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Alain Montoudis - Academia.edu

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class="js-profile-total-view-text">Public Views</span></p><p class="data"><span 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="31309978" href="https://www.academia.edu/Documents/in/Nutrition"><div id="js-react-on-rails-context" style="display:none" data-rails-context="{&quot;inMailer&quot;:false,&quot;i18nLocale&quot;:&quot;en&quot;,&quot;i18nDefaultLocale&quot;:&quot;en&quot;,&quot;href&quot;:&quot;https://independent.academia.edu/AlainMontoudis&quot;,&quot;location&quot;:&quot;/AlainMontoudis&quot;,&quot;scheme&quot;:&quot;https&quot;,&quot;host&quot;:&quot;independent.academia.edu&quot;,&quot;port&quot;:null,&quot;pathname&quot;:&quot;/AlainMontoudis&quot;,&quot;search&quot;:null,&quot;httpAcceptLanguage&quot;:null,&quot;serverSide&quot;:false}"></div> <div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{&quot;color&quot;:&quot;gray&quot;,&quot;children&quot;:[&quot;Nutrition&quot;]}" data-trace="false" data-dom-id="Pill-react-component-021dc274-10f2-4b33-8aac-5e27b8c2de41"></div> <div id="Pill-react-component-021dc274-10f2-4b33-8aac-5e27b8c2de41"></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 Alain Montoudis</h3></div><div class="js-work-strip profile--work_container" data-work-id="12472808"><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/12472808/Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites"><img alt="Research paper thumbnail of Evaluation of 3-hydroxy-3-methylglutaryl-COA-reductase, cholesterol-7?-hydroxylase and acyl-COA:cholesterol acyltransferase activities: alternative chromatographic methods to separate metabolites" 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/12472808/Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites">Evaluation of 3-hydroxy-3-methylglutaryl-COA-reductase, cholesterol-7?-hydroxylase and acyl-COA:cholesterol acyltransferase activities: alternative chromatographic methods to separate metabolites</a></div><div class="wp-workCard_item"><span>Biomedical Chromatography</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites...</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">Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites of enzymes involved in cholesterol metabolism in rabbit liver microsomes: hydroxyl-methylglutaryl-CoA reductase, cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase. A comparison method of thin-layer chromatography and solid-phase extraction column were assayed to separate substrate and metabolite of hydroxy-methylglutaryl-CoA reductase, whereas for cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase, this comparison was done between thin layer chromatography and HPLC. The results obtained by the new analytical chromatographic methods are not significantly different than those observed in literature. Moreover a larger percentage recovery was obtained for analysed metabolites. Our results demonstrate the reliability of these alternative chromatographic techniques and showed that they are valuable tools to precisely and rapidly measure the activity of those enzymes.</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="12472808"><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="12472808"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472808; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472808]").text(description); $(".js-view-count[data-work-id=12472808]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472808; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472808']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472808, 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" } } $('.js-work-strip[data-work-id=12472808]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472808,"title":"Evaluation of 3-hydroxy-3-methylglutaryl-COA-reductase, cholesterol-7?-hydroxylase and acyl-COA:cholesterol acyltransferase activities: alternative chromatographic methods to separate metabolites","translated_title":"","metadata":{"abstract":"Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites of enzymes involved in cholesterol metabolism in rabbit liver microsomes: hydroxyl-methylglutaryl-CoA reductase, cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase. A comparison method of thin-layer chromatography and solid-phase extraction column were assayed to separate substrate and metabolite of hydroxy-methylglutaryl-CoA reductase, whereas for cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase, this comparison was done between thin layer chromatography and HPLC. The results obtained by the new analytical chromatographic methods are not significantly different than those observed in literature. Moreover a larger percentage recovery was obtained for analysed metabolites. Our results demonstrate the reliability of these alternative chromatographic techniques and showed that they are valuable tools to precisely and rapidly measure the activity of those enzymes.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Biomedical Chromatography"},"translated_abstract":"Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites of enzymes involved in cholesterol metabolism in rabbit liver microsomes: hydroxyl-methylglutaryl-CoA reductase, cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase. A comparison method of thin-layer chromatography and solid-phase extraction column were assayed to separate substrate and metabolite of hydroxy-methylglutaryl-CoA reductase, whereas for cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase, this comparison was done between thin layer chromatography and HPLC. The results obtained by the new analytical chromatographic methods are not significantly different than those observed in literature. Moreover a larger percentage recovery was obtained for analysed metabolites. Our results demonstrate the reliability of these alternative chromatographic techniques and showed that they are valuable tools to precisely and rapidly measure the activity of those enzymes.","internal_url":"https://www.academia.edu/12472808/Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites","translated_internal_url":"","created_at":"2015-05-19T13:56:32.644-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31309978,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":31309978,"first_name":"Alain","middle_initials":null,"last_name":"Montoudis","page_name":"AlainMontoudis","domain_name":"independent","created_at":"2015-05-19T13:55:47.683-07:00","display_name":"Alain Montoudis","url":"https://independent.academia.edu/AlainMontoudis"},"attachments":[],"research_interests":[{"id":524,"name":"Analytical Chemistry","url":"https://www.academia.edu/Documents/in/Analytical_Chemistry"},{"id":5769,"name":"Mass Spectrometry","url":"https://www.academia.edu/Documents/in/Mass_Spectrometry"},{"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":246560,"name":"High Pressure Liquid Chromatography","url":"https://www.academia.edu/Documents/in/High_Pressure_Liquid_Chromatography"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":549972,"name":"Microchemistry","url":"https://www.academia.edu/Documents/in/Microchemistry"},{"id":788677,"name":"Rabbits","url":"https://www.academia.edu/Documents/in/Rabbits"},{"id":806387,"name":"Analytical Biochemistry","url":"https://www.academia.edu/Documents/in/Analytical_Biochemistry"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"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="12472805"><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/12472805/Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7alpha_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites"><img alt="Research paper thumbnail of Evaluation of 3-hydroxy-3-methylglutaryl-COA-reductase, cholesterol-7alpha-hydroxylase and acyl-COA:cholesterol acyltransferase activities: alternative chromatographic methods to separate metabolites" 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/12472805/Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7alpha_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites">Evaluation of 3-hydroxy-3-methylglutaryl-COA-reductase, cholesterol-7alpha-hydroxylase and acyl-COA:cholesterol acyltransferase activities: alternative chromatographic methods to separate metabolites</a></div><div class="wp-workCard_item"><span>Biomedical chromatography : BMC</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites...