (13%), IDL-cholesterol (24%) and primarily LDL-cholesterol (45%). Neither HDL-cholesterol nor chemical composition of VLDL, IDL, LDL and HDL was altered. When the aortic atherosclerotic involvement was evaluated by computerized planimetry, a 24% reduction of lesions was noted in clentiazem treated animals (P less than 0.05). Similarly, cholesterol content extracted from aortic wall was decreased. Our data therefore demonstrated that clentiazem is a potential antiatherosclerotic agent capable of decreasing plasma lipids and atherogenic lipoproteins as well as aortic fatty streaks.","internal_url":"https://www.academia.edu/19380177/Effect_of_clentiazem_on_lipid_profile_lipoprotein_composition_and_aortic_fatty_streaks_in_cholesterol_fed_rabbits","translated_internal_url":"","created_at":"2015-12-02T14:00:34.776-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":39643530,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":11545763,"work_id":19380177,"tagging_user_id":39643530,"tagged_user_id":31248312,"co_author_invite_id":null,"email":"e***y@recherche-ste-justine.qc.ca","affiliation":"Universit茅 de Montr茅al","display_order":0,"name":"Emile Levy","title":"Effect of clentiazem on lipid profile, lipoprotein composition and aortic fatty streaks in cholesterol-fed rabbits"},{"id":11545799,"work_id":19380177,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":2077458,"email":"d***l@lhrionhealth.ca","display_order":4194304,"name":"D. Bouthillier","title":"Effect of clentiazem on lipid profile, lipoprotein composition and aortic fatty streaks in cholesterol-fed rabbits"}],"downloadable_attachments":[],"slug":"Effect_of_clentiazem_on_lipid_profile_lipoprotein_composition_and_aortic_fatty_streaks_in_cholesterol_fed_rabbits","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":39643530,"first_name":"Carole","middle_initials":null,"last_name":"Garofalo","page_name":"CaroleGarofalo","domain_name":"independent","created_at":"2015-12-02T13:59:52.848-08:00","display_name":"Carole Garofalo","url":"https://independent.academia.edu/CaroleGarofalo"},"attachments":[],"research_interests":[{"id":8015,"name":"Atherosclerosis","url":"https://www.academia.edu/Documents/in/Atherosclerosis"},{"id":52055,"name":"Lipids","url":"https://www.academia.edu/Documents/in/Lipids"},{"id":90514,"name":"Cholesterol","url":"https://www.academia.edu/Documents/in/Cholesterol"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":184609,"name":"Lipid metabolism","url":"https://www.academia.edu/Documents/in/Lipid_metabolism"},{"id":227285,"name":"Lipoprotein(a)","url":"https://www.academia.edu/Documents/in/Lipoprotein_a_-1"},{"id":227299,"name":"Triglycerides","url":"https://www.academia.edu/Documents/in/Triglycerides"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":458879,"name":"Lipoproteins","url":"https://www.academia.edu/Documents/in/Lipoproteins"},{"id":788677,"name":"Rabbits","url":"https://www.academia.edu/Documents/in/Rabbits"},{"id":801998,"name":"Lipid Profile","url":"https://www.academia.edu/Documents/in/Lipid_Profile"},{"id":1035092,"name":"Aorta","url":"https://www.academia.edu/Documents/in/Aorta"}],"urls":[{"id":6101555,"url":"http://linkinghub.elsevier.com/retrieve/pii/002191509190108F"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="12440504"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/12440504/Circulating_Docosahexaenoic_Acid_Levels_Are_Associated_with_Fetal_Insulin_Sensitivity"><img alt="Research paper thumbnail of Circulating Docosahexaenoic Acid Levels Are Associated with Fetal Insulin Sensitivity" class="work-thumbnail" src="https://attachments.academia-assets.com/46182787/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/12440504/Circulating_Docosahexaenoic_Acid_Levels_Are_Associated_with_Fetal_Insulin_Sensitivity">Circulating Docosahexaenoic Acid Levels Are Associated with Fetal Insulin Sensitivity</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/CaroleGarofalo">Carole Garofalo</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://umontreal.academia.edu/EmileLevy">Emile Levy</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/AlainMontoudis">Alain Montoudis</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/AnnemoniqueNuyt">Anne-monique Nuyt</a></span></div><div class="wp-workCard_item"><span>PLoS ONE</span><span>, 2014</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="74cb523c9d02cddd30106248f46aedf3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":46182787,"asset_id":12440504,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/46182787/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="12440504"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="12440504"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12440504; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "74cb523c9d02cddd30106248f46aedf3" } } $('.js-work-strip[data-work-id=12440504]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12440504,"title":"Circulating Docosahexaenoic Acid Levels Are Associated with Fetal Insulin Sensitivity","translated_title":"","metadata":{"grobid_abstract":"Background: Arachidonic acid (AA; C20:4 n-6) and docosahexaenoic acid (DHA; C22:6 n-3) are important long-chain polyunsaturated fatty acids (LC-PUFA) in maintaining pancreatic beta-cell structure and function. Newborns of gestational diabetic mothers are more susceptible to the development of type 2 diabetes in adulthood. It is not known whether low circulating AA or DHA is involved in perinatally ''programming'' this susceptibility. This study aimed to assess whether circulating concentrations of AA, DHA and other fatty acids are associated with fetal insulin sensitivity or beta-cell function, and whether low circulating concentrations of AA or DHA are involved in compromised fetal insulin sensitivity in gestational diabetic pregnancies.","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"PLoS ONE","grobid_abstract_attachment_id":46182787},"translated_abstract":null,"internal_url":"https://www.academia.edu/12440504/Circulating_Docosahexaenoic_Acid_Levels_Are_Associated_with_Fetal_Insulin_Sensitivity","translated_internal_url":"","created_at":"2015-05-18T05:12:39.014-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31248312,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":564457,"work_id":12440504,"tagging_user_id":31248312,"tagged_user_id":39643530,"co_author_invite_id":217969,"email":"c***o@recherche-ste-justine.qc.ca","display_order":0,"name":"Carole Garofalo","title":"Circulating Docosahexaenoic Acid Levels Are Associated with Fetal Insulin Sensitivity"},{"id":564386,"work_id":12440504,"tagging_user_id":31248312,"tagged_user_id":null,"co_author_invite_id":217937,"email":"z***3@163.com","display_order":null,"name":"Zhong-Cheng Luo","title":"Circulating Docosahexaenoic Acid Levels Are Associated with 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"profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19380176"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380176/Maternal_and_fetal_leptin_adiponectin_levels_and_associations_with_fetal_insulin_sensitivity"><img alt="Research paper thumbnail of Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380176/Maternal_and_fetal_leptin_adiponectin_levels_and_associations_with_fetal_insulin_sensitivity">Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity</a></div><div class="wp-workCard_item"><span>Obesity</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">It remains uncertain whether leptin and adiponectin levels are correlated in maternal vs. fetal c...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">It remains uncertain whether leptin and adiponectin levels are correlated in maternal vs. fetal circulations. Little is known about whether leptin and adiponectin affect insulin sensitivity during fetal life. In a prospective singleton pregnancy cohort (n = 248), we investigated leptin and adiponectin concentrations in maternal (at 24-28 and 32-35 weeks of gestation) and fetal circulations, and their associations with fetal insulin sensitivity (glucose/insulin ratio, proinsulin level). Comparing concentrations in cord vs. maternal blood, leptin levels were 50% lower, but adiponectin levels more than doubled. Adjusting for gestational age at blood sampling, consistent and similar positive correlations (correlation coefficients: 0.31-0.34, all P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.0001) were observed in leptin or adiponectin levels in maternal (at 24-28 or 32-25 weeks of gestation) vs. fetal circulations. For each SD increase in maternal plasma concentration at 24-28 weeks, cord plasma concentration increased by 12.7 (95% confidence interval 6.8-18.5) ng/ml for leptin, and 2.9 (1.8-4.0) 碌g/ml for adiponectin, respectively (adjusted P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.0001). Fetal insulin sensitivity was negatively associated with cord blood leptin (each SD increase was associated with a 5.4 (2.1-8.7) mg/dl/碌U/ml reduction in cord plasma glucose/insulin ratio, and a 5.6 (3.9, 7.4) pmol/l increase in proinsulin level, all adjusted P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.01) but not adiponectin (P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt; 0.4) levels). Similar associations were observed in nondiabetic full-term pregnancies (n = 211). The results consistently suggest a maternal impact on fetal leptin and adiponectin levels, which may be an early life pathway in maternal-fetal transmission of the propensity to obesity and insulin resistance.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380176"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380176"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380176; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380176]").text(description); $(".js-view-count[data-work-id=19380176]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19380176; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19380176']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19380176, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=19380176]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380176,"title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity","translated_title":"","metadata":{"abstract":"It remains uncertain whether leptin and adiponectin levels are correlated in maternal vs. fetal circulations. 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Adjusting for gestational age at blood sampling, consistent and similar positive correlations (correlation coefficients: 0.31-0.34, all P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.0001) were observed in leptin or adiponectin levels in maternal (at 24-28 or 32-25 weeks of gestation) vs. fetal circulations. For each SD increase in maternal plasma concentration at 24-28 weeks, cord plasma concentration increased by 12.7 (95% confidence interval 6.8-18.5) ng/ml for leptin, and 2.9 (1.8-4.0) 碌g/ml for adiponectin, respectively (adjusted P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.0001). Fetal insulin sensitivity was negatively associated with cord blood leptin (each SD increase was associated with a 5.4 (2.1-8.7) mg/dl/碌U/ml reduction in cord plasma glucose/insulin ratio, and a 5.6 (3.9, 7.4) pmol/l increase in proinsulin level, all adjusted P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.01) but not adiponectin (P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt; 0.4) levels). Similar associations were observed in nondiabetic full-term pregnancies (n = 211). The results consistently suggest a maternal impact on fetal leptin and adiponectin levels, which may be an early life pathway in maternal-fetal transmission of the propensity to obesity and insulin resistance.","publication_date":{"day":null,"month":null,"year":2013,"errors":{}},"publication_name":"Obesity"},"translated_abstract":"It remains uncertain whether leptin and adiponectin levels are correlated in maternal vs. fetal circulations. Little is known about whether leptin and adiponectin affect insulin sensitivity during fetal life. In a prospective singleton pregnancy cohort (n = 248), we investigated leptin and adiponectin concentrations in maternal (at 24-28 and 32-35 weeks of gestation) and fetal circulations, and their associations with fetal insulin sensitivity (glucose/insulin ratio, proinsulin level). Comparing concentrations in cord vs. maternal blood, leptin levels were 50% lower, but adiponectin levels more than doubled. Adjusting for gestational age at blood sampling, consistent and similar positive correlations (correlation coefficients: 0.31-0.34, all P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.0001) were observed in leptin or adiponectin levels in maternal (at 24-28 or 32-25 weeks of gestation) vs. fetal circulations. For each SD increase in maternal plasma concentration at 24-28 weeks, cord plasma concentration increased by 12.7 (95% confidence interval 6.8-18.5) ng/ml for leptin, and 2.9 (1.8-4.0) 碌g/ml for adiponectin, respectively (adjusted P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.0001). Fetal insulin sensitivity was negatively associated with cord blood leptin (each SD increase was associated with a 5.4 (2.1-8.7) mg/dl/碌U/ml reduction in cord plasma glucose/insulin ratio, and a 5.6 (3.9, 7.4) pmol/l increase in proinsulin level, all adjusted P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.01) but not adiponectin (P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt; 0.4) levels). Similar associations were observed in nondiabetic full-term pregnancies (n = 211). The results consistently suggest a maternal impact on fetal leptin and adiponectin levels, which may be an early life pathway in maternal-fetal transmission of the propensity to obesity and insulin resistance.","internal_url":"https://www.academia.edu/19380176/Maternal_and_fetal_leptin_adiponectin_levels_and_associations_with_fetal_insulin_sensitivity","translated_internal_url":"","created_at":"2015-12-02T14:00:34.587-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":39643530,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":11545754,"work_id":19380176,"tagging_user_id":39643530,"tagged_user_id":31248312,"co_author_invite_id":null,"email":"e***y@recherche-ste-justine.qc.ca","affiliation":"Universit茅 de Montr茅al","display_order":0,"name":"Emile Levy","title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity"},{"id":11545770,"work_id":19380176,"tagging_user_id":39643530,"tagged_user_id":31223745,"co_author_invite_id":null,"email":"e***n@recherche-ste-justine.qc.ca","display_order":4194304,"name":"Edgard Delvin","title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity"},{"id":11545778,"work_id":19380176,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":217937,"email":"z***3@163.com","display_order":6291456,"name":"Zhong-cheng Luo","title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity"},{"id":11545780,"work_id":19380176,"tagging_user_id":39643530,"tagged_user_id":31459997,"co_author_invite_id":null,"email":"a***t@recherche-ste-justine.qc.ca","display_order":7340032,"name":"Anne-monique Nuyt","title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity"},{"id":11545786,"work_id":19380176,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":217939,"email":"w***r@umontreal.qc.ca","display_order":7864320,"name":"William Fraser","title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity"},{"id":11545791,"work_id":19380176,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":873919,"email":"b***n@umontreal.ca","display_order":8126464,"name":"Bryna Shatenstein","title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity"},{"id":11545792,"work_id":19380176,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":236514,"email":"c***a@dani.umontreal.ca","display_order":8257536,"name":"Cheri Deal","title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity"}],"downloadable_attachments":[],"slug":"Maternal_and_fetal_leptin_adiponectin_levels_and_associations_with_fetal_insulin_sensitivity","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":39643530,"first_name":"Carole","middle_initials":null,"last_name":"Garofalo","page_name":"CaroleGarofalo","domain_name":"independent","created_at":"2015-12-02T13:59:52.848-08:00","display_name":"Carole Garofalo","url":"https://independent.academia.edu/CaroleGarofalo"},"attachments":[],"research_interests":[{"id":3851,"name":"Obesity","url":"https://www.academia.edu/Documents/in/Obesity"},{"id":28235,"name":"Multidisciplinary","url":"https://www.academia.edu/Documents/in/Multidisciplinary"},{"id":51373,"name":"Insulin Resistance","url":"https://www.academia.edu/Documents/in/Insulin_Resistance"},{"id":62112,"name":"Prospective studies","url":"https://www.academia.edu/Documents/in/Prospective_studies"},{"id":62550,"name":"Pregnancy","url":"https://www.academia.edu/Documents/in/Pregnancy"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":71300,"name":"Blood Glucose","url":"https://www.academia.edu/Documents/in/Blood_Glucose"},{"id":71400,"name":"Insulin","url":"https://www.academia.edu/Documents/in/Insulin"},{"id":98925,"name":"Female","url":"https://www.academia.edu/Documents/in/Female"},{"id":135357,"name":"Leptin","url":"https://www.academia.edu/Documents/in/Leptin"},{"id":346660,"name":"Adiponectin","url":"https://www.academia.edu/Documents/in/Adiponectin"},{"id":382075,"name":"Adult","url":"https://www.academia.edu/Documents/in/Adult"},{"id":770944,"name":"Fetus","url":"https://www.academia.edu/Documents/in/Fetus"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="12440495"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/12440495/Asymmetrical_regulation_of_scavenger_receptor_class_B_type_I_by_apical_and_basolateral_stimuli_using_Caco_2_cells"><img alt="Research paper thumbnail of Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco-2 cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/12440495/Asymmetrical_regulation_of_scavenger_receptor_class_B_type_I_by_apical_and_basolateral_stimuli_using_Caco_2_cells">Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco-2 cells</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/CaroleGarofalo">Carole Garofalo</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://umontreal.academia.edu/EmileLevy">Emile Levy</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/ValerieMarcil">Valerie Marcil</a></span></div><div class="wp-workCard_item"><span>Journal of Cellular Biochemistry</span><span>, 2007</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Cholesterol uptake and the mechanisms that regulate cholesterol translocation from the intestinal...