</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">Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites of enzymes involved in cholesterol metabolism in rabbit liver microsomes: hydroxyl-methylglutaryl-CoA reductase, cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase. A comparison method of thin-layer chromatography and solid-phase extraction column were assayed to separate substrate and metabolite of hydroxy-methylglutaryl-CoA reductase, whereas for cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase, this comparison was done between thin layer chromatography and HPLC. The results obtained by the new analytical chromatographic methods are not significantly different than those observed in literature. Moreover a larger percentage recovery was obtained for analysed metabolites. Our results demonstrate the reliability of these alternative chromatographic techniques and showed that they are valuable tools to precisely and rapidly measure the activity ...</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="12472805"><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="12472805"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472805; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472805]").text(description); $(".js-view-count[data-work-id=12472805]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472805; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472805']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472805, 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" } } $('.js-work-strip[data-work-id=12472805]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472805,"title":"Evaluation of 3-hydroxy-3-methylglutaryl-COA-reductase, cholesterol-7alpha-hydroxylase and acyl-COA:cholesterol acyltransferase activities: alternative chromatographic methods to separate metabolites","translated_title":"","metadata":{"abstract":"Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites of enzymes involved in cholesterol metabolism in rabbit liver microsomes: hydroxyl-methylglutaryl-CoA reductase, cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase. A comparison method of thin-layer chromatography and solid-phase extraction column were assayed to separate substrate and metabolite of hydroxy-methylglutaryl-CoA reductase, whereas for cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase, this comparison was done between thin layer chromatography and HPLC. The results obtained by the new analytical chromatographic methods are not significantly different than those observed in literature. Moreover a larger percentage recovery was obtained for analysed metabolites. Our results demonstrate the reliability of these alternative chromatographic techniques and showed that they are valuable tools to precisely and rapidly measure the activity ...","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Biomedical chromatography : BMC"},"translated_abstract":"Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites of enzymes involved in cholesterol metabolism in rabbit liver microsomes: hydroxyl-methylglutaryl-CoA reductase, cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase. A comparison method of thin-layer chromatography and solid-phase extraction column were assayed to separate substrate and metabolite of hydroxy-methylglutaryl-CoA reductase, whereas for cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase, this comparison was done between thin layer chromatography and HPLC. The results obtained by the new analytical chromatographic methods are not significantly different than those observed in literature. Moreover a larger percentage recovery was obtained for analysed metabolites. Our results demonstrate the reliability of these alternative chromatographic techniques and showed that they are valuable tools to precisely and rapidly measure the activity ...","internal_url":"https://www.academia.edu/12472805/Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7alpha_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites","translated_internal_url":"","created_at":"2015-05-19T13:56:27.691-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31309978,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7alpha_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":31309978,"first_name":"Alain","middle_initials":null,"last_name":"Montoudis","page_name":"AlainMontoudis","domain_name":"independent","created_at":"2015-05-19T13:55:47.683-07:00","display_name":"Alain Montoudis","url":"https://independent.academia.edu/AlainMontoudis"},"attachments":[],"research_interests":[{"id":524,"name":"Analytical Chemistry","url":"https://www.academia.edu/Documents/in/Analytical_Chemistry"},{"id":5769,"name":"Mass Spectrometry","url":"https://www.academia.edu/Documents/in/Mass_Spectrometry"},{"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":246560,"name":"High Pressure Liquid Chromatography","url":"https://www.academia.edu/Documents/in/High_Pressure_Liquid_Chromatography"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":549972,"name":"Microchemistry","url":"https://www.academia.edu/Documents/in/Microchemistry"},{"id":788677,"name":"Rabbits","url":"https://www.academia.edu/Documents/in/Rabbits"},{"id":806387,"name":"Analytical Biochemistry","url":"https://www.academia.edu/Documents/in/Analytical_Biochemistry"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"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="12472804"><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/12472804/Influence_of_a_maternal_cholesterol_enriched_diet_on_1_14C_linoleic_acid_and_L_4_5_3H_leucine_entry_in_plasma_of_rabbit_offspring"><img alt="Research paper thumbnail of Influence of a maternal cholesterol-enriched diet on [1-14C]-linoleic acid and L-[4, 5-3H]-leucine entry in plasma of rabbit offspring" class="work-thumbnail" src="https://attachments.academia-assets.com/46157157/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/12472804/Influence_of_a_maternal_cholesterol_enriched_diet_on_1_14C_linoleic_acid_and_L_4_5_3H_leucine_entry_in_plasma_of_rabbit_offspring">Influence of a maternal cholesterol-enriched diet on [1-14C]-linoleic acid and L-[4, 5-3H]-leucine entry in plasma of rabbit offspring</a></div><div class="wp-workCard_item"><span>Life sciences</span><span>, Jan 20, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Fetal development requires an important entry of essential free fatty acids (EFFA) and essential ...</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">Fetal development requires an important entry of essential free fatty acids (EFFA) and essential amino acids (EAA) into the fetal circulation. We have reported that a 0.2% enriched-cholesterol diet (ECD) during rabbit gestation significantly reduces fetus weight compared to control diet. It is known that dietary linoleic acid deficiency, an EFFA, during the fetal development induces an important impair to the somatic development. Moreover, intrauterine growth retardation induced a reduction of the flux of leucine, an EAA, from maternal to fetal circulation. Therefore, we hypothesized that the administration of an ECD induces modifications of placental lipid composition concomitant alterations of the transfer of linoleic acid and leucine in fetal circulation. Quantification of placental lipids revealed that in the ECD group a reduction of total-cholesterol (TC) and free-cholesterol (FC) is observed, however an increased in FFA and phospholipids is noticed when compared to the control...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b011f6ac7a41651cca17e40019719970" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{&quot;attachment_id&quot;:46157157,&quot;asset_id&quot;:12472804,&quot;asset_type&quot;:&quot;Work&quot;,&quot;button_location&quot;:&quot;profile&quot;}" href="https://www.academia.edu/attachments/46157157/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&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="12472804"><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="12472804"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472804; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472804]").text(description); $(".js-view-count[data-work-id=12472804]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472804; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472804']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472804, 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: "b011f6ac7a41651cca17e40019719970" } } $('.js-work-strip[data-work-id=12472804]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472804,"title":"Influence of a maternal cholesterol-enriched diet on [1-14C]-linoleic acid and L-[4, 5-3H]-leucine entry in plasma of rabbit offspring","translated_title":"","metadata":{"abstract":"Fetal development requires an important entry of essential free fatty acids (EFFA) and essential amino acids (EAA) into the fetal circulation. 