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Cholesterol uptake and the mechanisms that regulate cholesterol translocation from the intestinal lumen into enterocytes remain for the most part unclear. Since scavenger receptor class B type I (SR-BI) has been suggested to play a role in cholesterol absorption, we investigated cellular SR-BI modulation by various potential effectors administered in both apical and basolateral sides of Caco-2 cells. With differentiation, Caco-2 cells increased SR-BI protein expression. Western blot analysis showed the ability of cholesterol and oxysterols in both cell compartments to reduce SR-BI protein expression. Among the n-3, n-6, and n-9 fatty acid families, only eicosapentaenoic acid was able to lower SR-BI protein expression on both sides, whereas apical alpha-linolenic acid decreased SR-BI abundance and basolateral arachidonic acid (AA) raised it. Epidermal growth factor and growth hormone, either in the apical or basolateral medium, diminished SR-BI cellular content, while insulin displayed the same effect only on the basolateral side. In the presence of proinflammatory agents (LPS, TNF-alpha, IFN-gamma), Caco-2 cells exhibited differential behavior. SR-BI was downregulated by lipopolysaccharide on both sides. Finally, WY-14643 fibrate diminished SR-BI protein expression when it was added to the apical medium. Biotinylation studies in response to selected stimuli revealed that regulatory modifications in SR-BI protein expression occurred for the most part at the apical cell surface irrespective of the effector location. Our data indicate that various effectors supplied to the apical and basolateral compartments may impact on SR-BI at the apical membrane, thus suggesting potential regulation of intestinal cholesterol absorption and distribution in various intracellular pools.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="12440495"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="12440495"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12440495; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12440495]").text(description); $(".js-view-count[data-work-id=12440495]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12440495; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12440495']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12440495, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=12440495]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12440495,"title":"Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco-2 cells","translated_title":"","metadata":{"abstract":"Cholesterol uptake and the mechanisms that regulate cholesterol translocation from the intestinal lumen into enterocytes remain for the most part unclear. Since scavenger receptor class B type I (SR-BI) has been suggested to play a role in cholesterol absorption, we investigated cellular SR-BI modulation by various potential effectors administered in both apical and basolateral sides of Caco-2 cells. With differentiation, Caco-2 cells increased SR-BI protein expression. Western blot analysis showed the ability of cholesterol and oxysterols in both cell compartments to reduce SR-BI protein expression. Among the n-3, n-6, and n-9 fatty acid families, only eicosapentaenoic acid was able to lower SR-BI protein expression on both sides, whereas apical alpha-linolenic acid decreased SR-BI abundance and basolateral arachidonic acid (AA) raised it. Epidermal growth factor and growth hormone, either in the apical or basolateral medium, diminished SR-BI cellular content, while insulin displayed the same effect only on the basolateral side. In the presence of proinflammatory agents (LPS, TNF-alpha, IFN-gamma), Caco-2 cells exhibited differential behavior. SR-BI was downregulated by lipopolysaccharide on both sides. Finally, WY-14643 fibrate diminished SR-BI protein expression when it was added to the apical medium. Biotinylation studies in response to selected stimuli revealed that regulatory modifications in SR-BI protein expression occurred for the most part at the apical cell surface irrespective of the effector location. Our data indicate that various effectors supplied to the apical and basolateral compartments may impact on SR-BI at the apical membrane, thus suggesting potential regulation of intestinal cholesterol absorption and distribution in various intracellular pools.","publication_date":{"day":null,"month":null,"year":2007,"errors":{}},"publication_name":"Journal of Cellular Biochemistry"},"translated_abstract":"Cholesterol uptake and the mechanisms that regulate cholesterol translocation from the intestinal lumen into enterocytes remain for the most part unclear. Since scavenger receptor class B type I (SR-BI) has been suggested to play a role in cholesterol absorption, we investigated cellular SR-BI modulation by various potential effectors administered in both apical and basolateral sides of Caco-2 cells. With differentiation, Caco-2 cells increased SR-BI protein expression. Western blot analysis showed the ability of cholesterol and oxysterols in both cell compartments to reduce SR-BI protein expression. Among the n-3, n-6, and n-9 fatty acid families, only eicosapentaenoic acid was able to lower SR-BI protein expression on both sides, whereas apical alpha-linolenic acid decreased SR-BI abundance and basolateral arachidonic acid (AA) raised it. Epidermal growth factor and growth hormone, either in the apical or basolateral medium, diminished SR-BI cellular content, while insulin displayed the same effect only on the basolateral side. In the presence of proinflammatory agents (LPS, TNF-alpha, IFN-gamma), Caco-2 cells exhibited differential behavior. SR-BI was downregulated by lipopolysaccharide on both sides. Finally, WY-14643 fibrate diminished SR-BI protein expression when it was added to the apical medium. Biotinylation studies in response to selected stimuli revealed that regulatory modifications in SR-BI protein expression occurred for the most part at the apical cell surface irrespective of the effector location. Our data indicate that various effectors supplied to the apical and basolateral compartments may impact on SR-BI at the apical membrane, thus suggesting potential regulation of intestinal cholesterol absorption and distribution in various intracellular pools.","internal_url":"https://www.academia.edu/12440495/Asymmetrical_regulation_of_scavenger_receptor_class_B_type_I_by_apical_and_basolateral_stimuli_using_Caco_2_cells","translated_internal_url":"","created_at":"2015-05-18T05:12:38.213-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31248312,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":564456,"work_id":12440495,"tagging_user_id":31248312,"tagged_user_id":39643530,"co_author_invite_id":217969,"email":"c***o@recherche-ste-justine.qc.ca","display_order":0,"name":"Carole Garofalo","title":"Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco-2 cells"},{"id":564438,"work_id":12440495,"tagging_user_id":31248312,"tagged_user_id":31307255,"co_author_invite_id":217967,"email":"v***l@hotmail.com","display_order":null,"name":"Valerie Marcil","title":"Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco-2 cells"},{"id":564474,"work_id":12440495,"tagging_user_id":31248312,"tagged_user_id":31223745,"co_author_invite_id":null,"email":"e***n@recherche-ste-justine.qc.ca","display_order":null,"name":"Edgard Delvin","title":"Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco-2 cells"},{"id":564446,"work_id":12440495,"tagging_user_id":31248312,"tagged_user_id":32265331,"co_author_invite_id":217968,"email":"d***t@umontreal.ca","display_order":null,"name":"Daniel Sinnett","title":"Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco-2 cells"}],"downloadable_attachments":[],"slug":"Asymmetrical_regulation_of_scavenger_receptor_class_B_type_I_by_apical_and_basolateral_stimuli_using_Caco_2_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":31248312,"first_name":"Emile","middle_initials":null,"last_name":"Levy","page_name":"EmileLevy","domain_name":"umontreal","created_at":"2015-05-18T05:12:19.584-07:00","display_name":"Emile Levy","url":"https://umontreal.academia.edu/EmileLevy"},"attachments":[],"research_interests":[{"id":60436,"name":"Cell Differentiation","url":"https://www.academia.edu/Documents/in/Cell_Differentiation"},{"id":60915,"name":"Cellular","url":"https://www.academia.edu/Documents/in/Cellular"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":72314,"name":"Fatty acids","url":"https://www.academia.edu/Documents/in/Fatty_acids"},{"id":90514,"name":"Cholesterol","url":"https://www.academia.edu/Documents/in/Cholesterol"},{"id":104853,"name":"Hormones","url":"https://www.academia.edu/Documents/in/Hormones"},{"id":122569,"name":"Cell Polarity","url":"https://www.academia.edu/Documents/in/Cell_Polarity"},{"id":314125,"name":"Caco-2 cells","url":"https://www.academia.edu/Documents/in/Caco-2_cells"},{"id":335983,"name":"Lipopolysaccharides","url":"https://www.academia.edu/Documents/in/Lipopolysaccharides"},{"id":782251,"name":"Cell Proliferation","url":"https://www.academia.edu/Documents/in/Cell_Proliferation"},{"id":989723,"name":"Caco 2 Cell","url":"https://www.academia.edu/Documents/in/Caco_2_Cell"},{"id":1296969,"name":"Molecular and Cellular Biochemistry","url":"https://www.academia.edu/Documents/in/Molecular_and_Cellular_Biochemistry"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":2468093,"name":"Cell Membrane","url":"https://www.academia.edu/Documents/in/Cell_Membrane"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="12440494"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/12440494/Modulation_of_intestinal_and_liver_fatty_acid_binding_proteins_in_Caco_2_cells_by_lipids_hormones_and_cytokines"><img alt="Research paper thumbnail of Modulation of intestinal and liver fatty acid-binding proteins in Caco-2 cells by lipids, hormones and cytokines" class="work-thumbnail" src="https://attachments.academia-assets.com/46182774/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/12440494/Modulation_of_intestinal_and_liver_fatty_acid_binding_proteins_in_Caco_2_cells_by_lipids_hormones_and_cytokines">Modulation of intestinal and liver fatty acid-binding proteins in Caco-2 cells by lipids, hormones and cytokines</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/CaroleGarofalo">Carole Garofalo</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://umontreal.academia.edu/EmileLevy">Emile Levy</a></span></div><div class="wp-workCard_item"><span>Journal of Cellular Biochemistry</span><span>, 2001</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c4c0869e78e30b744972dd69ceda3a4f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":46182774,"asset_id":12440494,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/46182774/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="12440494"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="12440494"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12440494; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12440494]").text(description); $(".js-view-count[data-work-id=12440494]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12440494; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12440494']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12440494, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "c4c0869e78e30b744972dd69ceda3a4f" } } $('.js-work-strip[data-work-id=12440494]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12440494,"title":"Modulation of intestinal and liver fatty acid-binding proteins in Caco-2 cells by lipids, hormones and cytokines","translated_title":"","metadata":{"grobid_abstract":"Intestinal and liver fatty acid binding proteins (I-and L-FABP) are thought to play a role in enterocyte fatty acid (FA) traf庐cking. Their modulation by cell differentiation and various potential effectors was investigated in the human Caco-2 cell line. With the acquisition of enterocytic features, Caco-2 cells seeded on plastic progressively increased L-FABP quantities, whereas I-FABP was not detectable even very late in the maturation process. On permeable 庐lters that improved differentiation markers (sucrase, alkaline phosphatase, transepithelial resistance), Caco-2 cells furthered their L-FABP content and expressed I-FABP. Western blot analysis showed a signi庐cant increase in I-and L-FABP expression following an 8-hour incubation period with butyric acid, oleic acid, and phosphatidylcholine. However, in all cases, I-FABP levels were higher than L-FABP concentrations regardless of the lipid substrates added. Similarly, hydrocortisone and insulin enhanced the cellular content of I-and L-FABP whereas leptin triggered I-FABP expression only after an 8-hour incubation. Finally, tumor necrosis factor-a was more effective in increasing the cytosolic amount of I-FABP levels. In conclusion, our data demonstrate that I-FABP expression is limited to fully differentiated Caco-2 cells and can be more easily regulated than L-FABP by lipids, hormones, and cytokines.","publication_date":{"day":null,"month":null,"year":2001,"errors":{}},"publication_name":"Journal of Cellular Biochemistry","grobid_abstract_attachment_id":46182774},"translated_abstract":null,"internal_url":"https://www.academia.edu/12440494/Modulation_of_intestinal_and_liver_fatty_acid_binding_proteins_in_Caco_2_cells_by_lipids_hormones_and_cytokines","translated_internal_url":"","created_at":"2015-05-18T05:12:38.104-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31248312,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":564455,"work_id":12440494,"tagging_user_id":31248312,"tagged_user_id":39643530,"co_author_invite_id":217969,"email":"c***o@recherche-ste-justine.qc.ca","display_order":0,"name":"Carole 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(HEPATOLOGY fine whether essential fatty acid (EFA) deficiency modi-1996;23:848-857.) fies the intrahepatic metabolism and biliary output of sterols in rats. EFA-deficient diet caused an impoverishment in linoleic, arachidonic, and docosahexaenoic","publication_date":{"day":null,"month":null,"year":1996,"errors":{}},"publication_name":"Hepatology","grobid_abstract_attachment_id":40587801},"translated_abstract":null,"internal_url":"https://www.academia.edu/19380175/Impact_of_essential_fatty_acid_deficiency_on_hepatic_sterol_metabolism_in_rats","translated_internal_url":"","created_at":"2015-12-02T14:00:34.303-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":39643530,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":11545756,"work_id":19380175,"tagging_user_id":39643530,"tagged_user_id":31248312,"co_author_invite_id":null,"email":"e***y@recherche-ste-justine.qc.ca","affiliation":"Universit茅 de Montr茅al","display_order":0,"name":"Emile Levy","title":"Impact of essential fatty acid deficiency on hepatic sterol metabolism in rats"},{"id":11545784,"work_id":19380175,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":217965,"email":"m***n@umontreal.ca","display_order":4194304,"name":"Moise Bendayan","title":"Impact of essential fatty acid deficiency on hepatic sterol metabolism in rats"},{"id":11545798,"work_id":19380175,"tagging_user_id":39643530,"tagged_user_id":57133755,"co_author_invite_id":217928,"email":"t***u@recherche-ste-justine.qc.ca","display_order":6291456,"name":"Th茅r猫se Rouleau","title":"Impact of essential fatty acid deficiency on hepatic sterol metabolism in rats"}],"downloadable_attachments":[{"id":40587801,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/40587801/thumbnails/1.jpg","file_name":"hep.510230428.pdf20151202-17091-1l73mne","download_url":"https://www.academia.edu/attachments/40587801/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Impact_of_essential_fatty_acid_deficienc.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/40587801/hep.510230428-libre.pdf20151202-17091-1l73mne?1449093975=\u0026response-content-disposition=attachment%3B+filename%3DImpact_of_essential_fatty_acid_deficienc.pdf\u0026Expires=1732617198\u0026Signature=BlGLy1iEsYKbcHDFlWFUslSGYIl8-t6vVigDbuladTsgH6gfzAaiPG3zLAHuSYLyb9TRp19aIxUNnXoC0UhaCAMHuWfwadDu43zI724xIhoY9dJ4i616VpCA6JQBWP4~9ZnmMsl80WqE3Bac9UqeYA4nRw27WiPvUn073bz3Y5QiBRJ0GqV2-nvBTTpqRYTcwLPCfJdJk9XrSij1MOgIcil0r6EK2slkl1om1ZMTA3EIl4KD0g9qao5h~L5UpywzFCShDpagkoiMl8d70ZKORG3O8~OrhXyEGC0UQdHxqS~rcuBLldExk-dHBPtoLjJNnBAyMHn2J4etD~2pl6omPw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Impact_of_essential_fatty_acid_deficiency_on_hepatic_sterol_metabolism_in_rats","translated_slug":"","page_count":10,"language":"en","content_type":"Work","owner":{"id":39643530,"first_name":"Carole","middle_initials":null,"last_name":"Garofalo","page_name":"CaroleGarofalo","domain_name":"independent","created_at":"2015-12-02T13:59:52.848-08:00","display_name":"Carole Garofalo","url":"https://independent.academia.edu/CaroleGarofalo"},"attachments":[{"id":40587801,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/40587801/thumbnails/1.jpg","file_name":"hep.510230428.pdf20151202-17091-1l73mne","download_url":"https://www.academia.edu/attachments/40587801/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Impact_of_essential_fatty_acid_deficienc.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/40587801/hep.510230428-libre.pdf20151202-17091-1l73mne?1449093975=\u0026response-content-disposition=attachment%3B+filename%3DImpact_of_essential_fatty_acid_deficienc.pdf\u0026Expires=1732617198\u0026Signature=BlGLy1iEsYKbcHDFlWFUslSGYIl8-t6vVigDbuladTsgH6gfzAaiPG3zLAHuSYLyb9TRp19aIxUNnXoC0UhaCAMHuWfwadDu43zI724xIhoY9dJ4i616VpCA6JQBWP4~9ZnmMsl80WqE3Bac9UqeYA4nRw27WiPvUn073bz3Y5QiBRJ0GqV2-nvBTTpqRYTcwLPCfJdJk9XrSij1MOgIcil0r6EK2slkl1om1ZMTA3EIl4KD0g9qao5h~L5UpywzFCShDpagkoiMl8d70ZKORG3O8~OrhXyEGC0UQdHxqS~rcuBLldExk-dHBPtoLjJNnBAyMHn2J4etD~2pl6omPw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":37773,"name":"Hepatology","url":"https://www.academia.edu/Documents/in/Hepatology"},{"id":71437,"name":"Liver","url":"https://www.academia.edu/Documents/in/Liver"},{"id":90514,"name":"Cholesterol","url":"https://www.academia.edu/Documents/in/Cholesterol"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":1611350,"name":"Docosahexaenoic Acid","url":"https://www.academia.edu/Documents/in/Docosahexaenoic_Acid"},{"id":2061395,"name":"Bile","url":"https://www.academia.edu/Documents/in/Bile-6"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19380174"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380174/The_distribution_of_microsomal_transfer_protein_MTP_and_apolipoprotein_b_in_endoplasmic_reticulum_ER_and_golgi_of_intestinal_absorptive_cells_possible_role_of_the_golgi_in_the_assembly_of_chylomicrons"><img alt="Research paper thumbnail of The distribution of microsomal transfer protein (MTP) and apolipoprotein b in endoplasmic reticulum (ER) and golgi of intestinal absorptive cells: possible role of the golgi in the assembly of chylomicrons" class="work-thumbnail" src="https://attachments.academia-assets.com/40587802/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380174/The_distribution_of_microsomal_transfer_protein_MTP_and_apolipoprotein_b_in_endoplasmic_reticulum_ER_and_golgi_of_intestinal_absorptive_cells_possible_role_of_the_golgi_in_the_assembly_of_chylomicrons">The distribution of microsomal transfer protein (MTP) and apolipoprotein b in endoplasmic reticulum (ER) and golgi of intestinal absorptive cells: possible role of the golgi in the assembly of chylomicrons</a></div><div class="wp-workCard_item"><span>Gastroenterology</span><span>, 2000</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="e3c269ea313f65b545cf5979dc3656d3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":40587802,"asset_id":19380174,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/40587802/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380174"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380174"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380174; 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These studies aim to identify regions of the lactase promoter involved in mediating the spatio-temporal expression pattern of the lactase gene and to utilize a novel photonic detection method for in vivo monitoring of promoter-reporter transgene expression in animals. Methods: 2.0-and 0.8kilobase fragments of the 5' flanking region of the rat lactase gene were cloned upstream of a firefly luciferase reporter and transfected into intestinal Caco-2 cells as a culture correlate of promoter activity. Transgenic mice harboring those same lactase promoter-reporter constructs were generated and screened for transgene expression by in vivo photonic detection with an intensified charge-coupled device (ICCD) camera. Luciferase activity was measured quantitatively by luminometer assays in multiple organs, including intestinal segments, harvested from pre and post-weaned mice. Results: Pre-weaned offspring of a 2-kb lactase promoter-reporter transgenic line express high-level luciferase activity in the small intestine (\u003e 8,000 fold over background) with maximal expression in the middle segments. Luciferase expression was barely detectable 芦 3 fold over background) in colon, stomach, kidney, lung, liver, spleen, and brain. Post-weaned 30-day offspring undergo a region-specific decline in luciferase expression in the small intestine (25% activity in the proximal and middle segments and 1% in the distal segments) relative to pre-weaned levels. In comparison to the full length promoter, the 0.8 -kb promoterreporter construct expressed low-level luciferase activity 芦 50 fold over background) in multiple organs and throughout the GI tract in transgenic mice. Conclusions: A 2.0-kilobase fragment of the lactase promoter directs region-specific expression in the small intestine of transgenic mice. The pattern of expression mimics that of endogenous lactase with respect to spatial restriction during maturation and differs from that described for related transgenic constructs. Important tissue-specific enhancing elements may reside in the region between 0.8-2.0 kb upstream of the lactase transcription start-site. Photonic detection with the ICCD camera is a sensitive method to rapidly screen for intestinal expression of a luciferase reporter gene in living transgenic mice.","publication_date":{"day":null,"month":null,"year":2000,"errors":{}},"publication_name":"Gastroenterology","grobid_abstract_attachment_id":40587802},"translated_abstract":null,"internal_url":"https://www.academia.edu/19380174/The_distribution_of_microsomal_transfer_protein_MTP_and_apolipoprotein_b_in_endoplasmic_reticulum_ER_and_golgi_of_intestinal_absorptive_cells_possible_role_of_the_golgi_in_the_assembly_of_chylomicrons","translated_internal_url":"","created_at":"2015-12-02T14:00:34.192-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":39643530,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":11545759,"work_id":19380174,"tagging_user_id":39643530,"tagged_user_id":31248312,"co_author_invite_id":null,"email":"e***y@recherche-ste-justine.qc.ca","affiliation":"Universit茅 de Montr茅al","display_order":0,"name":"Emile Levy","title":"The distribution of microsomal transfer protein (MTP) and apolipoprotein b in endoplasmic reticulum (ER) and golgi of intestinal absorptive cells: possible role of the golgi in the assembly of chylomicrons"},{"id":11545785,"work_id":19380174,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":217965,"email":"m***n@umontreal.ca","display_order":4194304,"name":"Moise Bendayan","title":"The distribution of microsomal transfer protein (MTP) and apolipoprotein b in endoplasmic reticulum (ER) and golgi of intestinal absorptive cells: possible role of the golgi in the assembly of 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Reticulum","url":"https://www.academia.edu/Documents/in/Endoplasmic_Reticulum"},{"id":227277,"name":"Apolipoprotein B","url":"https://www.academia.edu/Documents/in/Apolipoprotein_B"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":288383,"name":"Intestinal absorption","url":"https://www.academia.edu/Documents/in/Intestinal_absorption"},{"id":1239755,"name":"Neurosciences","url":"https://www.academia.edu/Documents/in/Neurosciences"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="12440489"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/12440489/Immunolocalization_ontogeny_and_regulation_of_microsomal_transfer_protein_MTP_in_human_fetal_intestine"><img alt="Research paper thumbnail of Immunolocalization, ontogeny and regulation of microsomal transfer protein (MTP) in human fetal intestine" class="work-thumbnail" src="https://attachments.academia-assets.com/46182797/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/12440489/Immunolocalization_ontogeny_and_regulation_of_microsomal_transfer_protein_MTP_in_human_fetal_intestine">Immunolocalization, ontogeny and regulation of microsomal transfer protein (MTP) in human fetal intestine</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/CaroleGarofalo">Carole Garofalo</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://umontreal.academia.edu/EmileLevy">Emile Levy</a></span></div><div class="wp-workCard_item"><span>Gastroenterology</span><span>, 2000</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="10b0f7e7060d980ea014810cbba9a8bd" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":46182797,"asset_id":12440489,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/46182797/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="12440489"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="12440489"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12440489; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12440489]").text(description); $(".js-view-count[data-work-id=12440489]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12440489; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12440489']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12440489, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "10b0f7e7060d980ea014810cbba9a8bd" } } $('.js-work-strip[data-work-id=12440489]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12440489,"title":"Immunolocalization, ontogeny and regulation of microsomal transfer protein (MTP) in human fetal intestine","translated_title":"","metadata":{"grobid_abstract":"Background and Aims: Lactase gene transcription is spatially restricted to the proximal and middle small intestine of the developing mouse. These studies aim to identify regions of the lactase promoter involved in mediating the spatio-temporal expression pattern of the lactase gene and to utilize a novel photonic detection method for in vivo monitoring of promoter-reporter transgene expression in animals. Methods: 2.0-and 0.8kilobase fragments of the 5' flanking region of the rat lactase gene were cloned upstream of a firefly luciferase reporter and transfected into intestinal Caco-2 cells as a culture correlate of promoter activity. Transgenic mice harboring those same lactase promoter-reporter constructs were generated and screened for transgene expression by in vivo photonic detection with an intensified charge-coupled device (ICCD) camera. Luciferase activity was measured quantitatively by luminometer assays in multiple organs, including intestinal segments, harvested from pre and post-weaned mice. Results: Pre-weaned offspring of a 2-kb lactase promoter-reporter transgenic line express high-level luciferase activity in the small intestine (\u003e 8,000 fold over background) with maximal expression in the middle segments. Luciferase expression was barely detectable 芦 3 fold over background) in colon, stomach, kidney, lung, liver, spleen, and brain. Post-weaned 30-day offspring undergo a region-specific decline in luciferase expression in the small intestine (25% activity in the proximal and middle segments and 1% in the distal segments) relative to pre-weaned levels. In comparison to the full length promoter, the 0.8 -kb promoterreporter construct expressed low-level luciferase activity 芦 50 fold over background) in multiple organs and throughout the GI tract in transgenic mice. Conclusions: A 2.0-kilobase fragment of the lactase promoter directs region-specific expression in the small intestine of transgenic mice. The pattern of expression mimics that of endogenous lactase with respect to spatial restriction during maturation and differs from that described for related transgenic constructs. Important tissue-specific enhancing elements may reside in the region between 0.8-2.0 kb upstream of the lactase transcription start-site. Photonic detection with the ICCD camera is a sensitive method to rapidly screen for intestinal expression of a luciferase reporter gene in living transgenic mice.","publication_date":{"day":null,"month":null,"year":2000,"errors":{}},"publication_name":"Gastroenterology","grobid_abstract_attachment_id":46182797},"translated_abstract":null,"internal_url":"https://www.academia.edu/12440489/Immunolocalization_ontogeny_and_regulation_of_microsomal_transfer_protein_MTP_in_human_fetal_intestine","translated_internal_url":"","created_at":"2015-05-18T05:12:37.504-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31248312,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":564454,"work_id":12440489,"tagging_user_id":31248312,"tagged_user_id":39643530,"co_author_invite_id":217969,"email":"c***o@recherche-ste-justine.qc.ca","display_order":0,"name":"Carole Garofalo","title":"Immunolocalization, ontogeny and regulation of microsomal transfer protein (MTP) in human fetal intestine"},{"id":564469,"work_id":12440489,"tagging_user_id":31248312,"tagged_user_id":31223745,"co_author_invite_id":null,"email":"e***n@recherche-ste-justine.qc.ca","display_order":null,"name":"Edgard Delvin","title":"Immunolocalization, ontogeny and regulation of microsomal transfer protein (MTP) in human fetal intestine"}],"downloadable_attachments":[{"id":46182797,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/46182797/thumbnails/1.jpg","file_name":"S0016-5085_2800_2983249-720160602-19467-l6tizl.pdf","download_url":"https://www.academia.edu/attachments/46182797/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Immunolocalization_ontogeny_and_regulati.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/46182797/S0016-5085_2800_2983249-720160602-19467-l6tizl-libre.pdf?1464914830=\u0026response-content-disposition=attachment%3B+filename%3DImmunolocalization_ontogeny_and_regulati.pdf\u0026Expires=1731934979\u0026Signature=NCWtUOA3lobIi5Xy69lMTyoen4R8cUArEuJ4dxAQYmR66pHK2L8n7nknCY~WOI~fopXP8EXqLolRDwDmULCK7M-Qq5FJCGq4rkoL~mrHkuUAvdYV0MvDAfW4SKXeZ4JeFlKzDMY5AYiIpAo8~nTosmrRsQyJ3mwdim9bKf~yICrpkKgBBRx~npGO9CQYnp0554il~01G6YzkbP1agXS~FIYT~3DV66FnbxI4aA93pBqxCISVhEi2lnX3WEsttYOhc5N46hBwfjiLbqjFfUujetdqI-u6dLODqjLdXDvHalFvKYGc24eRe~KERQ1GzVyvqsb7tAVz8JEySdFXdLkF5Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Immunolocalization_ontogeny_and_regulation_of_microsomal_transfer_protein_MTP_in_human_fetal_intestine","translated_slug":"","page_count":1,"language":"en","content_type":"Work","owner":{"id":31248312,"first_name":"Emile","middle_initials":null,"last_name":"Levy","page_name":"EmileLevy","domain_name":"umontreal","created_at":"2015-05-18T05:12:19.584-07:00","display_name":"Emile Levy","url":"https://umontreal.academia.edu/EmileLevy"},"attachments":[{"id":46182797,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/46182797/thumbnails/1.jpg","file_name":"S0016-5085_2800_2983249-720160602-19467-l6tizl.pdf","download_url":"https://www.academia.edu/attachments/46182797/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Immunolocalization_ontogeny_and_regulati.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/46182797/S0016-5085_2800_2983249-720160602-19467-l6tizl-libre.pdf?1464914830=\u0026response-content-disposition=attachment%3B+filename%3DImmunolocalization_ontogeny_and_regulati.pdf\u0026Expires=1731934979\u0026Signature=NCWtUOA3lobIi5Xy69lMTyoen4R8cUArEuJ4dxAQYmR66pHK2L8n7nknCY~WOI~fopXP8EXqLolRDwDmULCK7M-Qq5FJCGq4rkoL~mrHkuUAvdYV0MvDAfW4SKXeZ4JeFlKzDMY5AYiIpAo8~nTosmrRsQyJ3mwdim9bKf~yICrpkKgBBRx~npGO9CQYnp0554il~01G6YzkbP1agXS~FIYT~3DV66FnbxI4aA93pBqxCISVhEi2lnX3WEsttYOhc5N46hBwfjiLbqjFfUujetdqI-u6dLODqjLdXDvHalFvKYGc24eRe~KERQ1GzVyvqsb7tAVz8JEySdFXdLkF5Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":3274,"name":"Gastroenterology","url":"https://www.academia.edu/Documents/in/Gastroenterology"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":1239755,"name":"Neurosciences","url":"https://www.academia.edu/Documents/in/Neurosciences"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> </div><div class="profile--tab_content_container js-tab-pane tab-pane" data-section-id="4213235" id="papers"><div class="js-work-strip profile--work_container" data-work-id="19380187"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380187/Localization_Structure_and_Regulation_of_AMP_Activated_Protein_Kinase_in_the_Small_Intestine"><img alt="Research paper thumbnail of Localization, Structure and Regulation of AMP-Activated Protein Kinase in the Small Intestine" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380187/Localization_Structure_and_Regulation_of_AMP_Activated_Protein_Kinase_in_the_Small_Intestine">Localization, Structure and Regulation of AMP-Activated Protein Kinase in the Small Intestine</a></div><div class="wp-workCard_item"><span>Gastroenterology</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380187"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380187"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380187; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19380185"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380185/Combined_n_3_and_n_6_essential_fatty_deficiency_is_a_potent_modulator_of_plasma_lipids_lipoprotein_composition_and_lipolytic_enzymes"><img alt="Research paper thumbnail of Combined (n-3 and n-6) essential fatty deficiency is a potent modulator of plasma lipids, lipoprotein composition, and lipolytic enzymes" class="work-thumbnail" src="https://attachments.academia-assets.com/40587781/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380185/Combined_n_3_and_n_6_essential_fatty_deficiency_is_a_potent_modulator_of_plasma_lipids_lipoprotein_composition_and_lipolytic_enzymes">Combined (n-3 and n-6) essential fatty deficiency is a potent modulator of plasma lipids, lipoprotein composition, and lipolytic enzymes</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Essential fatty acids (EFA) are important structural and functional components of cell membranes....</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Essential fatty acids (EFA) are important structural and functional components of cell membranes. Their deficiency has been associated with several clinical and biochemical abnor- malities. In the present study, the lipid profile as well as the concentration, composition, and metabolism of lipoproteins were examined in rats rendered EFA-deficient over a period of 12 weeks. 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/></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/12440530/An_Intervention_to_Promote_Breast_Milk_Production_in_Mothers_of_Preterm_Infants">An Intervention to Promote Breast Milk Production in Mothers of Preterm Infants</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/CaroleGarofalo">Carole Garofalo</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://umontreal.academia.edu/EmileLevy">Emile Levy</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/AnnemoniqueNuyt">Anne-monique Nuyt</a></span></div><div class="wp-workCard_item"><span>Western journal of nursing research</span><span>, Jan 13, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">A pilot study was conducted to estimate the effects of a breast milk expression education and sup...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">A pilot study was conducted to estimate the effects of a breast milk expression education and support intervention on breast milk production outcomes in mothers of very and extremely preterm infants. Forty mothers of hospitalized preterm infants (&lt;30 weeks of gestation) were randomized to the experimental intervention or standard care for 6 weeks. Duration and frequency of breast milk expressions and volume of expressed breast milk were measured daily. Samples of breast milk were collected thrice during the study and analyzed for their lipid concentration. Mothers in the experimental group had a statistically significant higher duration of breast milk expression in min/day (p = .043). Differences observed between the two groups regarding the frequency of breast milk expression, volume of breast milk, and lipid concentration were not statistically significant. 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Other biological functions attribu...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Gastrointestinal peptides are involved in modulating appetite. Other biological functions attributed to them include the regulation of lipid homeostasis. However, data concerning PYY remain fragmentary. The objectives of the study were: (i) To determine the effect of PYY on intestinal transport and synthesis of cholesterol, the biogenesis of apolipoproteins (apos) and assembly of lipoproteins and (ii) To analyze whether the effects of PYY are similar according to whether cells are exposed to PYY on apical or basolateral surface. Caco-2/15 cells were incubated with PYY (1-36) administered either to the apical or basolateral medium, at concentrations of 50 or 200 nM for 24 hours. De novo synthesis of cholesterol, cholesterol uptake, and assembly of lipoproteins were evaluated through the incorporation of [(14)C]-acetate, [(14)C]-cholesterol, and [(14)C]-oleate, respectively. Biogenesis of apos (A-I, A-IV, E, B-48 and B-100) was examined by the incorporation of [(35)S]-methionine. 