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Quantification of placental lipids revealed that in the ECD group a reduction of total-cholesterol (TC) and free-cholesterol (FC) is observed, however an increased in FFA and phospholipids is noticed when compared to the control...","publication_date":{"day":20,"month":1,"year":2004,"errors":{}},"publication_name":"Life sciences"},"translated_abstract":"Fetal development requires an important entry of essential free fatty acids (EFFA) and essential amino acids (EAA) into the fetal circulation. We have reported that a 0.2% enriched-cholesterol diet (ECD) during rabbit gestation significantly reduces fetus weight compared to control diet. It is known that dietary linoleic acid deficiency, an EFFA, during the fetal development induces an important impair to the somatic development. Moreover, intrauterine growth retardation induced a reduction of the flux of leucine, an EAA, from maternal to fetal circulation. 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hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/12472803/Impact_of_an_enriched_cholesterol_diet_on_enzymatic_cholesterol_metabolism_during_rabbit_gestation"><img alt="Research paper thumbnail of Impact of an enriched-cholesterol diet on enzymatic cholesterol metabolism during rabbit gestation" class="work-thumbnail" src="https://attachments.academia-assets.com/46157152/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/12472803/Impact_of_an_enriched_cholesterol_diet_on_enzymatic_cholesterol_metabolism_during_rabbit_gestation">Impact of an enriched-cholesterol diet on enzymatic cholesterol metabolism during rabbit gestation</a></div><div class="wp-workCard_item"><span>Life sciences</span><span>, 2003</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">An appropriate cholesterol homeostasis is vital for the maintenance and the optimal fetal develop...</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">An appropriate cholesterol homeostasis is vital for the maintenance and the optimal fetal development. The cholesterol is essential for the synthesis of progesterone and 17beta-estradiol, hormones that actively participate to sustain gestation. However, the administration of 0.2% enriched cholesterol diet (ECD) during rabbit gestation significantly increased the cholesterol blood profile (total-cholesterol, LDL, HDL, esterified-cholesterol and free-cholesterol) of dams and offspring, and induced a reduction of the offspring weight of 15% as compared to the control group. Enzymes involved in cholesterol metabolism (ACAT, HMG-CoA-reductase and cholesterol-7alpha-hydroxylase) are greatly influenced by cholesterol profile. We hypothesized that the administration of an ECD during rabbit gestation modifies the activity of those enzymes. Female rabbits (pregnant or not) were fed with a standard diet or an ECD. At term, livers (dams and offspring) and placentas were collected and ACAT, HMG-...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="e82f990b6b2c7ff9f0931b46e464636d" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{&quot;attachment_id&quot;:46157152,&quot;asset_id&quot;:12472803,&quot;asset_type&quot;:&quot;Work&quot;,&quot;button_location&quot;:&quot;profile&quot;}" href="https://www.academia.edu/attachments/46157152/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&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="12472803"><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="12472803"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472803; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472803]").text(description); $(".js-view-count[data-work-id=12472803]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472803; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472803']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472803, 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: "e82f990b6b2c7ff9f0931b46e464636d" } } $('.js-work-strip[data-work-id=12472803]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472803,"title":"Impact of an enriched-cholesterol diet on enzymatic cholesterol metabolism during rabbit gestation","translated_title":"","metadata":{"abstract":"An appropriate cholesterol homeostasis is vital for the maintenance and the optimal fetal development. The cholesterol is essential for the synthesis of progesterone and 17beta-estradiol, hormones that actively participate to sustain gestation. However, the administration of 0.2% enriched cholesterol diet (ECD) during rabbit gestation significantly increased the cholesterol blood profile (total-cholesterol, LDL, HDL, esterified-cholesterol and free-cholesterol) of dams and offspring, and induced a reduction of the offspring weight of 15% as compared to the control group. Enzymes involved in cholesterol metabolism (ACAT, HMG-CoA-reductase and cholesterol-7alpha-hydroxylase) are greatly influenced by cholesterol profile. We hypothesized that the administration of an ECD during rabbit gestation modifies the activity of those enzymes. Female rabbits (pregnant or not) were fed with a standard diet or an ECD. At term, livers (dams and offspring) and placentas were collected and ACAT, HMG-...","publication_date":{"day":null,"month":null,"year":2003,"errors":{}},"publication_name":"Life sciences"},"translated_abstract":"An appropriate cholesterol homeostasis is vital for the maintenance and the optimal fetal development. The cholesterol is essential for the synthesis of progesterone and 17beta-estradiol, hormones that actively participate to sustain gestation. However, the administration of 0.2% enriched cholesterol diet (ECD) during rabbit gestation significantly increased the cholesterol blood profile (total-cholesterol, LDL, HDL, esterified-cholesterol and free-cholesterol) of dams and offspring, and induced a reduction of the offspring weight of 15% as compared to the control group. Enzymes involved in cholesterol metabolism (ACAT, HMG-CoA-reductase and cholesterol-7alpha-hydroxylase) are greatly influenced by cholesterol profile. We hypothesized that the administration of an ECD during rabbit gestation modifies the activity of those enzymes. Female rabbits (pregnant or not) were fed with a standard diet or an ECD. 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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="12472802"><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/12472802/Influence_of_a_maternal_cholesterol_enriched_diet_on_1_14C_linoleic_acid_and_L_4_5_3H_leucine_entry_in_plasma_of_rabbit_offspring"><img alt="Research paper thumbnail of Influence of a maternal cholesterol-enriched diet on [1-14C]-linoleic acid and L-[4, 5-3H]-leucine entry in plasma of rabbit offspring" class="work-thumbnail" src="https://attachments.academia-assets.com/46157158/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/12472802/Influence_of_a_maternal_cholesterol_enriched_diet_on_1_14C_linoleic_acid_and_L_4_5_3H_leucine_entry_in_plasma_of_rabbit_offspring">Influence of a maternal cholesterol-enriched diet on [1-14C]-linoleic acid and L-[4, 5-3H]-leucine entry in plasma of rabbit offspring</a></div><div class="wp-workCard_item"><span>Life Sciences</span><span>, 2004</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f62095d7d3b3885fc8b7c8a50a30265b" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{&quot;attachment_id&quot;:46157158,&quot;asset_id&quot;:12472802,&quot;asset_type&quot;:&quot;Work&quot;,&quot;button_location&quot;:&quot;profile&quot;}" href="https://www.academia.edu/attachments/46157158/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&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="12472802"><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="12472802"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472802; 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We have reported that a 0.2% enriched-cholesterol diet (ECD) during rabbit gestation significantly