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The ...","publication_date":{"day":null,"month":null,"year":2012,"errors":{}},"publication_name":"PloS one"},"translated_abstract":"Gastrointestinal peptides are involved in modulating appetite. Other biological functions attributed to them include the regulation of lipid homeostasis. However, data concerning PYY remain fragmentary. The objectives of the study were: (i) To determine the effect of PYY on intestinal transport and synthesis of cholesterol, the biogenesis of apolipoproteins (apos) and assembly of lipoproteins and (ii) To analyze whether the effects of PYY are similar according to whether cells are exposed to PYY on apical or basolateral surface. Caco-2/15 cells were incubated with PYY (1-36) administered either to the apical or basolateral medium, at concentrations of 50 or 200 nM for 24 hours. De novo synthesis of cholesterol, cholesterol uptake, and assembly of lipoproteins were evaluated through the incorporation of [(14)C]-acetate, [(14)C]-cholesterol, and [(14)C]-oleate, respectively. Biogenesis of apos (A-I, A-IV, E, B-48 and B-100) was examined by the incorporation of [(35)S]-methionine. 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We investigated in vitro some of the mechanisms of this transport. Caco-2/15 cells internalize leptin from the apical medium and release it through transcytosis in the basal medium in a time- temperature-dependent and saturable fashion. Leptin receptors are revealed on the apical brush-border membrane of the Caco-2 cells. RNA-mediated silencing of the receptor led to decreases in the uptake and basolateral release. Leptin in the basal medium was found bound to the soluble form of its receptor. An inhibitor of clathrin-dependent endocytosis (chlorpromazine) decreased leptin uptake. Confocal immunocytochemistry and the use of brefeldin A and okadaic acid revealed the passage of leptin through the Golgi apparatus. We propose that leptin transcytosis by intestinal cells depends on its receptor, on clathrin-coated vesicles and transits through the Golgi apparatus.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="49eec4b9e24dda6aa9bc3511cc7c0614" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":40587796,"asset_id":19380183,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/40587796/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380183"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380183"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380183; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380183]").text(description); $(".js-view-count[data-work-id=19380183]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19380183; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19380183']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19380183, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "49eec4b9e24dda6aa9bc3511cc7c0614" } } $('.js-work-strip[data-work-id=19380183]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380183,"title":"Receptor-Mediated Transcytosis of Leptin through Human Intestinal Cells In Vitro","translated_title":"","metadata":{"abstract":"Gastric Leptin is absorbed by duodenal enterocytes and released on the basolateral side towards the bloodstream. 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We propose that leptin transcytosis by intestinal cells depends on its receptor, on clathrin-coated vesicles and transits through the Golgi apparatus.","publication_date":{"day":null,"month":null,"year":2010,"errors":{}},"publication_name":"International journal of cell biology"},"translated_abstract":"Gastric Leptin is absorbed by duodenal enterocytes and released on the basolateral side towards the bloodstream. We investigated in vitro some of the mechanisms of this transport. Caco-2/15 cells internalize leptin from the apical medium and release it through transcytosis in the basal medium in a time- temperature-dependent and saturable fashion. Leptin receptors are revealed on the apical brush-border membrane of the Caco-2 cells. RNA-mediated silencing of the receptor led to decreases in the uptake and basolateral release. Leptin in the basal medium was found bound to the soluble form of its receptor. An inhibitor of clathrin-dependent endocytosis (chlorpromazine) decreased leptin uptake. Confocal immunocytochemistry and the use of brefeldin A and okadaic acid revealed the passage of leptin through the Golgi apparatus. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19380182"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380182/TUBERCULOSIS_SOCIETY"><img alt="Research paper thumbnail of TUBERCULOSIS SOCIETY" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380182/TUBERCULOSIS_SOCIETY">TUBERCULOSIS SOCIETY</a></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380182"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380182"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380182; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19380181"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380181/Sar1b_transgenic_male_mice_are_more_susceptible_to_high_fat_diet_induced_obesity_insulin_insensitivity_and_intestinal_chylomicron_overproduction"><img alt="Research paper thumbnail of Sar1b transgenic male mice are more susceptible to high-fat diet-induced obesity, insulin insensitivity and intestinal chylomicron overproduction" class="work-thumbnail" src="https://attachments.academia-assets.com/42094697/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380181/Sar1b_transgenic_male_mice_are_more_susceptible_to_high_fat_diet_induced_obesity_insulin_insensitivity_and_intestinal_chylomicron_overproduction">Sar1b transgenic male mice are more susceptible to high-fat diet-induced obesity, insulin insensitivity and intestinal chylomicron overproduction</a></div><div class="wp-workCard_item"><span>The Journal of nutritional biochemistry</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In the intracellular secretory network, nascent proteins are shuttled from the endoplasmic reticu...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">In the intracellular secretory network, nascent proteins are shuttled from the endoplasmic reticulum to the Golgi by transport vesicles requiring Sar1b, a small GTPase. Mutations in this key enzyme impair intestinal lipid transport and cause chylomicron retention disease. The main aim of this study was to assess whether Sar1b overexpression under a hypercaloric diet accelerated lipid production and chylomicron (CM) secretion, thereby inducing cardiometabolic abnormalities. To this end, we generated transgenic mice overexpressing human Sar1b (Sar1b(+/+)) using pBROAD3-mcs that features the ubiquitous mouse ROSA26 promoter. In response to a high-fat diet (HFD), Sar1b(+/+) mice displayed significantly increased body weight and adiposity compared with Sar1b(+/+) mice under the same regimen or with wild-type (WT) mice exposed to chow diet or HFD. Furthermore, Sar1b(+/+) mice were prone to liver steatosis as revealed by significantly elevated hepatic triglycerides (TG) and cholesterol in ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b9f0c58be08cd3a8d6074a7d93bb50cf" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":42094697,"asset_id":19380181,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/42094697/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380181"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380181"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380181; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380181]").text(description); $(".js-view-count[data-work-id=19380181]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19380181; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19380181']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19380181, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "b9f0c58be08cd3a8d6074a7d93bb50cf" } } $('.js-work-strip[data-work-id=19380181]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380181,"title":"Sar1b transgenic male mice are more susceptible to high-fat diet-induced obesity, insulin insensitivity and intestinal chylomicron overproduction","translated_title":"","metadata":{"abstract":"In the intracellular secretory network, nascent proteins are shuttled from the endoplasmic reticulum to the Golgi by transport vesicles requiring Sar1b, a small GTPase. 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href="https://www.academia.edu/12440523/A_polyphenol_rich_cranberry_extract_protects_from_diet_induced_obesity_insulin_resistance_and_intestinal_inflammation_in_association_with_increased_Akkermansia_spp_population_in_the_gut_microbiota_of_mice"><img alt="Research paper thumbnail of A polyphenol-rich cranberry extract protects from diet-induced obesity, insulin resistance and intestinal inflammation in association with increased Akkermansia spp. population in the gut microbiota of mice" class="work-thumbnail" src="https://attachments.academia-assets.com/46182959/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/12440523/A_polyphenol_rich_cranberry_extract_protects_from_diet_induced_obesity_insulin_resistance_and_intestinal_inflammation_in_association_with_increased_Akkermansia_spp_population_in_the_gut_microbiota_of_mice">A polyphenol-rich cranberry extract protects from diet-induced obesity, insulin resistance and intestinal inflammation in association with increased Akkermansia spp. population in the gut microbiota of mice</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/CaroleGarofalo">Carole Garofalo</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://umontreal.academia.edu/EmileLevy">Emile Levy</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/Genevi%C3%A8vePilon">Genevi猫ve Pilon</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://ulaval.academia.edu/DenisRoy">Denis Roy</a></span></div><div class="wp-workCard_item"><span>Gut</span><span>, Jan 30, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The increasing prevalence of obesity and type 2 diabetes (T2D) demonstrates the failure of conven...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The increasing prevalence of obesity and type 2 diabetes (T2D) demonstrates the failure of conventional treatments to curb these diseases. The gut microbiota has been put forward as a key player in the pathophysiology of diet-induced T2D. Importantly, cranberry (Vaccinium macrocarpon Aiton) is associated with a number of beneficial health effects. We aimed to investigate the metabolic impact of a cranberry extract (CE) on high fat/high sucrose (HFHS)-fed mice and to determine whether its consequent antidiabetic effects are related to modulations in the gut microbiota. C57BL/6J mice were fed either a chow or a HFHS diet. HFHS-fed mice were gavaged daily either with vehicle (water) or CE (200鈥卪g/kg) for 8鈥厀eeks. The composition of the gut microbiota was assessed by analysing 16S rRNA gene sequences with 454 pyrosequencing. CE treatment was found to reduce HFHS-induced weight gain and visceral obesity. CE treatment also decreased liver weight and triglyceride accumulation in associatio...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="10523ea6e051192f1bcf2d3ebf701e8e" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":46182959,"asset_id":12440523,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/46182959/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="12440523"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="12440523"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12440523; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12440523]").text(description); $(".js-view-count[data-work-id=12440523]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12440523; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12440523']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12440523, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "10523ea6e051192f1bcf2d3ebf701e8e" } } $('.js-work-strip[data-work-id=12440523]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12440523,"title":"A polyphenol-rich cranberry extract protects from diet-induced obesity, insulin resistance and intestinal inflammation in association with increased Akkermansia spp. population in the gut microbiota of mice","translated_title":"","metadata":{"abstract":"The increasing prevalence of obesity and type 2 diabetes (T2D) demonstrates the failure of conventional treatments to curb these diseases. The gut microbiota has been put forward as a key player in the pathophysiology of diet-induced T2D. Importantly, cranberry (Vaccinium macrocarpon Aiton) is associated with a number of beneficial health effects. We aimed to investigate the metabolic impact of a cranberry extract (CE) on high fat/high sucrose (HFHS)-fed mice and to determine whether its consequent antidiabetic effects are related to modulations in the gut microbiota. C57BL/6J mice were fed either a chow or a HFHS diet. HFHS-fed mice were gavaged daily either with vehicle (water) or CE (200鈥卪g/kg) for 8鈥厀eeks. The composition of the gut microbiota was assessed by analysing 16S rRNA gene sequences with 454 pyrosequencing. CE treatment was found to reduce HFHS-induced weight gain and visceral obesity. 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}); </script> <div class="js-work-strip profile--work_container" data-work-id="19380180"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380180/Effect_of_retinoic_acid_on_cell_proliferation_and_differentiation_as_well_as_on_lipid_synthesis_lipoprotein_secretion_and_apolipoprotein_biogenesis"><img alt="Research paper thumbnail of Effect of retinoic acid on cell proliferation and differentiation as well as on lipid synthesis, lipoprotein secretion, and apolipoprotein biogenesis" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380180/Effect_of_retinoic_acid_on_cell_proliferation_and_differentiation_as_well_as_on_lipid_synthesis_lipoprotein_secretion_and_apolipoprotein_biogenesis">Effect of retinoic acid on cell proliferation and differentiation as well as on lipid synthesis, lipoprotein secretion, and apolipoprotein biogenesis</a></div><div class="wp-workCard_item"><span>American Journal of Physiology-gastrointestinal and Liver Physiology</span><span>, 2007</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Dietary vitamin A and its active metabolites are essential nutrients for many functions as well a...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Dietary vitamin A and its active metabolites are essential nutrients for many functions as well as potent regulators of gene transcription and growth. Although the epithelium of the small intestine is characterized by rapid and constant renewal and enterocytes play a central role in the absorption and metabolism of alimentary retinol, very little is known about the function of retinoids in the human gastrointestinal epithelium and mechanisms by which programs engage the cell cycle are poorly understood. We have assessed the effects of 10 microM 9- and 13-cis-retinoic acid (RA) on proliferation and differentiation processes, lipid esterification, apolipoprotein (apo) biogenesis and lipoprotein secretion along with nuclear factor gene transcription. Treatment of Caco-2 cells with RA at different concentrations and incubation periods revealed the reduction of thymidine incorporation in 60% preconfluent or 100% confluent cells. Concomitantly, RA 1) modulated D-type cyclins by reducing the mitogen-sensitive cyclin D1 and upregulating cyclin D3 expressions and 2) caused a trend of increase in p38 MAPK, which triggers CDX2, a central protein in cell differentiation. RA remained without effect on lipoprotein output and apo synthesis, even for apo A-I that possesses RARE in its promoter. RA, in combination with 22-hydroxycholesterol, could induce apo A-I gene expression without any impact on apo A-I mass. Only the gene expression of peroxisome proliferator-activated receptor (PPAR)beta, retinoic receptor (RAR)beta, and RARgamma was augmented and no alteration was noted in PPARalpha, PPARgamma, liver X receptor (LXR)alpha, LXRbeta, and retinoid X receptors. Taken together, these data highlight RA-induced cell differentiation via specific signaling without a significant impact on apo A-I synthesis.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380180"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380180"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380180; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380180]").text(description); $(".js-view-count[data-work-id=19380180]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19380180; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19380180']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19380180, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=19380180]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380180,"title":"Effect of retinoic acid on cell proliferation and differentiation as well as on lipid synthesis, lipoprotein secretion, and apolipoprotein biogenesis","translated_title":"","metadata":{"abstract":"Dietary vitamin A and its active metabolites are essential nutrients for many functions as well as potent regulators of gene transcription and growth. Although the epithelium of the small intestine is characterized by rapid and constant renewal and enterocytes play a central role in the absorption and metabolism of alimentary retinol, very little is known about the function of retinoids in the human gastrointestinal epithelium and mechanisms by which programs engage the cell cycle are poorly understood. We have assessed the effects of 10 microM 9- and 13-cis-retinoic acid (RA) on proliferation and differentiation processes, lipid esterification, apolipoprotein (apo) biogenesis and lipoprotein secretion along with nuclear factor gene transcription. Treatment of Caco-2 cells with RA at different concentrations and incubation periods revealed the reduction of thymidine incorporation in 60% preconfluent or 100% confluent cells. Concomitantly, RA 1) modulated D-type cyclins by reducing the mitogen-sensitive cyclin D1 and upregulating cyclin D3 expressions and 2) caused a trend of increase in p38 MAPK, which triggers CDX2, a central protein in cell differentiation. RA remained without effect on lipoprotein output and apo synthesis, even for apo A-I that possesses RARE in its promoter. RA, in combination with 22-hydroxycholesterol, could induce apo A-I gene expression without any impact on apo A-I mass. Only the gene expression of peroxisome proliferator-activated receptor (PPAR)beta, retinoic receptor (RAR)beta, and RARgamma was augmented and no alteration was noted in PPARalpha, PPARgamma, liver X receptor (LXR)alpha, LXRbeta, and retinoid X receptors. 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We have assessed the effects of 10 microM 9- and 13-cis-retinoic acid (RA) on proliferation and differentiation processes, lipid esterification, apolipoprotein (apo) biogenesis and lipoprotein secretion along with nuclear factor gene transcription. Treatment of Caco-2 cells with RA at different concentrations and incubation periods revealed the reduction of thymidine incorporation in 60% preconfluent or 100% confluent cells. Concomitantly, RA 1) modulated D-type cyclins by reducing the mitogen-sensitive cyclin D1 and upregulating cyclin D3 expressions and 2) caused a trend of increase in p38 MAPK, which triggers CDX2, a central protein in cell differentiation. RA remained without effect on lipoprotein output and apo synthesis, even for apo A-I that possesses RARE in its promoter. RA, in combination with 22-hydroxycholesterol, could induce apo A-I gene expression without any impact on apo A-I mass. Only the gene expression of peroxisome proliferator-activated receptor (PPAR)beta, retinoic receptor (RAR)beta, and RARgamma was augmented and no alteration was noted in PPARalpha, PPARgamma, liver X receptor (LXR)alpha, LXRbeta, and retinoid X receptors. 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Vitamin E is not produced in the body; it can only be obtained by mean of food from plant sources or through natural and synthetic supplements. Vitamin E is commercially extracted primarily from vegetable oils such as palm, canola, corn, cotton or soybean oils. Studies have shown that during industrial production a significant loss of tocopherols occurs in the range of 25% to 35% due to either thermal breakdown or chemical reactions. the majority of the tocopherol loss during oil processing is due to oxidation which renders the molecule ineffective with respect to its vitamin's function. Tocopherolquinone is one of the major oxidation products of vitamin E. The present study is the first to demonstrate that stannous chloride (SnCl 2 .2H 2 O) ion is capable of reducing 伪tocopherolquinone (TQ) back to 伪-tocopherol. Experiments conducted by reacting pure commercial standard 伪-TQ with stannous chloride (II) in organic solvent (methanol) yield promising results by reducing 95% of the 伪-TQ and producing vitamin E. These results led us to the isolation by HPLC of a fraction of TQ that was successfully reduced back to TOH. the TQ was obtained by oxidation reaction in vitro of a small quantity of commercial standard 伪-TOH and copper chloride (CuCl 2 ). in this study, stannous chloride has also proven to provide an important antioxidation effect by preventing the oxidation of TOH when exposed to a powerful oxidation catalyst such as CuCl 2 . the present study has shown as well for the first time the reaction of chromium (III) hexahydrate CrCl 3 .6 (H 2 O) with 伪tocopherolquinone resulting in the formation of 伪-tocopherol. This discovery presents a double advantage with regard to its applications: on one hand it can help reduce significantly the loss of vitamin E during industrial processing and on the other hand it could explain the still unanswered question on the potential antioxidant properties of chromium (III) reported in several publications. Background: It has been shown that dietary supplementation with Malaysian red palm oil improves functional recovery and reduces infarct size, following ischaemia/reperfusion (IR) in rat hearts. We subsequently investigated the composition of several other palm oils. These palm oils are consumed as a regular part of the diet in many parts of Africa and South-America. Materials and Methods: Oils were analyzed for fatty acid composition, antioxidant and trace metal content. Results: Fatty acid and antioxidant composition of palm oils from Africa yielded similar results to that of the Malaysian product. South-American palm oil however showed some differences in fatty acid composition, as well as significant differences in antioxidant content, especially with respect to vitamin E content. Trace metal analysis of oils are under way. Conclusion: Malaysian red palm oil supplementation reduces myocardial ischaemia/reperfusion injury and infarct size, through its natural antioxidant and fatty acid content. We hypothesize that African palm oil will have similar effects than the Malaysian counterpart with regards to cardiovascular protection. Further studies need to be done with the South-American palm oil to determine its effects on cardiovascular protection in the rat model. a (BPA), an important occupational and environmental chemical, causes toxicity to several organ systems including the liver. However, very little is known regarding the precise molecular mechanisms and cellular targets responsible for BPA toxicity. Studies in experimental animal models report that mitochondrial damage could be involved in BPA-induced liver injury. Given that BPA adversely affects the liver, and considering the central role of the liver in whole body energy metabolism and homeostasis, it is critical to understand the mechanisms behind BPA-induced hepatotoxicity. the aim of the present study was to evaluate the effects of BPA on metabolism and mitochondrial function by measuring the oxygen consumption rate (OCR) in primary rat hepatocytes using an XF24 analyzer (Seahorse Bioscience). Primary rat hepatocytes were plated in collagencoated Seahorse 24-well plates, allowed to attach for 5 h, and then exposed to various concentrations of BPA (0, 1,10, and 100 碌M) for 12 h before measuring OCR. Basal and maximal respiration, as well as the proton leak, were significantly increased following exposure to 100 碌M BPA compared to untreated control hepatocytes. Cell viability was unaffected in rat hepatocytes exposed to 1 碌M BPA, and decreased by only 22% and 30% with 10 碌M and 100 碌M BPA concentrations, respectively. Importantly, these results are in agreement with previous studies showing BPA-mediated increases in the rate of state 4 oxygen consumption in isolated mitochondria. These findings suggest that BPA may cause bioenergetic stress in cells by uncoupling. in summary, our results show that BPA negatively impacts mitochondrial function leading to critical alterations in the metabolic profile of hepatocytes.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Free Radical Biology and Medicine","grobid_abstract_attachment_id":40587799},"translated_abstract":null,"internal_url":"https://www.academia.edu/19380179/Dried_Apple_Peel_Extract_Prevents_Oxidative_Stress_and_Inflammation_in_Intestinal_Cells","translated_internal_url":"","created_at":"2015-12-02T14:00:35.014-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":39643530,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":11545764,"work_id":19380179,"tagging_user_id":39643530,"tagged_user_id":31248312,"co_author_invite_id":null,"email":"e***y@recherche-ste-justine.qc.ca","affiliation":"Universit茅 de Montr茅al","display_order":0,"name":"Emile Levy","title":"Dried Apple Peel Extract Prevents Oxidative Stress and Inflammation in Intestinal Cells"},{"id":11545774,"work_id":19380179,"tagging_user_id":39643530,"tagged_user_id":31223745,"co_author_invite_id":null,"email":"e***n@recherche-ste-justine.qc.ca","display_order":4194304,"name":"Edgard Delvin","title":"Dried Apple Peel Extract Prevents Oxidative Stress and Inflammation in Intestinal Cells"}],"downloadable_attachments":[{"id":40587799,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/40587799/thumbnails/1.jpg","file_name":"j.freeradbiomed.2011.10.143.pdf20151202-22750-1ar7eso","download_url":"https://www.academia.edu/attachments/40587799/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Dried_Apple_Peel_Extract_Prevents_Oxidat.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/40587799/j.freeradbiomed.2011.10.143-libre.pdf20151202-22750-1ar7eso?1449093975=\u0026response-content-disposition=attachment%3B+filename%3DDried_Apple_Peel_Extract_Prevents_Oxidat.pdf\u0026Expires=1732020033\u0026Signature=HcNjqE6lfPoDNMXfBY8f3Z9whavewHNLEyQjZR3MaZk0XjTKoS~~pLQD8i8CPTXwbHvLAisJWvxsNSO4lcVk0tI-5u08W5aGmp2sCsKC-e9-v5wC994wR2xzyEdCJrgcnTKCgRE11Ha-c2FbeLS52fbAcO3QkbFy6ANpcqri3kuVnZSGz6pLl~iNCbPyUMpOahMO-edNkdwRrWoktrBwBKtRqjvPvtu7EpIccjUFneyhrHt9XMh-K6OWzwoLib8~b-Ln6hUEN-HxD8C2nnCV-Hp1vOAIgIfi3VNtqYCDhlzADquE-NBVmxvpx9CSRb5q5toF8uUT7E6D9fTNL2HB9Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Dried_Apple_Peel_Extract_Prevents_Oxidative_Stress_and_Inflammation_in_Intestinal_Cells","translated_slug":"","page_count":2,"language":"en","content_type":"Work","owner":{"id":39643530,"first_name":"Carole","middle_initials":null,"last_name":"Garofalo","page_name":"CaroleGarofalo","domain_name":"independent","created_at":"2015-12-02T13:59:52.848-08:00","display_name":"Carole Garofalo","url":"https://independent.academia.edu/CaroleGarofalo"},"attachments":[{"id":40587799,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/40587799/thumbnails/1.jpg","file_name":"j.freeradbiomed.2011.10.143.pdf20151202-22750-1ar7eso","download_url":"https://www.academia.edu/attachments/40587799/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Dried_Apple_Peel_Extract_Prevents_Oxidat.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/40587799/j.freeradbiomed.2011.10.143-libre.pdf20151202-22750-1ar7eso?1449093975=\u0026response-content-disposition=attachment%3B+filename%3DDried_Apple_Peel_Extract_Prevents_Oxidat.pdf\u0026Expires=1732020033\u0026Signature=HcNjqE6lfPoDNMXfBY8f3Z9whavewHNLEyQjZR3MaZk0XjTKoS~~pLQD8i8CPTXwbHvLAisJWvxsNSO4lcVk0tI-5u08W5aGmp2sCsKC-e9-v5wC994wR2xzyEdCJrgcnTKCgRE11Ha-c2FbeLS52fbAcO3QkbFy6ANpcqri3kuVnZSGz6pLl~iNCbPyUMpOahMO-edNkdwRrWoktrBwBKtRqjvPvtu7EpIccjUFneyhrHt9XMh-K6OWzwoLib8~b-Ln6hUEN-HxD8C2nnCV-Hp1vOAIgIfi3VNtqYCDhlzADquE-NBVmxvpx9CSRb5q5toF8uUT7E6D9fTNL2HB9Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"urls":[{"id":6101556,"url":"http://www.sciencedirect.com/science/article/pii/S0891584911007726"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19380178"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380178/Prevention_of_oxidative_stress_inflammation_and_mitochondrial_dysfunction_in_the_intestine_by_different_cranberry_phenolic_fractions"><img alt="Research paper thumbnail of Prevention of oxidative stress, inflammation and mitochondrial dysfunction in the intestine by different cranberry phenolic fractions" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380178/Prevention_of_oxidative_stress_inflammation_and_mitochondrial_dysfunction_in_the_intestine_by_different_cranberry_phenolic_fractions">Prevention of oxidative stress, inflammation and mitochondrial dysfunction in the intestine by different cranberry phenolic fractions</a></div><div class="wp-workCard_item"><span>Clinical Science</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Cranberry fruit has been reported to have high antioxidant effectiveness that is potentially link...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Cranberry fruit has been reported to have high antioxidant effectiveness that is potentially linked to its richness in diversified polyphenolic content. The aim of the present study was to determine the role of cranberry polyphenolic fractions in oxidative stress (OxS), inflammation and mitochondrial functions using intestinal Caco-2/15 cells. The combination of HPLC and UltraPerformance LC庐-tandem quadrupole (UPLC-TQD) techniques allowed us to characterize the profile of low, medium and high molecular mass polyphenolic compounds in cranberry extracts. The medium molecular mass fraction was enriched with flavonoids and procyanidin dimers whereas procyanidin oligomers (DP &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt; 4) were the dominant class of polyphenols in the high molecular mass fraction. Pre-incubation of Caco-2/15 cells with these cranberry extracts prevented iron/ascorbate-mediated lipid peroxidation and counteracted lipopolysaccharide-mediated inflammation as evidenced by the decrease in pro-inflammatory cytokines (TNF-伪 and interleukin-6), cyclo-oxygenase-2 and prostaglandin E2. Cranberry polyphenols (CP) fractions limited both nuclear factor 魏B activation and Nrf2 down-regulation. Consistently, cranberry procyanidins alleviated OxS-dependent mitochondrial dysfunctions as shown by the rise in ATP production and the up-regulation of Bcl-2, as well as the decline of protein expression of cytochrome c and apoptotic-inducing factor. These mitochondrial effects were associated with a significant stimulation of peroxisome-proliferator-activated receptor 纬 co-activator-1-伪, a central inducing factor of mitochondrial biogenesis and transcriptional co-activator of numerous downstream mediators. Finally, cranberry procyanidins forestalled the effect of iron/ascorbate on the protein expression of mitochondrial transcription factors (mtTFA, mtTFB1, mtTFB2). Our findings provide evidence for the capacity of CP to reduce intestinal OxS and inflammation while improving mitochondrial dysfunction.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380178"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380178"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380178; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380178]").text(description); $(".js-view-count[data-work-id=19380178]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19380178; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19380178']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19380178, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=19380178]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380178,"title":"Prevention of oxidative stress, inflammation and mitochondrial dysfunction in the intestine by different cranberry phenolic fractions","translated_title":"","metadata":{"abstract":"Cranberry fruit has been reported to have high antioxidant effectiveness that is potentially linked to its richness in diversified polyphenolic content. The aim of the present study was to determine the role of cranberry polyphenolic fractions in oxidative stress (OxS), inflammation and mitochondrial functions using intestinal Caco-2/15 cells. The combination of HPLC and UltraPerformance LC庐-tandem quadrupole (UPLC-TQD) techniques allowed us to characterize the profile of low, medium and high molecular mass polyphenolic compounds in cranberry extracts. The medium molecular mass fraction was enriched with flavonoids and procyanidin dimers whereas procyanidin oligomers (DP \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt; 4) were the dominant class of polyphenols in the high molecular mass fraction. Pre-incubation of Caco-2/15 cells with these cranberry extracts prevented iron/ascorbate-mediated lipid peroxidation and counteracted lipopolysaccharide-mediated inflammation as evidenced by the decrease in pro-inflammatory cytokines (TNF-伪 and interleukin-6), cyclo-oxygenase-2 and prostaglandin E2. Cranberry polyphenols (CP) fractions limited both nuclear factor 魏B activation and Nrf2 down-regulation. Consistently, cranberry procyanidins alleviated OxS-dependent mitochondrial dysfunctions as shown by the rise in ATP production and the up-regulation of Bcl-2, as well as the decline of protein expression of cytochrome c and apoptotic-inducing factor. These mitochondrial effects were associated with a significant stimulation of peroxisome-proliferator-activated receptor 纬 co-activator-1-伪, a central inducing factor of mitochondrial biogenesis and transcriptional co-activator of numerous downstream mediators. Finally, cranberry procyanidins forestalled the effect of iron/ascorbate on the protein expression of mitochondrial transcription factors (mtTFA, mtTFB1, mtTFB2). Our findings provide evidence for the capacity of CP to reduce intestinal OxS and inflammation while improving mitochondrial dysfunction.","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Clinical Science"},"translated_abstract":"Cranberry fruit has been reported to have high antioxidant effectiveness that is potentially linked to its richness in diversified polyphenolic content. The aim of the present study was to determine the role of cranberry polyphenolic fractions in oxidative stress (OxS), inflammation and mitochondrial functions using intestinal Caco-2/15 cells. The combination of HPLC and UltraPerformance LC庐-tandem quadrupole (UPLC-TQD) techniques allowed us to characterize the profile of low, medium and high molecular mass polyphenolic compounds in cranberry extracts. The medium molecular mass fraction was enriched with flavonoids and procyanidin dimers whereas procyanidin oligomers (DP \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt; 4) were the dominant class of polyphenols in the high molecular mass fraction. Pre-incubation of Caco-2/15 cells with these cranberry extracts prevented iron/ascorbate-mediated lipid peroxidation and counteracted lipopolysaccharide-mediated inflammation as evidenced by the decrease in pro-inflammatory cytokines (TNF-伪 and interleukin-6), cyclo-oxygenase-2 and prostaglandin E2. Cranberry polyphenols (CP) fractions limited both nuclear factor 魏B activation and Nrf2 down-regulation. Consistently, cranberry procyanidins alleviated OxS-dependent mitochondrial dysfunctions as shown by the rise in ATP production and the up-regulation of Bcl-2, as well as the decline of protein expression of cytochrome c and apoptotic-inducing factor. These mitochondrial effects were associated with a significant stimulation of peroxisome-proliferator-activated receptor 纬 co-activator-1-伪, a central inducing factor of mitochondrial biogenesis and transcriptional co-activator of numerous downstream mediators. Finally, cranberry procyanidins forestalled the effect of iron/ascorbate on the protein expression of mitochondrial transcription factors (mtTFA, mtTFB1, mtTFB2). Our findings provide evidence for the capacity of CP to reduce intestinal OxS and inflammation while improving mitochondrial dysfunction.","internal_url":"https://www.academia.edu/19380178/Prevention_of_oxidative_stress_inflammation_and_mitochondrial_dysfunction_in_the_intestine_by_different_cranberry_phenolic_fractions","translated_internal_url":"","created_at":"2015-12-02T14:00:34.930-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":39643530,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":11545760,"work_id":19380178,"tagging_user_id":39643530,"tagged_user_id":31248312,"co_author_invite_id":null,"email":"e***y@recherche-ste-justine.qc.ca","affiliation":"Universit茅 de Montr茅al","display_order":0,"name":"Emile Levy","title":"Prevention of oxidative stress, inflammation and mitochondrial dysfunction in the intestine by different cranberry phenolic fractions"},{"id":11545772,"work_id":19380178,"tagging_user_id":39643530,"tagged_user_id":31223745,"co_author_invite_id":null,"email":"e***n@recherche-ste-justine.qc.ca","display_order":4194304,"name":"Edgard Delvin","title":"Prevention of oxidative stress, inflammation and mitochondrial dysfunction in the intestine by different cranberry phenolic fractions"},{"id":11545782,"work_id":19380178,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":217950,"email":"a***e@criucpq.ulaval.ca","display_order":7340032,"name":"Andr茅 