reduces fetus weight compared to control diet. It is known that dietary linoleic acid deficiency, an EFFA, during the fetal development induces an important impair to the somatic development. Moreover, intrauterine growth retardation induced a reduction of the flux of leucine, an EAA, from maternal to fetal circulation. Therefore, we hypothesized that the administration of an ECD induces modifications of placental lipid composition concomitant alterations of the transfer of linoleic acid and leucine in fetal circulation. Quantification of placental lipids revealed that in the ECD group a reduction of total-cholesterol (TC) and free-cholesterol (FC) is observed, however an increased in FFA and phospholipids is noticed when compared to the control group. In placenta from the ECD group, the FC/ TC ratio is significantly reduced compared to the control group. In the ECD group, the liver shows an increase of TC, FC and FFA compared to the control group. However, the quantity of triacylglycerol present in the liver from the ECD is significantly reduced compared to the control group. To evaluate the placental transfer of some essential nutrients, intravenous injection of [1-14 C]-linoleic acid or L-[4, 5-3 H]-leucine to term rabbit (control and ECD group) were done. Two hours later, rabbits were euthanized and we collected placenta, livers and blood from dams and offspring. The concentrations of both radiolabeled molecules (linoleic acid and its esterified form or leucine) were higher in the plasma of ECD offspring than those found in offspring from control diet. Despite 0024-3205/$ -see front matter D (J. Lafond). www.elsevier.com/locate/lifescie Life Sciences 74 (2004) 1751 -1762","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Life 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sampling","url":"https://www.academia.edu/Documents/in/Blood_sampling"},{"id":130343,"name":"Hypercholesterolemia","url":"https://www.academia.edu/Documents/in/Hypercholesterolemia"},{"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":283379,"name":"Glycerol","url":"https://www.academia.edu/Documents/in/Glycerol"},{"id":564878,"name":"Body Weight","url":"https://www.academia.edu/Documents/in/Body_Weight"},{"id":770944,"name":"Fetus","url":"https://www.academia.edu/Documents/in/Fetus"},{"id":788677,"name":"Rabbits","url":"https://www.academia.edu/Documents/in/Rabbits"},{"id":818710,"name":"Free Fatty Acid","url":"https://www.academia.edu/Documents/in/Free_Fatty_Acid"},{"id":1274497,"name":"Total Cholesterol","url":"https://www.academia.edu/Documents/in/Total_Cholesterol"},{"id":1631043,"name":"Control Group","url":"https://www.academia.edu/Documents/in/Control_Group"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":2349258,"name":"Serum albumin","url":"https://www.academia.edu/Documents/in/Serum_albumin"}],"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="12472800"><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/12472800/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/46157167/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/12472800/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="a5ab33323cae8a64d5cb5c8dc49175cb" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{&quot;attachment_id&quot;:46157167,&quot;asset_id&quot;:12472800,&quot;asset_type&quot;:&quot;Work&quot;,&quot;button_location&quot;:&quot;profile&quot;}" href="https://www.academia.edu/attachments/46157167/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&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="12472800"><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="12472800"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472800; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472800]").text(description); $(".js-view-count[data-work-id=12472800]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472800; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472800']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472800, 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: "a5ab33323cae8a64d5cb5c8dc49175cb" } } $('.js-work-strip[data-work-id=12472800]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472800,"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. 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 ...","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"The Journal of nutritional biochemistry"},"translated_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. 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 ...","internal_url":"https://www.academia.edu/12472800/Sar1b_transgenic_male_mice_are_more_susceptible_to_high_fat_diet_induced_obesity_insulin_insensitivity_and_intestinal_chylomicron_overproduction","translated_internal_url":"","created_at":"2015-05-19T13:56:27.089-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31309978,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":46157167,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/46157167/thumbnails/1.jpg","file_name":"j.jnutbio.2014.01.00420160602-3400-11s5qdz.pdf","download_url":"https://www.academia.edu/attachments/46157167/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Sar1b_transgenic_male_mice_are_more_susc.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/46157167/j.jnutbio.2014.01.00420160602-3400-11s5qdz-libre.pdf?1464855339=\u0026response-content-disposition=attachment%3B+filename%3DSar1b_transgenic_male_mice_are_more_susc.pdf\u0026Expires=1731603140\u0026Signature=CcLTGaaWMuh-DMox01O~4~sFTSn~btkYxvXYG8rEjnQCXWHUwq-Mfj4uWetrTEfKpCdhFUTNay3xssmJJFlkBnEu9PK2b0lQLR5-vv0lz4Dq55LF2eeYqpo-I7-nwMvqjqB244My9d-dIjdPtGL8zWksEO8oXEJOXMj2xT7I9yh9S5q--DXAOsUJnVDq2~U4Ou9Y6i0VLaBo4~gTP5AyMoq9V37auzWgtbROWAQzQ~9258MVuvpEImLcpjBnaSEJ5gL2-Q3ezGDvTxbqpqoiTZnnDRwLxKgLm7f4eQLF8pv7YR3lkfYmqKx0kmXV-5j707hL0TVFEPV23lPjJUlo~A__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Sar1b_transgenic_male_mice_are_more_susceptible_to_high_fat_diet_induced_obesity_insulin_insensitivity_and_intestinal_chylomicron_overproduction","translated_slug":"","page_count":9,"language":"en","content_type":"Work","owner":{"id":31309978,"first_name":"Alain","middle_initials":null,"last_name":"Montoudis","page_name":"AlainMontoudis","domain_name":"independent","created_at":"2015-05-19T13:55:47.683-07:00","display_name":"Alain Montoudis","url":"https://independent.academia.edu/AlainMontoudis"},"attachments":[{"id":46157167,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/46157167/thumbnails/1.jpg","file_name":"j.jnutbio.2014.01.00420160602-3400-11s5qdz.pdf","download_url":"https://www.academia.edu/attachments/46157167/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Sar1b_transgenic_male_mice_are_more_susc.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/46157167/j.jnutbio.2014.01.00420160602-3400-11s5qdz-libre.pdf?1464855339=\u0026response-content-disposition=attachment%3B+filename%3DSar1b_transgenic_male_mice_are_more_susc.pdf\u0026Expires=1731603140\u0026Signature=CcLTGaaWMuh-DMox01O~4~sFTSn~btkYxvXYG8rEjnQCXWHUwq-Mfj4uWetrTEfKpCdhFUTNay3xssmJJFlkBnEu9PK2b0lQLR5-vv0lz4Dq55LF2eeYqpo-I7-nwMvqjqB244My9d-dIjdPtGL8zWksEO8oXEJOXMj2xT7I9yh9S5q--DXAOsUJnVDq2~U4Ou9Y6i0VLaBo4~gTP5AyMoq9V37auzWgtbROWAQzQ~9258MVuvpEImLcpjBnaSEJ5gL2-Q3ezGDvTxbqpqoiTZnnDRwLxKgLm7f4eQLF8pv7YR3lkfYmqKx0kmXV-5j707hL0TVFEPV23lPjJUlo~A__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":591,"name":"Nutrition and Dietetics","url":"https://www.academia.edu/Documents/in/Nutrition_and_Dietetics"},{"id":3851,"name":"Obesity","url":"https://www.academia.edu/Documents/in/Obesity"},{"id":51373,"name":"Insulin Resistance","url":"https://www.academia.edu/Documents/in/Insulin_Resistance"},{"id":52055,"name":"Lipids","url":"https://www.academia.edu/Documents/in/Lipids"},{"id":72314,"name":"Fatty acids","url":"https://www.academia.edu/Documents/in/Fatty_acids"},{"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":218820,"name":"Eating","url":"https://www.academia.edu/Documents/in/Eating"},{"id":227299,"name":"Triglycerides","url":"https://www.academia.edu/Documents/in/Triglycerides"},{"id":288383,"name":"Intestinal absorption","url":"https://www.academia.edu/Documents/in/Intestinal_absorption"},{"id":291136,"name":"Intestines","url":"https://www.academia.edu/Documents/in/Intestines"},{"id":564878,"name":"Body Weight","url":"https://www.academia.edu/Documents/in/Body_Weight"},{"id":573653,"name":"Food Sciences","url":"https://www.academia.edu/Documents/in/Food_Sciences"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":1763968,"name":"Gene Expression Regulation","url":"https://www.academia.edu/Documents/in/Gene_Expression_Regulation"}],"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="12472799"><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/12472799/Intestinal_fatty_acid_binding_protein_and_lipid_transport_in_human_intestinal_epithelial_cells"><img alt="Research paper thumbnail of Intestinal-fatty acid binding protein and lipid transport in human intestinal epithelial cells" class="work-thumbnail" src="https://attachments.academia-assets.com/46157159/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/12472799/Intestinal_fatty_acid_binding_protein_and_lipid_transport_in_human_intestinal_epithelial_cells">Intestinal-fatty acid binding protein and lipid transport in human intestinal epithelial cells</a></div><div class="wp-workCard_item"><span>Biochemical and biophysical research communications</span><span>, Jan 6, 2006</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Intestinal-fatty acid binding protein (I-FABP) is a 14-15 kDa cytoplasmic molecule highly express...