Marette","title":"Prevention of oxidative stress, inflammation and mitochondrial dysfunction in the intestine by different cranberry phenolic fractions"},{"id":11545787,"work_id":19380178,"tagging_user_id":39643530,"tagged_user_id":31309978,"co_author_invite_id":2711269,"email":"m***n@gmail.com","display_order":7864320,"name":"Alain Montoudis","title":"Prevention of oxidative stress, inflammation and mitochondrial dysfunction in the intestine by different cranberry phenolic fractions"}],"downloadable_attachments":[],"slug":"Prevention_of_oxidative_stress_inflammation_and_mitochondrial_dysfunction_in_the_intestine_by_different_cranberry_phenolic_fractions","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":39643530,"first_name":"Carole","middle_initials":null,"last_name":"Garofalo","page_name":"CaroleGarofalo","domain_name":"independent","created_at":"2015-12-02T13:59:52.848-08:00","display_name":"Carole Garofalo","url":"https://independent.academia.edu/CaroleGarofalo"},"attachments":[],"research_interests":[{"id":9334,"name":"Inflammation","url":"https://www.academia.edu/Documents/in/Inflammation"},{"id":14292,"name":"Oxidative Stress","url":"https://www.academia.edu/Documents/in/Oxidative_Stress"},{"id":15719,"name":"Mitochondria","url":"https://www.academia.edu/Documents/in/Mitochondria"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":51711,"name":"Antioxidants","url":"https://www.academia.edu/Documents/in/Antioxidants"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":72314,"name":"Fatty acids","url":"https://www.academia.edu/Documents/in/Fatty_acids"},{"id":233372,"name":"Lipid peroxidation","url":"https://www.academia.edu/Documents/in/Lipid_peroxidation"},{"id":291136,"name":"Intestines","url":"https://www.academia.edu/Documents/in/Intestines"},{"id":314125,"name":"Caco-2 cells","url":"https://www.academia.edu/Documents/in/Caco-2_cells"},{"id":354056,"name":"Plant extracts","url":"https://www.academia.edu/Documents/in/Plant_extracts"},{"id":434453,"name":"Oxidative phosphorylation","url":"https://www.academia.edu/Documents/in/Oxidative_phosphorylation"},{"id":690437,"name":"Vaccinium Macrocarpon","url":"https://www.academia.edu/Documents/in/Vaccinium_Macrocarpon"},{"id":948028,"name":"Proanthocyanidins","url":"https://www.academia.edu/Documents/in/Proanthocyanidins"},{"id":1223957,"name":"Catechin","url":"https://www.academia.edu/Documents/in/Catechin"},{"id":1816594,"name":"Adenosine Triphosphate","url":"https://www.academia.edu/Documents/in/Adenosine_Triphosphate"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19380177"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380177/Effect_of_clentiazem_on_lipid_profile_lipoprotein_composition_and_aortic_fatty_streaks_in_cholesterol_fed_rabbits"><img alt="Research paper thumbnail of Effect of clentiazem on lipid profile, lipoprotein composition and aortic fatty streaks in cholesterol-fed rabbits" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380177/Effect_of_clentiazem_on_lipid_profile_lipoprotein_composition_and_aortic_fatty_streaks_in_cholesterol_fed_rabbits">Effect of clentiazem on lipid profile, lipoprotein composition and aortic fatty streaks in cholesterol-fed rabbits</a></div><div class="wp-workCard_item"><span>Atherosclerosis</span><span>, 1991</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Numerous experimental studies have reported that common antihypertensive drugs such as diuretics,...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Numerous experimental studies have reported that common antihypertensive drugs such as diuretics, beta-blockers, and methyldopa have adverse effects on plasma lipids and lipoproteins. The present study was designed to define the effect of clentiazem (10 mg/kg/day) an antihypertensive drug, on hyperlipidemia in rabbits on a cholesterol-rich diet (1%) for 12 weeks. Compared with controls, clentiazem treated rabbits had lower plasma concentrations of triglycerides (55%), total cholesterol (24%), free cholesterol (27%), esterified cholesterol (23%) and phospholipids (24%). The decrease in cholesterol was accounted for by a reduction of VLDL-cholesterol (13%), IDL-cholesterol (24%) and primarily LDL-cholesterol (45%). Neither HDL-cholesterol nor chemical composition of VLDL, IDL, LDL and HDL was altered. When the aortic atherosclerotic involvement was evaluated by computerized planimetry, a 24% reduction of lesions was noted in clentiazem treated animals (P less than 0.05). Similarly, cholesterol content extracted from aortic wall was decreased. Our data therefore demonstrated that clentiazem is a potential antiatherosclerotic agent capable of decreasing plasma lipids and atherogenic lipoproteins as well as aortic fatty streaks.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380177"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380177"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380177; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380177]").text(description); $(".js-view-count[data-work-id=19380177]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19380177; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19380177']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19380177, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=19380177]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380177,"title":"Effect of clentiazem on lipid profile, lipoprotein composition and aortic fatty streaks in cholesterol-fed rabbits","translated_title":"","metadata":{"abstract":"Numerous experimental studies have reported that common antihypertensive drugs such as diuretics, beta-blockers, and methyldopa have adverse effects on plasma lipids and lipoproteins. The present study was designed to define the effect of clentiazem (10 mg/kg/day) an antihypertensive drug, on hyperlipidemia in rabbits on a cholesterol-rich diet (1%) for 12 weeks. Compared with controls, clentiazem treated rabbits had lower plasma concentrations of triglycerides (55%), total cholesterol (24%), free cholesterol (27%), esterified cholesterol (23%) and phospholipids (24%). The decrease in cholesterol was accounted for by a reduction of VLDL-cholesterol (13%), IDL-cholesterol (24%) and primarily LDL-cholesterol (45%). Neither HDL-cholesterol nor chemical composition of VLDL, IDL, LDL and HDL was altered. When the aortic atherosclerotic involvement was evaluated by computerized planimetry, a 24% reduction of lesions was noted in clentiazem treated animals (P less than 0.05). Similarly, cholesterol content extracted from aortic wall was decreased. Our data therefore demonstrated that clentiazem is a potential antiatherosclerotic agent capable of decreasing plasma lipids and atherogenic lipoproteins as well as aortic fatty streaks.","publication_date":{"day":null,"month":null,"year":1991,"errors":{}},"publication_name":"Atherosclerosis"},"translated_abstract":"Numerous experimental studies have reported that common antihypertensive drugs such as diuretics, beta-blockers, and methyldopa have adverse effects on plasma lipids and lipoproteins. The present study was designed to define the effect of clentiazem (10 mg/kg/day) an antihypertensive drug, on hyperlipidemia in rabbits on a cholesterol-rich diet (1%) for 12 weeks. Compared with controls, clentiazem treated rabbits had lower plasma concentrations of triglycerides (55%), total cholesterol (24%), free cholesterol (27%), esterified cholesterol (23%) and phospholipids (24%). The decrease in cholesterol was accounted for by a reduction of VLDL-cholesterol (13%), IDL-cholesterol (24%) and primarily LDL-cholesterol (45%). Neither HDL-cholesterol nor chemical composition of VLDL, IDL, LDL and HDL was altered. When the aortic atherosclerotic involvement was evaluated by computerized planimetry, a 24% reduction of lesions was noted in clentiazem treated animals (P less than 0.05). Similarly, cholesterol content extracted from aortic wall was decreased. Our data therefore demonstrated that clentiazem is a potential antiatherosclerotic agent capable of decreasing plasma lipids and atherogenic lipoproteins as well as aortic fatty streaks.","internal_url":"https://www.academia.edu/19380177/Effect_of_clentiazem_on_lipid_profile_lipoprotein_composition_and_aortic_fatty_streaks_in_cholesterol_fed_rabbits","translated_internal_url":"","created_at":"2015-12-02T14:00:34.776-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":39643530,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":11545763,"work_id":19380177,"tagging_user_id":39643530,"tagged_user_id":31248312,"co_author_invite_id":null,"email":"e***y@recherche-ste-justine.qc.ca","affiliation":"Universit茅 de Montr茅al","display_order":0,"name":"Emile Levy","title":"Effect of clentiazem on lipid profile, lipoprotein composition and aortic fatty streaks in cholesterol-fed rabbits"},{"id":11545799,"work_id":19380177,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":2077458,"email":"d***l@lhrionhealth.ca","display_order":4194304,"name":"D. Bouthillier","title":"Effect of clentiazem on lipid profile, lipoprotein composition and aortic fatty streaks in cholesterol-fed rabbits"}],"downloadable_attachments":[],"slug":"Effect_of_clentiazem_on_lipid_profile_lipoprotein_composition_and_aortic_fatty_streaks_in_cholesterol_fed_rabbits","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":39643530,"first_name":"Carole","middle_initials":null,"last_name":"Garofalo","page_name":"CaroleGarofalo","domain_name":"independent","created_at":"2015-12-02T13:59:52.848-08:00","display_name":"Carole Garofalo","url":"https://independent.academia.edu/CaroleGarofalo"},"attachments":[],"research_interests":[{"id":8015,"name":"Atherosclerosis","url":"https://www.academia.edu/Documents/in/Atherosclerosis"},{"id":52055,"name":"Lipids","url":"https://www.academia.edu/Documents/in/Lipids"},{"id":90514,"name":"Cholesterol","url":"https://www.academia.edu/Documents/in/Cholesterol"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":184609,"name":"Lipid metabolism","url":"https://www.academia.edu/Documents/in/Lipid_metabolism"},{"id":227285,"name":"Lipoprotein(a)","url":"https://www.academia.edu/Documents/in/Lipoprotein_a_-1"},{"id":227299,"name":"Triglycerides","url":"https://www.academia.edu/Documents/in/Triglycerides"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":458879,"name":"Lipoproteins","url":"https://www.academia.edu/Documents/in/Lipoproteins"},{"id":788677,"name":"Rabbits","url":"https://www.academia.edu/Documents/in/Rabbits"},{"id":801998,"name":"Lipid Profile","url":"https://www.academia.edu/Documents/in/Lipid_Profile"},{"id":1035092,"name":"Aorta","url":"https://www.academia.edu/Documents/in/Aorta"}],"urls":[{"id":6101555,"url":"http://linkinghub.elsevier.com/retrieve/pii/002191509190108F"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="12440504"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/12440504/Circulating_Docosahexaenoic_Acid_Levels_Are_Associated_with_Fetal_Insulin_Sensitivity"><img alt="Research paper thumbnail of Circulating Docosahexaenoic Acid Levels Are Associated with Fetal Insulin Sensitivity" class="work-thumbnail" src="https://attachments.academia-assets.com/46182787/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/12440504/Circulating_Docosahexaenoic_Acid_Levels_Are_Associated_with_Fetal_Insulin_Sensitivity">Circulating Docosahexaenoic Acid Levels Are Associated with Fetal Insulin Sensitivity</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/CaroleGarofalo">Carole Garofalo</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://umontreal.academia.edu/EmileLevy">Emile Levy</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/AlainMontoudis">Alain Montoudis</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/AnnemoniqueNuyt">Anne-monique Nuyt</a></span></div><div class="wp-workCard_item"><span>PLoS ONE</span><span>, 2014</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="74cb523c9d02cddd30106248f46aedf3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":46182787,"asset_id":12440504,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/46182787/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="12440504"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="12440504"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12440504; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12440504]").text(description); $(".js-view-count[data-work-id=12440504]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12440504; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12440504']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12440504, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "74cb523c9d02cddd30106248f46aedf3" } } $('.js-work-strip[data-work-id=12440504]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12440504,"title":"Circulating Docosahexaenoic Acid Levels Are Associated with Fetal Insulin Sensitivity","translated_title":"","metadata":{"grobid_abstract":"Background: Arachidonic acid (AA; C20:4 n-6) and docosahexaenoic acid (DHA; C22:6 n-3) are important long-chain polyunsaturated fatty acids (LC-PUFA) in maintaining pancreatic beta-cell structure and function. Newborns of gestational diabetic mothers are more susceptible to the development of type 2 diabetes in adulthood. It is not known whether low circulating AA or DHA is involved in perinatally ''programming'' this susceptibility. This study aimed to assess whether circulating concentrations of AA, DHA and other fatty acids are associated with fetal insulin sensitivity or beta-cell function, and whether low circulating concentrations of AA or DHA are involved in compromised fetal insulin sensitivity in gestational diabetic pregnancies.","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"PLoS ONE","grobid_abstract_attachment_id":46182787},"translated_abstract":null,"internal_url":"https://www.academia.edu/12440504/Circulating_Docosahexaenoic_Acid_Levels_Are_Associated_with_Fetal_Insulin_Sensitivity","translated_internal_url":"","created_at":"2015-05-18T05:12:39.014-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31248312,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":564457,"work_id":12440504,"tagging_user_id":31248312,"tagged_user_id":39643530,"co_author_invite_id":217969,"email":"c***o@recherche-ste-justine.qc.ca","display_order":0,"name":"Carole Garofalo","title":"Circulating Docosahexaenoic Acid Levels Are Associated with Fetal Insulin Sensitivity"},{"id":564386,"work_id":12440504,"tagging_user_id":31248312,"tagged_user_id":null,"co_author_invite_id":217937,"email":"z***3@163.com","display_order":null,"name":"Zhong-Cheng Luo","title":"Circulating Docosahexaenoic Acid Levels Are Associated with 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"profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19380176"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380176/Maternal_and_fetal_leptin_adiponectin_levels_and_associations_with_fetal_insulin_sensitivity"><img alt="Research paper thumbnail of Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380176/Maternal_and_fetal_leptin_adiponectin_levels_and_associations_with_fetal_insulin_sensitivity">Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity</a></div><div class="wp-workCard_item"><span>Obesity</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">It remains uncertain whether leptin and adiponectin levels are correlated in maternal vs. fetal c...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">It remains uncertain whether leptin and adiponectin levels are correlated in maternal vs. fetal circulations. Little is known about whether leptin and adiponectin affect insulin sensitivity during fetal life. In a prospective singleton pregnancy cohort (n = 248), we investigated leptin and adiponectin concentrations in maternal (at 24-28 and 32-35 weeks of gestation) and fetal circulations, and their associations with fetal insulin sensitivity (glucose/insulin ratio, proinsulin level). Comparing concentrations in cord vs. maternal blood, leptin levels were 50% lower, but adiponectin levels more than doubled. Adjusting for gestational age at blood sampling, consistent and similar positive correlations (correlation coefficients: 0.31-0.34, all P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.0001) were observed in leptin or adiponectin levels in maternal (at 24-28 or 32-25 weeks of gestation) vs. fetal circulations. For each SD increase in maternal plasma concentration at 24-28 weeks, cord plasma concentration increased by 12.7 (95% confidence interval 6.8-18.5) ng/ml for leptin, and 2.9 (1.8-4.0) 碌g/ml for adiponectin, respectively (adjusted P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.0001). Fetal insulin sensitivity was negatively associated with cord blood leptin (each SD increase was associated with a 5.4 (2.1-8.7) mg/dl/碌U/ml reduction in cord plasma glucose/insulin ratio, and a 5.6 (3.9, 7.4) pmol/l increase in proinsulin level, all adjusted P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.01) but not adiponectin (P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt; 0.4) levels). Similar associations were observed in nondiabetic full-term pregnancies (n = 211). The results consistently suggest a maternal impact on fetal leptin and adiponectin levels, which may be an early life pathway in maternal-fetal transmission of the propensity to obesity and insulin resistance.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380176"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380176"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380176; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=19380176]").text(description); $(".js-view-count[data-work-id=19380176]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 19380176; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='19380176']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 19380176, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=19380176]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":19380176,"title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity","translated_title":"","metadata":{"abstract":"It remains uncertain whether leptin and adiponectin levels are correlated in maternal vs. fetal circulations. 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Adjusting for gestational age at blood sampling, consistent and similar positive correlations (correlation coefficients: 0.31-0.34, all P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.0001) were observed in leptin or adiponectin levels in maternal (at 24-28 or 32-25 weeks of gestation) vs. fetal circulations. For each SD increase in maternal plasma concentration at 24-28 weeks, cord plasma concentration increased by 12.7 (95% confidence interval 6.8-18.5) ng/ml for leptin, and 2.9 (1.8-4.0) 碌g/ml for adiponectin, respectively (adjusted P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.0001). Fetal insulin sensitivity was negatively associated with cord blood leptin (each SD increase was associated with a 5.4 (2.1-8.7) mg/dl/碌U/ml reduction in cord plasma glucose/insulin ratio, and a 5.6 (3.9, 7.4) pmol/l increase in proinsulin level, all adjusted P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.01) but not adiponectin (P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt; 0.4) levels). Similar associations were observed in nondiabetic full-term pregnancies (n = 211). The results consistently suggest a maternal impact on fetal leptin and adiponectin levels, which may be an early life pathway in maternal-fetal transmission of the propensity to obesity and insulin resistance.","publication_date":{"day":null,"month":null,"year":2013,"errors":{}},"publication_name":"Obesity"},"translated_abstract":"It remains uncertain whether leptin and adiponectin levels are correlated in maternal vs. fetal circulations. Little is known about whether leptin and adiponectin affect insulin sensitivity during fetal life. In a prospective singleton pregnancy cohort (n = 248), we investigated leptin and adiponectin concentrations in maternal (at 24-28 and 32-35 weeks of gestation) and fetal circulations, and their associations with fetal insulin sensitivity (glucose/insulin ratio, proinsulin level). Comparing concentrations in cord vs. maternal blood, leptin levels were 50% lower, but adiponectin levels more than doubled. Adjusting for gestational age at blood sampling, consistent and similar positive correlations (correlation coefficients: 0.31-0.34, all P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.0001) were observed in leptin or adiponectin levels in maternal (at 24-28 or 32-25 weeks of gestation) vs. fetal circulations. For each SD increase in maternal plasma concentration at 24-28 weeks, cord plasma concentration increased by 12.7 (95% confidence interval 6.8-18.5) ng/ml for leptin, and 2.9 (1.8-4.0) 碌g/ml for adiponectin, respectively (adjusted P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.0001). Fetal insulin sensitivity was negatively associated with cord blood leptin (each SD increase was associated with a 5.4 (2.1-8.7) mg/dl/碌U/ml reduction in cord plasma glucose/insulin ratio, and a 5.6 (3.9, 7.4) pmol/l increase in proinsulin level, all adjusted P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.01) but not adiponectin (P \u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt; 0.4) levels). Similar associations were observed in nondiabetic full-term pregnancies (n = 211). The results consistently suggest a maternal impact on fetal leptin and adiponectin levels, which may be an early life pathway in maternal-fetal transmission of the propensity to obesity and insulin resistance.","internal_url":"https://www.academia.edu/19380176/Maternal_and_fetal_leptin_adiponectin_levels_and_associations_with_fetal_insulin_sensitivity","translated_internal_url":"","created_at":"2015-12-02T14:00:34.587-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":39643530,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":11545754,"work_id":19380176,"tagging_user_id":39643530,"tagged_user_id":31248312,"co_author_invite_id":null,"email":"e***y@recherche-ste-justine.qc.ca","affiliation":"Universit茅 de Montr茅al","display_order":0,"name":"Emile Levy","title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity"},{"id":11545770,"work_id":19380176,"tagging_user_id":39643530,"tagged_user_id":31223745,"co_author_invite_id":null,"email":"e***n@recherche-ste-justine.qc.ca","display_order":4194304,"name":"Edgard Delvin","title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity"},{"id":11545778,"work_id":19380176,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":217937,"email":"z***3@163.com","display_order":6291456,"name":"Zhong-cheng Luo","title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity"},{"id":11545780,"work_id":19380176,"tagging_user_id":39643530,"tagged_user_id":31459997,"co_author_invite_id":null,"email":"a***t@recherche-ste-justine.qc.ca","display_order":7340032,"name":"Anne-monique Nuyt","title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity"},{"id":11545786,"work_id":19380176,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":217939,"email":"w***r@umontreal.qc.ca","display_order":7864320,"name":"William Fraser","title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity"},{"id":11545791,"work_id":19380176,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":873919,"email":"b***n@umontreal.ca","display_order":8126464,"name":"Bryna Shatenstein","title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity"},{"id":11545792,"work_id":19380176,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":236514,"email":"c***a@dani.umontreal.ca","display_order":8257536,"name":"Cheri Deal","title":"Maternal and fetal leptin, adiponectin levels and associations with fetal insulin sensitivity"}],"downloadable_attachments":[],"slug":"Maternal_and_fetal_leptin_adiponectin_levels_and_associations_with_fetal_insulin_sensitivity","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":39643530,"first_name":"Carole","middle_initials":null,"last_name":"Garofalo","page_name":"CaroleGarofalo","domain_name":"independent","created_at":"2015-12-02T13:59:52.848-08:00","display_name":"Carole Garofalo","url":"https://independent.academia.edu/CaroleGarofalo"},"attachments":[],"research_interests":[{"id":3851,"name":"Obesity","url":"https://www.academia.edu/Documents/in/Obesity"},{"id":28235,"name":"Multidisciplinary","url":"https://www.academia.edu/Documents/in/Multidisciplinary"},{"id":51373,"name":"Insulin Resistance","url":"https://www.academia.edu/Documents/in/Insulin_Resistance"},{"id":62112,"name":"Prospective studies","url":"https://www.academia.edu/Documents/in/Prospective_studies"},{"id":62550,"name":"Pregnancy","url":"https://www.academia.edu/Documents/in/Pregnancy"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":71300,"name":"Blood Glucose","url":"https://www.academia.edu/Documents/in/Blood_Glucose"},{"id":71400,"name":"Insulin","url":"https://www.academia.edu/Documents/in/Insulin"},{"id":98925,"name":"Female","url":"https://www.academia.edu/Documents/in/Female"},{"id":135357,"name":"Leptin","url":"https://www.academia.edu/Documents/in/Leptin"},{"id":346660,"name":"Adiponectin","url":"https://www.academia.edu/Documents/in/Adiponectin"},{"id":382075,"name":"Adult","url":"https://www.academia.edu/Documents/in/Adult"},{"id":770944,"name":"Fetus","url":"https://www.academia.edu/Documents/in/Fetus"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="12440495"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/12440495/Asymmetrical_regulation_of_scavenger_receptor_class_B_type_I_by_apical_and_basolateral_stimuli_using_Caco_2_cells"><img alt="Research paper thumbnail of Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco-2 cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/12440495/Asymmetrical_regulation_of_scavenger_receptor_class_B_type_I_by_apical_and_basolateral_stimuli_using_Caco_2_cells">Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco-2 cells</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/CaroleGarofalo">Carole Garofalo</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://umontreal.academia.edu/EmileLevy">Emile Levy</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/ValerieMarcil">Valerie Marcil</a></span></div><div class="wp-workCard_item"><span>Journal of Cellular Biochemistry</span><span>, 2007</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Cholesterol uptake and the mechanisms that regulate cholesterol translocation from the intestinal...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Cholesterol uptake and the mechanisms that regulate cholesterol translocation from the intestinal lumen into enterocytes remain for the most part unclear. Since scavenger receptor class B type I (SR-BI) has been suggested to play a role in cholesterol absorption, we investigated cellular SR-BI modulation by various potential effectors administered in both apical and basolateral sides of Caco-2 cells. With differentiation, Caco-2 cells increased SR-BI protein expression. Western blot analysis showed the ability of cholesterol and oxysterols in both cell compartments to reduce SR-BI protein expression. Among the n-3, n-6, and n-9 fatty acid families, only eicosapentaenoic acid was able to lower SR-BI protein expression on both sides, whereas apical alpha-linolenic acid decreased SR-BI abundance and basolateral arachidonic acid (AA) raised it. Epidermal growth factor and growth hormone, either in the apical or basolateral medium, diminished SR-BI cellular content, while insulin displayed the same effect only on the basolateral side. In the presence of proinflammatory agents (LPS, TNF-alpha, IFN-gamma), Caco-2 cells exhibited differential behavior. SR-BI was downregulated by lipopolysaccharide on both sides. Finally, WY-14643 fibrate diminished SR-BI protein expression when it was added to the apical medium. Biotinylation studies in response to selected stimuli revealed that regulatory modifications in SR-BI protein expression occurred for the most part at the apical cell surface irrespective of the effector location. Our data indicate that various effectors supplied to the apical and basolateral compartments may impact on SR-BI at the apical membrane, thus suggesting potential regulation of intestinal cholesterol absorption and distribution in various intracellular pools.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="12440495"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="12440495"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12440495; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12440495]").text(description); $(".js-view-count[data-work-id=12440495]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12440495; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12440495']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12440495, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=12440495]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12440495,"title":"Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco-2 cells","translated_title":"","metadata":{"abstract":"Cholesterol uptake and the mechanisms that regulate cholesterol translocation from the intestinal lumen into enterocytes remain for the most part unclear. Since scavenger receptor class B type I (SR-BI) has been suggested to play a role in cholesterol absorption, we investigated cellular SR-BI modulation by various potential effectors administered in both apical and basolateral sides of Caco-2 cells. With differentiation, Caco-2 cells increased SR-BI protein expression. Western blot analysis showed the ability of cholesterol and oxysterols in both cell compartments to reduce SR-BI protein expression. Among the n-3, n-6, and n-9 fatty acid families, only eicosapentaenoic acid was able to lower SR-BI protein expression on both sides, whereas apical alpha-linolenic acid decreased SR-BI abundance and basolateral arachidonic acid (AA) raised it. Epidermal growth factor and growth hormone, either in the apical or basolateral medium, diminished SR-BI cellular content, while insulin displayed the same effect only on the basolateral side. In the presence of proinflammatory agents (LPS, TNF-alpha, IFN-gamma), Caco-2 cells exhibited differential behavior. SR-BI was downregulated by lipopolysaccharide on both sides. Finally, WY-14643 fibrate diminished SR-BI protein expression when it was added to the apical medium. Biotinylation studies in response to selected stimuli revealed that regulatory modifications in SR-BI protein expression occurred for the most part at the apical cell surface irrespective of the effector location. Our data indicate that various effectors supplied to the apical and basolateral compartments may impact on SR-BI at the apical membrane, thus suggesting potential regulation of intestinal cholesterol absorption and distribution in various intracellular pools.","publication_date":{"day":null,"month":null,"year":2007,"errors":{}},"publication_name":"Journal of Cellular Biochemistry"},"translated_abstract":"Cholesterol uptake and the mechanisms that regulate cholesterol translocation from the intestinal lumen into enterocytes remain for the most part unclear. Since scavenger receptor class B type I (SR-BI) has been suggested to play a role in cholesterol absorption, we investigated cellular SR-BI modulation by various potential effectors administered in both apical and basolateral sides of Caco-2 cells. With differentiation, Caco-2 cells increased SR-BI protein expression. Western blot analysis showed the ability of cholesterol and oxysterols in both cell compartments to reduce SR-BI protein expression. Among the n-3, n-6, and n-9 fatty acid families, only eicosapentaenoic acid was able to lower SR-BI protein expression on both sides, whereas apical alpha-linolenic acid decreased SR-BI abundance and basolateral arachidonic acid (AA) raised it. Epidermal growth factor and growth hormone, either in the apical or basolateral medium, diminished SR-BI cellular content, while insulin displayed the same effect only on the basolateral side. In the presence of proinflammatory agents (LPS, TNF-alpha, IFN-gamma), Caco-2 cells exhibited differential behavior. SR-BI was downregulated by lipopolysaccharide on both sides. Finally, WY-14643 fibrate diminished SR-BI protein expression when it was added to the apical medium. Biotinylation studies in response to selected stimuli revealed that regulatory modifications in SR-BI protein expression occurred for the most part at the apical cell surface irrespective of the effector location. Our data indicate that various effectors supplied to the apical and basolateral compartments may impact on SR-BI at the apical membrane, thus suggesting potential regulation of intestinal cholesterol absorption and distribution in various intracellular pools.","internal_url":"https://www.academia.edu/12440495/Asymmetrical_regulation_of_scavenger_receptor_class_B_type_I_by_apical_and_basolateral_stimuli_using_Caco_2_cells","translated_internal_url":"","created_at":"2015-05-18T05:12:38.213-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31248312,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":564456,"work_id":12440495,"tagging_user_id":31248312,"tagged_user_id":39643530,"co_author_invite_id":217969,"email":"c***o@recherche-ste-justine.qc.ca","display_order":0,"name":"Carole Garofalo","title":"Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco-2 cells"},{"id":564438,"work_id":12440495,"tagging_user_id":31248312,"tagged_user_id":31307255,"co_author_invite_id":217967,"email":"v***l@hotmail.com","display_order":null,"name":"Valerie Marcil","title":"Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco-2 cells"},{"id":564474,"work_id":12440495,"tagging_user_id":31248312,"tagged_user_id":31223745,"co_author_invite_id":null,"email":"e***n@recherche-ste-justine.qc.ca","display_order":null,"name":"Edgard Delvin","title":"Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco-2 cells"},{"id":564446,"work_id":12440495,"tagging_user_id":31248312,"tagged_user_id":32265331,"co_author_invite_id":217968,"email":"d***t@umontreal.ca","display_order":null,"name":"Daniel Sinnett","title":"Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco-2 cells"}],"downloadable_attachments":[],"slug":"Asymmetrical_regulation_of_scavenger_receptor_class_B_type_I_by_apical_and_basolateral_stimuli_using_Caco_2_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":31248312,"first_name":"Emile","middle_initials":null,"last_name":"Levy","page_name":"EmileLevy","domain_name":"umontreal","created_at":"2015-05-18T05:12:19.584-07:00","display_name":"Emile Levy","url":"https://umontreal.academia.edu/EmileLevy"},"attachments":[],"research_interests":[{"id":60436,"name":"Cell Differentiation","url":"https://www.academia.edu/Documents/in/Cell_Differentiation"},{"id":60915,"name":"Cellular","url":"https://www.academia.edu/Documents/in/Cellular"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":72314,"name":"Fatty acids","url":"https://www.academia.edu/Documents/in/Fatty_acids"},{"id":90514,"name":"Cholesterol","url":"https://www.academia.edu/Documents/in/Cholesterol"},{"id":104853,"name":"Hormones","url":"https://www.academia.edu/Documents/in/Hormones"},{"id":122569,"name":"Cell Polarity","url":"https://www.academia.edu/Documents/in/Cell_Polarity"},{"id":314125,"name":"Caco-2 cells","url":"https://www.academia.edu/Documents/in/Caco-2_cells"},{"id":335983,"name":"Lipopolysaccharides","url":"https://www.academia.edu/Documents/in/Lipopolysaccharides"},{"id":782251,"name":"Cell Proliferation","url":"https://www.academia.edu/Documents/in/Cell_Proliferation"},{"id":989723,"name":"Caco 2 Cell","url":"https://www.academia.edu/Documents/in/Caco_2_Cell"},{"id":1296969,"name":"Molecular and Cellular Biochemistry","url":"https://www.academia.edu/Documents/in/Molecular_and_Cellular_Biochemistry"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":2468093,"name":"Cell Membrane","url":"https://www.academia.edu/Documents/in/Cell_Membrane"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="12440494"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/12440494/Modulation_of_intestinal_and_liver_fatty_acid_binding_proteins_in_Caco_2_cells_by_lipids_hormones_and_cytokines"><img alt="Research paper thumbnail of Modulation of intestinal and liver fatty acid-binding proteins in Caco-2 cells by lipids, hormones and cytokines" class="work-thumbnail" src="https://attachments.academia-assets.com/46182774/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/12440494/Modulation_of_intestinal_and_liver_fatty_acid_binding_proteins_in_Caco_2_cells_by_lipids_hormones_and_cytokines">Modulation of intestinal and liver fatty acid-binding proteins in Caco-2 cells by lipids, hormones and cytokines</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/CaroleGarofalo">Carole Garofalo</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://umontreal.academia.edu/EmileLevy">Emile Levy</a></span></div><div class="wp-workCard_item"><span>Journal of Cellular Biochemistry</span><span>, 2001</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c4c0869e78e30b744972dd69ceda3a4f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":46182774,"asset_id":12440494,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/46182774/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="12440494"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="12440494"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12440494; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12440494]").text(description); $(".js-view-count[data-work-id=12440494]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12440494; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12440494']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12440494, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "c4c0869e78e30b744972dd69ceda3a4f" } } $('.js-work-strip[data-work-id=12440494]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12440494,"title":"Modulation