</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">Intestinal-fatty acid binding protein (I-FABP) is a 14-15 kDa cytoplasmic molecule highly expressed in the enterocyte. Although different functions have been proposed for various FABP family members, the specific function of I-FABP in human intestine remains unclear. Here, we studied the role of I-FABP in molecularly modified normal human intestinal epithelial cells (HIEC-6). cDNA transfection resulted in 90-fold I-FABP overexpression compared to cells treated with empty pQCXIP vector. The high-resolution immunogold technique revealed labeling mainly in the cytosol and confirmed the marked phenotype abundance of I-FABP in cDNA transfected cells. I-FABP overexpression was not associated with alterations in cell proliferation and viability. Studies using these transfected cells cultured with [14C]oleic acid did not reveal higher efficiency in de novo synthesis or secretion of triglycerides, phospholipids, and cholesteryl esters compared to cells treated with empty pQCXIP vector only. ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c60d4cf177d28699409d5b910f9a7c4c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{&quot;attachment_id&quot;:46157159,&quot;asset_id&quot;:12472799,&quot;asset_type&quot;:&quot;Work&quot;,&quot;button_location&quot;:&quot;profile&quot;}" href="https://www.academia.edu/attachments/46157159/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&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="12472799"><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="12472799"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472799; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472799]").text(description); $(".js-view-count[data-work-id=12472799]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472799; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472799']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472799, 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: "c60d4cf177d28699409d5b910f9a7c4c" } } $('.js-work-strip[data-work-id=12472799]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472799,"title":"Intestinal-fatty acid binding protein and lipid transport in human intestinal epithelial cells","translated_title":"","metadata":{"abstract":"Intestinal-fatty acid binding protein (I-FABP) is a 14-15 kDa cytoplasmic molecule highly expressed in the enterocyte. Although different functions have been proposed for various FABP family members, the specific function of I-FABP in human intestine remains unclear. Here, we studied the role of I-FABP in molecularly modified normal human intestinal epithelial cells (HIEC-6). cDNA transfection resulted in 90-fold I-FABP overexpression compared to cells treated with empty pQCXIP vector. The high-resolution immunogold technique revealed labeling mainly in the cytosol and confirmed the marked phenotype abundance of I-FABP in cDNA transfected cells. I-FABP overexpression was not associated with alterations in cell proliferation and viability. Studies using these transfected cells cultured with [14C]oleic acid did not reveal higher efficiency in de novo synthesis or secretion of triglycerides, phospholipids, and cholesteryl esters compared to cells treated with empty pQCXIP vector only. ...","publication_date":{"day":6,"month":1,"year":2006,"errors":{}},"publication_name":"Biochemical and biophysical research communications"},"translated_abstract":"Intestinal-fatty acid binding protein (I-FABP) is a 14-15 kDa cytoplasmic molecule highly expressed in the enterocyte. Although different functions have been proposed for various FABP family members, the specific function of I-FABP in human intestine remains unclear. Here, we studied the role of I-FABP in molecularly modified normal human intestinal epithelial cells (HIEC-6). cDNA transfection resulted in 90-fold I-FABP overexpression compared to cells treated with empty pQCXIP vector. The high-resolution immunogold technique revealed labeling mainly in the cytosol and confirmed the marked phenotype abundance of I-FABP in cDNA transfected cells. I-FABP overexpression was not associated with alterations in cell proliferation and viability. Studies using these transfected cells cultured with [14C]oleic acid did not reveal higher efficiency in de novo synthesis or secretion of triglycerides, phospholipids, and cholesteryl esters compared to cells treated with empty pQCXIP vector only. 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hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/12472798/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" rel="nofollow" href="https://www.academia.edu/12472798/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;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="12472798"><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="12472798"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472798; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472798]").text(description); $(".js-view-count[data-work-id=12472798]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472798; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472798']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472798, 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" } } $('.js-work-strip[data-work-id=12472798]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472798,"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;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;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/12472798/Prevention_of_oxidative_stress_inflammation_and_mitochondrial_dysfunction_in_the_intestine_by_different_cranberry_phenolic_fractions","translated_internal_url":"","created_at":"2015-05-19T13:56:26.889-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31309978,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"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":31309978,"first_name":"Alain","middle_initials":null,"last_name":"Montoudis","page_name":"AlainMontoudis","domain_name":"independent","created_at":"2015-05-19T13:55:47.683-07:00","display_name":"Alain Montoudis","url":"https://independent.academia.edu/AlainMontoudis"},"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="12472797"><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/12472797/Impact_of_an_enriched_cholesterol_diet_on_enzymatic_cholesterol_metabolism_during_rabbit_gestation"><img alt="Research paper thumbnail of Impact of an enriched-cholesterol diet on enzymatic cholesterol metabolism during rabbit gestation" class="work-thumbnail" src="https://attachments.academia-assets.com/46157153/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/12472797/Impact_of_an_enriched_cholesterol_diet_on_enzymatic_cholesterol_metabolism_during_rabbit_gestation">Impact of an enriched-cholesterol diet on enzymatic cholesterol metabolism during rabbit gestation</a></div><div class="wp-workCard_item"><span>Life Sciences</span><span>, 2003</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="658f64e3bdc92b834024aea4e28c1e3d" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{&quot;attachment_id&quot;:46157153,&quot;asset_id&quot;:12472797,&quot;asset_type&quot;:&quot;Work&quot;,&quot;button_location&quot;:&quot;profile&quot;}" href="https://www.academia.edu/attachments/46157153/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&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="12472797"><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="12472797"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472797; 