of intestinal and liver fatty acid-binding proteins in Caco-2 cells by lipids, hormones and cytokines","translated_title":"","metadata":{"grobid_abstract":"Intestinal and liver fatty acid binding proteins (I-and L-FABP) are thought to play a role in enterocyte fatty acid (FA) traf庐cking. Their modulation by cell differentiation and various potential effectors was investigated in the human Caco-2 cell line. With the acquisition of enterocytic features, Caco-2 cells seeded on plastic progressively increased L-FABP quantities, whereas I-FABP was not detectable even very late in the maturation process. On permeable 庐lters that improved differentiation markers (sucrase, alkaline phosphatase, transepithelial resistance), Caco-2 cells furthered their L-FABP content and expressed I-FABP. Western blot analysis showed a signi庐cant increase in I-and L-FABP expression following an 8-hour incubation period with butyric acid, oleic acid, and phosphatidylcholine. However, in all cases, I-FABP levels were higher than L-FABP concentrations regardless of the lipid substrates added. Similarly, hydrocortisone and insulin enhanced the cellular content of I-and L-FABP whereas leptin triggered I-FABP expression only after an 8-hour incubation. Finally, tumor necrosis factor-a was more effective in increasing the cytosolic amount of I-FABP levels. In conclusion, our data demonstrate that I-FABP expression is limited to fully differentiated Caco-2 cells and can be more easily regulated than L-FABP by lipids, hormones, and cytokines.","publication_date":{"day":null,"month":null,"year":2001,"errors":{}},"publication_name":"Journal of Cellular Biochemistry","grobid_abstract_attachment_id":46182774},"translated_abstract":null,"internal_url":"https://www.academia.edu/12440494/Modulation_of_intestinal_and_liver_fatty_acid_binding_proteins_in_Caco_2_cells_by_lipids_hormones_and_cytokines","translated_internal_url":"","created_at":"2015-05-18T05:12:38.104-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31248312,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":564455,"work_id":12440494,"tagging_user_id":31248312,"tagged_user_id":39643530,"co_author_invite_id":217969,"email":"c***o@recherche-ste-justine.qc.ca","display_order":0,"name":"Carole 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(HEPATOLOGY fine whether essential fatty acid (EFA) deficiency modi-1996;23:848-857.) fies the intrahepatic metabolism and biliary output of sterols in rats. EFA-deficient diet caused an impoverishment in linoleic, arachidonic, and docosahexaenoic","publication_date":{"day":null,"month":null,"year":1996,"errors":{}},"publication_name":"Hepatology","grobid_abstract_attachment_id":40587801},"translated_abstract":null,"internal_url":"https://www.academia.edu/19380175/Impact_of_essential_fatty_acid_deficiency_on_hepatic_sterol_metabolism_in_rats","translated_internal_url":"","created_at":"2015-12-02T14:00:34.303-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":39643530,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":11545756,"work_id":19380175,"tagging_user_id":39643530,"tagged_user_id":31248312,"co_author_invite_id":null,"email":"e***y@recherche-ste-justine.qc.ca","affiliation":"Universit茅 de Montr茅al","display_order":0,"name":"Emile Levy","title":"Impact of essential fatty acid deficiency on hepatic sterol metabolism in rats"},{"id":11545784,"work_id":19380175,"tagging_user_id":39643530,"tagged_user_id":null,"co_author_invite_id":217965,"email":"m***n@umontreal.ca","display_order":4194304,"name":"Moise Bendayan","title":"Impact of essential fatty acid deficiency on hepatic sterol metabolism in rats"},{"id":11545798,"work_id":19380175,"tagging_user_id":39643530,"tagged_user_id":57133755,"co_author_invite_id":217928,"email":"t***u@recherche-ste-justine.qc.ca","display_order":6291456,"name":"Th茅r猫se Rouleau","title":"Impact of essential fatty acid deficiency on hepatic sterol metabolism in rats"}],"downloadable_attachments":[{"id":40587801,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/40587801/thumbnails/1.jpg","file_name":"hep.510230428.pdf20151202-17091-1l73mne","download_url":"https://www.academia.edu/attachments/40587801/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Impact_of_essential_fatty_acid_deficienc.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/40587801/hep.510230428-libre.pdf20151202-17091-1l73mne?1449093975=\u0026response-content-disposition=attachment%3B+filename%3DImpact_of_essential_fatty_acid_deficienc.pdf\u0026Expires=1732617198\u0026Signature=BlGLy1iEsYKbcHDFlWFUslSGYIl8-t6vVigDbuladTsgH6gfzAaiPG3zLAHuSYLyb9TRp19aIxUNnXoC0UhaCAMHuWfwadDu43zI724xIhoY9dJ4i616VpCA6JQBWP4~9ZnmMsl80WqE3Bac9UqeYA4nRw27WiPvUn073bz3Y5QiBRJ0GqV2-nvBTTpqRYTcwLPCfJdJk9XrSij1MOgIcil0r6EK2slkl1om1ZMTA3EIl4KD0g9qao5h~L5UpywzFCShDpagkoiMl8d70ZKORG3O8~OrhXyEGC0UQdHxqS~rcuBLldExk-dHBPtoLjJNnBAyMHn2J4etD~2pl6omPw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Impact_of_essential_fatty_acid_deficiency_on_hepatic_sterol_metabolism_in_rats","translated_slug":"","page_count":10,"language":"en","content_type":"Work","owner":{"id":39643530,"first_name":"Carole","middle_initials":null,"last_name":"Garofalo","page_name":"CaroleGarofalo","domain_name":"independent","created_at":"2015-12-02T13:59:52.848-08:00","display_name":"Carole Garofalo","url":"https://independent.academia.edu/CaroleGarofalo"},"attachments":[{"id":40587801,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/40587801/thumbnails/1.jpg","file_name":"hep.510230428.pdf20151202-17091-1l73mne","download_url":"https://www.academia.edu/attachments/40587801/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Impact_of_essential_fatty_acid_deficienc.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/40587801/hep.510230428-libre.pdf20151202-17091-1l73mne?1449093975=\u0026response-content-disposition=attachment%3B+filename%3DImpact_of_essential_fatty_acid_deficienc.pdf\u0026Expires=1732617198\u0026Signature=BlGLy1iEsYKbcHDFlWFUslSGYIl8-t6vVigDbuladTsgH6gfzAaiPG3zLAHuSYLyb9TRp19aIxUNnXoC0UhaCAMHuWfwadDu43zI724xIhoY9dJ4i616VpCA6JQBWP4~9ZnmMsl80WqE3Bac9UqeYA4nRw27WiPvUn073bz3Y5QiBRJ0GqV2-nvBTTpqRYTcwLPCfJdJk9XrSij1MOgIcil0r6EK2slkl1om1ZMTA3EIl4KD0g9qao5h~L5UpywzFCShDpagkoiMl8d70ZKORG3O8~OrhXyEGC0UQdHxqS~rcuBLldExk-dHBPtoLjJNnBAyMHn2J4etD~2pl6omPw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":37773,"name":"Hepatology","url":"https://www.academia.edu/Documents/in/Hepatology"},{"id":71437,"name":"Liver","url":"https://www.academia.edu/Documents/in/Liver"},{"id":90514,"name":"Cholesterol","url":"https://www.academia.edu/Documents/in/Cholesterol"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":1611350,"name":"Docosahexaenoic Acid","url":"https://www.academia.edu/Documents/in/Docosahexaenoic_Acid"},{"id":2061395,"name":"Bile","url":"https://www.academia.edu/Documents/in/Bile-6"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="19380174"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/19380174/The_distribution_of_microsomal_transfer_protein_MTP_and_apolipoprotein_b_in_endoplasmic_reticulum_ER_and_golgi_of_intestinal_absorptive_cells_possible_role_of_the_golgi_in_the_assembly_of_chylomicrons"><img alt="Research paper thumbnail of The distribution of microsomal transfer protein (MTP) and apolipoprotein b in endoplasmic reticulum (ER) and golgi of intestinal absorptive cells: possible role of the golgi in the assembly of chylomicrons" class="work-thumbnail" src="https://attachments.academia-assets.com/40587802/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/19380174/The_distribution_of_microsomal_transfer_protein_MTP_and_apolipoprotein_b_in_endoplasmic_reticulum_ER_and_golgi_of_intestinal_absorptive_cells_possible_role_of_the_golgi_in_the_assembly_of_chylomicrons">The distribution of microsomal transfer protein (MTP) and apolipoprotein b in endoplasmic reticulum (ER) and golgi of intestinal absorptive cells: possible role of the golgi in the assembly of chylomicrons</a></div><div class="wp-workCard_item"><span>Gastroenterology</span><span>, 2000</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="e3c269ea313f65b545cf5979dc3656d3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":40587802,"asset_id":19380174,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/40587802/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="19380174"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="19380174"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 19380174; 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These studies aim to identify regions of the lactase promoter involved in mediating the spatio-temporal expression pattern of the lactase gene and to utilize a novel photonic detection method for in vivo monitoring of promoter-reporter transgene expression in animals. Methods: 2.0-and 0.8kilobase fragments of the 5' flanking region of the rat lactase gene were cloned upstream of a firefly luciferase reporter and transfected into intestinal Caco-2 cells as a culture correlate of promoter activity. Transgenic mice harboring those same lactase promoter-reporter constructs were generated and screened for transgene expression by in vivo photonic detection with an intensified charge-coupled device (ICCD) camera. Luciferase activity was measured quantitatively by luminometer assays in multiple organs, including intestinal segments, harvested from pre and post-weaned mice. Results: Pre-weaned offspring of a 2-kb lactase promoter-reporter transgenic line express high-level luciferase activity in the small intestine (\u003e 8,000 fold over background) with maximal expression in the middle segments. Luciferase expression was barely detectable 芦 3 fold over background) in colon, stomach, kidney, lung, liver, spleen, and brain. Post-weaned 30-day offspring undergo a region-specific decline in luciferase expression in the small intestine (25% activity in the proximal and middle segments and 1% in the distal segments) relative to pre-weaned levels. In comparison to the full length promoter, the 0.8 -kb promoterreporter construct expressed low-level luciferase activity 芦 50 fold over background) in multiple organs and throughout the GI tract in transgenic mice. Conclusions: A 2.0-kilobase fragment of the lactase promoter directs region-specific expression in the small intestine of transgenic mice. The pattern of expression mimics that of endogenous lactase with respect to spatial restriction during maturation and differs from that described for related transgenic constructs. Important tissue-specific enhancing elements may reside in the region between 0.8-2.0 kb upstream of the lactase transcription start-site. Photonic detection with the ICCD camera is a sensitive method to rapidly screen for intestinal expression of a luciferase reporter gene in living transgenic 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href="https://www.academia.edu/12440489/Immunolocalization_ontogeny_and_regulation_of_microsomal_transfer_protein_MTP_in_human_fetal_intestine"><img alt="Research paper thumbnail of Immunolocalization, ontogeny and regulation of microsomal transfer protein (MTP) in human fetal intestine" class="work-thumbnail" src="https://attachments.academia-assets.com/46182797/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/12440489/Immunolocalization_ontogeny_and_regulation_of_microsomal_transfer_protein_MTP_in_human_fetal_intestine">Immunolocalization, ontogeny and regulation of microsomal transfer protein (MTP) in human fetal intestine</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/CaroleGarofalo">Carole Garofalo</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://umontreal.academia.edu/EmileLevy">Emile Levy</a></span></div><div class="wp-workCard_item"><span>Gastroenterology</span><span>, 2000</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="10b0f7e7060d980ea014810cbba9a8bd" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":46182797,"asset_id":12440489,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/46182797/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper 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window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12440489']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12440489, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || 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These studies aim to identify regions of the lactase promoter involved in mediating the spatio-temporal expression pattern of the lactase gene and to utilize a novel photonic detection method for in vivo monitoring of promoter-reporter transgene expression in animals. Methods: 2.0-and 0.8kilobase fragments of the 5' flanking region of the rat lactase gene were cloned upstream of a firefly luciferase reporter and transfected into intestinal Caco-2 cells as a culture correlate of promoter activity. Transgenic mice harboring those same lactase promoter-reporter constructs were generated and screened for transgene expression by in vivo photonic detection with an intensified charge-coupled device (ICCD) camera. Luciferase activity was measured quantitatively by luminometer assays in multiple organs, including intestinal segments, harvested from pre and post-weaned mice. Results: Pre-weaned offspring of a 2-kb lactase promoter-reporter transgenic line express high-level luciferase activity in the small intestine (\u003e 8,000 fold over background) with maximal expression in the middle segments. Luciferase expression was barely detectable 芦 3 fold over background) in colon, stomach, kidney, lung, liver, spleen, and brain. Post-weaned 30-day offspring undergo a region-specific decline in luciferase expression in the small intestine (25% activity in the proximal and middle segments and 1% in the distal segments) relative to pre-weaned levels. In comparison to the full length promoter, the 0.8 -kb promoterreporter construct expressed low-level luciferase activity 芦 50 fold over background) in multiple organs and throughout the GI tract in transgenic mice. Conclusions: A 2.0-kilobase fragment of the lactase promoter directs region-specific expression in the small intestine of transgenic mice. The pattern of expression mimics that of endogenous lactase with respect to spatial restriction during maturation and differs from that described for related transgenic constructs. Important tissue-specific enhancing elements may reside in the region between 0.8-2.0 kb upstream of the lactase transcription start-site. Photonic detection with the ICCD camera is a sensitive method to rapidly screen for intestinal expression of a luciferase reporter gene in living transgenic mice.","publication_date":{"day":null,"month":null,"year":2000,"errors":{}},"publication_name":"Gastroenterology","grobid_abstract_attachment_id":46182797},"translated_abstract":null,"internal_url":"https://www.academia.edu/12440489/Immunolocalization_ontogeny_and_regulation_of_microsomal_transfer_protein_MTP_in_human_fetal_intestine","translated_internal_url":"","created_at":"2015-05-18T05:12:37.504-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31248312,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":564454,"work_id":12440489,"tagging_user_id":31248312,"tagged_user_id":39643530,"co_author_invite_id":217969,"email":"c***o@recherche-ste-justine.qc.ca","display_order":0,"name":"Carole Garofalo","title":"Immunolocalization, ontogeny and regulation of microsomal transfer protein (MTP) in human fetal intestine"},{"id":564469,"work_id":12440489,"tagging_user_id":31248312,"tagged_user_id":31223745,"co_author_invite_id":null,"email":"e***n@recherche-ste-justine.qc.ca","display_order":null,"name":"Edgard Delvin","title":"Immunolocalization, ontogeny and regulation of microsomal transfer protein (MTP) in human fetal intestine"}],"downloadable_attachments":[{"id":46182797,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/46182797/thumbnails/1.jpg","file_name":"S0016-5085_2800_2983249-720160602-19467-l6tizl.pdf","download_url":"https://www.academia.edu/attachments/46182797/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Immunolocalization_ontogeny_and_regulati.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/46182797/S0016-5085_2800_2983249-720160602-19467-l6tizl-libre.pdf?1464914830=\u0026response-content-disposition=attachment%3B+filename%3DImmunolocalization_ontogeny_and_regulati.pdf\u0026Expires=1731934979\u0026Signature=NCWtUOA3lobIi5Xy69lMTyoen4R8cUArEuJ4dxAQYmR66pHK2L8n7nknCY~WOI~fopXP8EXqLolRDwDmULCK7M-Qq5FJCGq4rkoL~mrHkuUAvdYV0MvDAfW4SKXeZ4JeFlKzDMY5AYiIpAo8~nTosmrRsQyJ3mwdim9bKf~yICrpkKgBBRx~npGO9CQYnp0554il~01G6YzkbP1agXS~FIYT~3DV66FnbxI4aA93pBqxCISVhEi2lnX3WEsttYOhc5N46hBwfjiLbqjFfUujetdqI-u6dLODqjLdXDvHalFvKYGc24eRe~KERQ1GzVyvqsb7tAVz8JEySdFXdLkF5Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Immunolocalization_ontogeny_and_regulation_of_microsomal_transfer_protein_MTP_in_human_fetal_intestine","translated_slug":"","page_count":1,"language":"en","content_type":"Work","owner":{"id":31248312,"first_name":"Emile","middle_initials":null,"last_name":"Levy","page_name":"EmileLevy","domain_name":"umontreal","created_at":"2015-05-18T05:12:19.584-07:00","display_name":"Emile Levy","url":"https://umontreal.academia.edu/EmileLevy"},"attachments":[{"id":46182797,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/46182797/thumbnails/1.jpg","file_name":"S0016-5085_2800_2983249-720160602-19467-l6tizl.pdf","download_url":"https://www.academia.edu/attachments/46182797/download_file?st=MTczMjcwOTc1Miw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Immunolocalization_ontogeny_and_regulati.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/46182797/S0016-5085_2800_2983249-720160602-19467-l6tizl-libre.pdf?1464914830=\u0026response-content-disposition=attachment%3B+filename%3DImmunolocalization_ontogeny_and_regulati.pdf\u0026Expires=1731934979\u0026Signature=NCWtUOA3lobIi5Xy69lMTyoen4R8cUArEuJ4dxAQYmR66pHK2L8n7nknCY~WOI~fopXP8EXqLolRDwDmULCK7M-Qq5FJCGq4rkoL~mrHkuUAvdYV0MvDAfW4SKXeZ4JeFlKzDMY5AYiIpAo8~nTosmrRsQyJ3mwdim9bKf~yICrpkKgBBRx~npGO9CQYnp0554il~01G6YzkbP1agXS~FIYT~3DV66FnbxI4aA93pBqxCISVhEi2lnX3WEsttYOhc5N46hBwfjiLbqjFfUujetdqI-u6dLODqjLdXDvHalFvKYGc24eRe~KERQ1GzVyvqsb7tAVz8JEySdFXdLkF5Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":3274,"name":"Gastroenterology","url":"https://www.academia.edu/Documents/in/Gastroenterology"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":1239755,"name":"Neurosciences","url":"https://www.academia.edu/Documents/in/Neurosciences"}],"urls":[]}, dispatcherData: dispatcherData }); 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