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The cholesterol is essential for the synthesis of progesterone and 17h-estradiol, hormones that actively participate to sustain gestation. However, the administration of 0.2% enriched cholesterol diet (ECD) during rabbit gestation significantly increased the cholesterol blood profile (total-cholesterol, LDL, HDL, esterified-cholesterol and freecholesterol) of dams and offspring, and induced a reduction of the offspring weight of 15% as compared to the control group. Enzymes involved in cholesterol metabolism (ACAT, HMG-CoA-reductase and cholesterol-7ahydroxylase) are greatly influenced by cholesterol profile. We hypothesized that the administration of an ECD during rabbit gestation modifies the activity of those enzymes. Female rabbits (pregnant or not) were fed with a standard diet or an ECD. At term, livers (dams and offspring) and placentas were collected and ACAT, HMG-CoA-reductase and cholesterol-7a-hydroxylase activities were assayed. Our results demonstrate that gestation induced a reduction of ACAT activity (48.9%) in dam's liver and, an augmentation of HMG-CoA-reductase activity (142.4%) whereas it has no effect on cholesterol-7a-hydroxylase activity. The administration of the ECD has no additive effect on ACAT, but significantly reduced the HMG-CoA-reductase activity and cholesterol-7a-hydroxylase activity as compared with the pregnant control group. In placentas the ECD supplementation has an influence for HMG-CoA-reductase activity, where a 43% increased in observed. Any ACAT activity was detected in placenta and the ECD has no influence on the cholesterol-7a-hydroxylase activity. Whereas their offspring's liver present a reduction of ACAT and HMG-CoA-reductase activity. Gestation associated with ECD reduces significantly the HMG-CoA-reductase activity, decreasing the 0024-3205/03/$ -see front matter D cholesterol synthesis, but placenta seems to compensate this effect by increasing its HMG-CoA-reductase activity. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="12472796"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/12472796/Intestinal_fatty_acid_binding_protein_regulates_mitochondrion_oxidation_and_cholesterol_uptake"><img alt="Research paper thumbnail of Intestinal fatty acid binding protein regulates mitochondrion 聽-oxidation and cholesterol uptake" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/12472796/Intestinal_fatty_acid_binding_protein_regulates_mitochondrion_oxidation_and_cholesterol_uptake">Intestinal fatty acid binding protein regulates mitochondrion 聽-oxidation and cholesterol uptake</a></div><div class="wp-workCard_item"><span>The Journal of Lipid Research</span><span>, 2008</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="12472796"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="12472796"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472796; 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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="12472795"><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/12472795/Localization_function_and_regulation_of_the_two_intestinal_fatty_acid_binding_protein_types"><img alt="Research paper thumbnail of Localization, function and regulation of the two intestinal fatty acid-binding protein types" 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/12472795/Localization_function_and_regulation_of_the_two_intestinal_fatty_acid_binding_protein_types">Localization, function and regulation of the two intestinal fatty acid-binding protein types</a></div><div class="wp-workCard_item"><span>Histochemistry and Cell Biology</span><span>, 2009</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Although intestinal (I) and liver (L) fatty acid binding proteins (FABP) have been widely studied...</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">Although intestinal (I) and liver (L) fatty acid binding proteins (FABP) have been widely studied, the physiological significance of the presence of the two FABP forms (I- and L-FABP) in absorptive cells remains unknown as do the differences related to their distribution along the crypt-villus axis, regional expression, ontogeny and regulation in the human intestine. Our morphological experiments supported the expression of I- and L-FABP as early as 13 weeks of gestation. Whereas cytoplasmic immunofluorescence staining of L-FABP was barely detectable in the lower half of the villus and in the crypt epithelial cells, I-FABP was visualized in epithelial cells of the crypt-villus axis in all intestinal segments until the adult period in which the staining was maximized in the upper part of the villus. Immunoelectron microscopy revealed more intense labeling of L-FABP compared with I-FABP, accompanied with a heterogeneous distribution in the cytoplasm, microvilli and basolateral membranes. By western blot analysis, I- and L-FABP at 15 weeks of gestation appeared predominant in jejunum compared with duodenum, ileum, proximal and distal colon. Exploration of the maturation aspect documented a rise in L-FABP in adult tissues. Permanent transfections of Caco-2 cells with I-FABP cDNA resulted in decreased lipid export, apolipoprotein (apo) biogenesis and chylomicron secretion. Additionally, supplementation of Caco-2 with insulin, hydrocortisone and epidermal growth factor differentially modulated the expression of I- and L-FABP, apo B-48 and microsomal triglyceride transfer protein (MTP), emphasizing that these key proteins do not exhibit a parallel modulation. Overall, our findings indicate that the two FABPs display differences in localization, regulation and developmental pattern.</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="12472795"><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="12472795"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472795; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472795]").text(description); $(".js-view-count[data-work-id=12472795]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472795; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472795']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472795, 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" } } $('.js-work-strip[data-work-id=12472795]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472795,"title":"Localization, function and regulation of the two intestinal fatty acid-binding protein types","translated_title":"","metadata":{"abstract":"Although intestinal (I) and liver (L) fatty acid binding proteins (FABP) have been widely studied, the physiological significance of the presence of the two FABP forms (I- and L-FABP) in absorptive cells remains unknown as do the differences related to their distribution along the crypt-villus axis, regional expression, ontogeny and regulation in the human intestine. Our morphological experiments supported the expression of I- and L-FABP as early as 13 weeks of gestation. Whereas cytoplasmic immunofluorescence staining of L-FABP was barely detectable in the lower half of the villus and in the crypt epithelial cells, I-FABP was visualized in epithelial cells of the crypt-villus axis in all intestinal segments until the adult period in which the staining was maximized in the upper part of the villus. Immunoelectron microscopy revealed more intense labeling of L-FABP compared with I-FABP, accompanied with a heterogeneous distribution in the cytoplasm, microvilli and basolateral membranes. By western blot analysis, I- and L-FABP at 15 weeks of gestation appeared predominant in jejunum compared with duodenum, ileum, proximal and distal colon. Exploration of the maturation aspect documented a rise in L-FABP in adult tissues. Permanent transfections of Caco-2 cells with I-FABP cDNA resulted in decreased lipid export, apolipoprotein (apo) biogenesis and chylomicron secretion. Additionally, supplementation of Caco-2 with insulin, hydrocortisone and epidermal growth factor differentially modulated the expression of I- and L-FABP, apo B-48 and microsomal triglyceride transfer protein (MTP), emphasizing that these key proteins do not exhibit a parallel modulation. Overall, our findings indicate that the two FABPs display differences in localization, regulation and developmental pattern.","publication_date":{"day":null,"month":null,"year":2009,"errors":{}},"publication_name":"Histochemistry and Cell Biology"},"translated_abstract":"Although intestinal (I) and liver (L) fatty acid binding proteins (FABP) have been widely studied, the physiological significance of the presence of the two FABP forms (I- and L-FABP) in absorptive cells remains unknown as do the differences related to their distribution along the crypt-villus axis, regional expression, ontogeny and regulation in the human intestine. Our morphological experiments supported the expression of I- and L-FABP as early as 13 weeks of gestation. Whereas cytoplasmic immunofluorescence staining of L-FABP was barely detectable in the lower half of the villus and in the crypt epithelial cells, I-FABP was visualized in epithelial cells of the crypt-villus axis in all intestinal segments until the adult period in which the staining was maximized in the upper part of the villus. Immunoelectron microscopy revealed more intense labeling of L-FABP compared with I-FABP, accompanied with a heterogeneous distribution in the cytoplasm, microvilli and basolateral membranes. By western blot analysis, I- and L-FABP at 15 weeks of gestation appeared predominant in jejunum compared with duodenum, ileum, proximal and distal colon. Exploration of the maturation aspect documented a rise in L-FABP in adult tissues. Permanent transfections of Caco-2 cells with I-FABP cDNA resulted in decreased lipid export, apolipoprotein (apo) biogenesis and chylomicron secretion. Additionally, supplementation of Caco-2 with insulin, hydrocortisone and epidermal growth factor differentially modulated the expression of I- and L-FABP, apo B-48 and microsomal triglyceride transfer protein (MTP), emphasizing that these key proteins do not exhibit a parallel modulation. Overall, our findings indicate that the two FABPs display differences in localization, regulation and developmental pattern.","internal_url":"https://www.academia.edu/12472795/Localization_function_and_regulation_of_the_two_intestinal_fatty_acid_binding_protein_types","translated_internal_url":"","created_at":"2015-05-19T13:56:26.603-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31309978,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Localization_function_and_regulation_of_the_two_intestinal_fatty_acid_binding_protein_types","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":31309978,"first_name":"Alain","middle_initials":null,"last_name":"Montoudis","page_name":"AlainMontoudis","domain_name":"independent","created_at":"2015-05-19T13:55:47.683-07:00","display_name":"Alain Montoudis","url":"https://independent.academia.edu/AlainMontoudis"},"attachments":[],"research_interests":[{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":104853,"name":"Hormones","url":"https://www.academia.edu/Documents/in/Hormones"},{"id":134346,"name":"Infant","url":"https://www.academia.edu/Documents/in/Infant"},{"id":176898,"name":"Jejunum","url":"https://www.academia.edu/Documents/in/Jejunum"},{"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":329263,"name":"Epidermal Growth Factor","url":"https://www.academia.edu/Documents/in/Epidermal_Growth_Factor"},{"id":458879,"name":"Lipoproteins","url":"https://www.academia.edu/Documents/in/Lipoproteins"},{"id":462111,"name":"Western blot","url":"https://www.academia.edu/Documents/in/Western_blot"},{"id":829416,"name":"Colon","url":"https://www.academia.edu/Documents/in/Colon"},{"id":989723,"name":"Caco 2 Cell","url":"https://www.academia.edu/Documents/in/Caco_2_Cell"},{"id":1509323,"name":"Fatty Acid Binding Protein","url":"https://www.academia.edu/Documents/in/Fatty_Acid_Binding_Protein"}],"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="12472794"><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/12472794/Hepatocyte_specific_Ptpn6_deletion_promotes_hepatic_lipid_accretion_but_reduces_NAFLD_in_diet_induced_obesity_Potential_role_of_PPAR%CE%B3"><img alt="Research paper thumbnail of Hepatocyte-specific Ptpn6 deletion promotes hepatic lipid accretion, but reduces NAFLD in diet-induced obesity: Potential role of PPAR纬" 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/12472794/Hepatocyte_specific_Ptpn6_deletion_promotes_hepatic_lipid_accretion_but_reduces_NAFLD_in_diet_induced_obesity_Potential_role_of_PPAR%CE%B3">Hepatocyte-specific Ptpn6 deletion promotes hepatic lipid accretion, but reduces NAFLD in diet-induced obesity: Potential role of PPAR纬</a></div><div class="wp-workCard_item"><span>Hepatology</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Hepatocyte-specific Shp1 knockout mice (Ptpn6(H-KO)) are protected from hepatic insulin resistanc...</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">Hepatocyte-specific Shp1 knockout mice (Ptpn6(H-KO)) are protected from hepatic insulin resistance evoked by high-fat diet (HFD) feeding for 8 weeks. Unexpectedly, we report herein that Ptpn6(H-KO) mice fed an HFD for up to 16 weeks are still protected from insulin resistance, but are more prone to hepatic steatosis, as compared with their HFD-fed Ptpn6(f/f) counterparts. The livers from HFD-fed Ptpn6(H-KO) mice displayed 1) augmented lipogenesis, marked by increased expression of several hepatic genes involved in fatty acid biosynthesis, 2) elevated postprandial fatty acid uptake, and 3) significantly reduced lipid export with enhanced degradation of apolipoprotein B (ApoB). Despite more extensive hepatic steatosis, the inflammatory profile of the HFD-fed Ptpn6(H-KO) liver was similar (8 weeks) or even improved (16 weeks) as compared to their HFD-fed Ptpn6(f/f) littermates, along with reduced hepatocellular damage as revealed by serum levels of hepatic enzymes. Interestingly, comparative microarray analysis revealed a significant up-regulation of peroxisome proliferator-activated receptor gamma (PPAR纬) gene expression, confirmed by quantitative polymerase chain reaction. Elevated PPAR纬 nuclear activity also was observed and found to be directly regulated by Shp1 in a cell-autonomous manner. These findings highlight a novel role for hepatocyte Shp1 in the regulation of PPAR纬 and hepatic lipid metabolism. Shp1 deficiency prevents the development of severe hepatic inflammation and hepatocellular damage in steatotic livers, presenting hepatocyte Shp1 as a potential novel mediator of nonalcoholic fatty liver diseases in obesity.</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="12472794"><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="12472794"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472794; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472794]").text(description); $(".js-view-count[data-work-id=12472794]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472794; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472794']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472794, 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" } } $('.js-work-strip[data-work-id=12472794]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472794,"title":"Hepatocyte-specific Ptpn6 deletion promotes hepatic lipid accretion, but reduces NAFLD in diet-induced obesity: Potential role of PPAR纬","translated_title":"","metadata":{"abstract":"Hepatocyte-specific Shp1 knockout mice (Ptpn6(H-KO)) are protected from hepatic insulin resistance evoked by high-fat diet (HFD) feeding for 8 weeks. Unexpectedly, we report herein that Ptpn6(H-KO) mice fed an HFD for up to 16 weeks are still protected from insulin resistance, but are more prone to hepatic steatosis, as compared with their HFD-fed Ptpn6(f/f) counterparts. The livers from HFD-fed Ptpn6(H-KO) mice displayed 1) augmented lipogenesis, marked by increased expression of several hepatic genes involved in fatty acid biosynthesis, 2) elevated postprandial fatty acid uptake, and 3) significantly reduced lipid export with enhanced degradation of apolipoprotein B (ApoB). Despite more extensive hepatic steatosis, the inflammatory profile of the HFD-fed Ptpn6(H-KO) liver was similar (8 weeks) or even improved (16 weeks) as compared to their HFD-fed Ptpn6(f/f) littermates, along with reduced hepatocellular damage as revealed by serum levels of hepatic enzymes. Interestingly, comparative microarray analysis revealed a significant up-regulation of peroxisome proliferator-activated receptor gamma (PPAR纬) gene expression, confirmed by quantitative polymerase chain reaction. Elevated PPAR纬 nuclear activity also was observed and found to be directly regulated by Shp1 in a cell-autonomous manner. These findings highlight a novel role for hepatocyte Shp1 in the regulation of PPAR纬 and hepatic lipid metabolism. Shp1 deficiency prevents the development of severe hepatic inflammation and hepatocellular damage in steatotic livers, presenting hepatocyte Shp1 as a potential novel mediator of nonalcoholic fatty liver diseases in obesity.","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Hepatology"},"translated_abstract":"Hepatocyte-specific Shp1 knockout mice (Ptpn6(H-KO)) are protected from hepatic insulin resistance evoked by high-fat diet (HFD) feeding for 8 weeks. Unexpectedly, we report herein that Ptpn6(H-KO) mice fed an HFD for up to 16 weeks are still protected from insulin resistance, but are more prone to hepatic steatosis, as compared with their HFD-fed Ptpn6(f/f) counterparts. The livers from HFD-fed Ptpn6(H-KO) mice displayed 1) augmented lipogenesis, marked by increased expression of several hepatic genes involved in fatty acid biosynthesis, 2) elevated postprandial fatty acid uptake, and 3) significantly reduced lipid export with enhanced degradation of apolipoprotein B (ApoB). Despite more extensive hepatic steatosis, the inflammatory profile of the HFD-fed Ptpn6(H-KO) liver was similar (8 weeks) or even improved (16 weeks) as compared to their HFD-fed Ptpn6(f/f) littermates, along with reduced hepatocellular damage as revealed by serum levels of hepatic enzymes. Interestingly, comparative microarray analysis revealed a significant up-regulation of peroxisome proliferator-activated receptor gamma (PPAR纬) gene expression, confirmed by quantitative polymerase chain reaction. Elevated PPAR纬 nuclear activity also was observed and found to be directly regulated by Shp1 in a cell-autonomous manner. These findings highlight a novel role for hepatocyte Shp1 in the regulation of PPAR纬 and hepatic lipid metabolism. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="12472793"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/12472793/Prevention_of_Lipid_oxidation_in_Paediatric_Parenteral_Nutrition"><img alt="Research paper thumbnail of Prevention of Lipid oxidation in Paediatric Parenteral Nutrition" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/12472793/Prevention_of_Lipid_oxidation_in_Paediatric_Parenteral_Nutrition">Prevention of Lipid oxidation in Paediatric Parenteral Nutrition</a></div><div class="wp-workCard_item"><span>Free Radical Biology and Medicine</span><span>, 2010</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="12472793"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="12472793"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472793; 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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="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="{&quot;attachment_id&quot;:46182787,&quot;asset_id&quot;:12440504,&quot;asset_type&quot;:&quot;Work&quot;,&quot;button_location&quot;:&quot;profile&quot;}" href="https://www.academia.edu/attachments/46182787/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&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); 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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. 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"profile_work_strip") }); </script> </div><div class="profile--tab_content_container js-tab-pane tab-pane" data-section-id="2955706" id="papers"><div class="js-work-strip profile--work_container" data-work-id="12472808"><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/12472808/Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites"><img alt="Research paper thumbnail of Evaluation of 3-hydroxy-3-methylglutaryl-COA-reductase, cholesterol-7?-hydroxylase and acyl-COA:cholesterol acyltransferase activities: alternative chromatographic methods to separate metabolites" 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/12472808/Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites">Evaluation of 3-hydroxy-3-methylglutaryl-COA-reductase, cholesterol-7?-hydroxylase and acyl-COA:cholesterol acyltransferase activities: alternative chromatographic methods to separate metabolites</a></div><div class="wp-workCard_item"><span>Biomedical Chromatography</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites...</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">Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites of enzymes involved in cholesterol metabolism in rabbit liver microsomes: hydroxyl-methylglutaryl-CoA reductase, cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase. A comparison method of thin-layer chromatography and solid-phase extraction column were assayed to separate substrate and metabolite of hydroxy-methylglutaryl-CoA reductase, whereas for cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase, this comparison was done between thin layer chromatography and HPLC. The results obtained by the new analytical chromatographic methods are not significantly different than those observed in literature. Moreover a larger percentage recovery was obtained for analysed metabolites. Our results demonstrate the reliability of these alternative chromatographic techniques and showed that they are valuable tools to precisely and rapidly measure the activity of those enzymes.</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="12472808"><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="12472808"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472808; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472808]").text(description); $(".js-view-count[data-work-id=12472808]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472808; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472808']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472808, 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" } } $('.js-work-strip[data-work-id=12472808]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472808,"title":"Evaluation of 3-hydroxy-3-methylglutaryl-COA-reductase, cholesterol-7?-hydroxylase and acyl-COA:cholesterol acyltransferase activities: alternative chromatographic methods to separate metabolites","translated_title":"","metadata":{"abstract":"Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites of enzymes involved in cholesterol metabolism in rabbit liver microsomes: hydroxyl-methylglutaryl-CoA reductase, cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase. A comparison method of thin-layer chromatography and solid-phase extraction column were assayed to separate substrate and metabolite of hydroxy-methylglutaryl-CoA reductase, whereas for cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase, this comparison was done between thin layer chromatography and HPLC. The results obtained by the new analytical chromatographic methods are not significantly different than those observed in literature. Moreover a larger percentage recovery was obtained for analysed metabolites. Our results demonstrate the reliability of these alternative chromatographic techniques and showed that they are valuable tools to precisely and rapidly measure the activity of those enzymes.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Biomedical Chromatography"},"translated_abstract":"Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites of enzymes involved in cholesterol metabolism in rabbit liver microsomes: hydroxyl-methylglutaryl-CoA reductase, cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase. A comparison method of thin-layer chromatography and solid-phase extraction column were assayed to separate substrate and metabolite of hydroxy-methylglutaryl-CoA reductase, whereas for cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase, this comparison was done between thin layer chromatography and HPLC. The results obtained by the new analytical chromatographic methods are not significantly different than those observed in literature. Moreover a larger percentage recovery was obtained for analysed metabolites. Our results demonstrate the reliability of these alternative chromatographic techniques and showed that they are valuable tools to precisely and rapidly measure the activity of those enzymes.","internal_url":"https://www.academia.edu/12472808/Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites","translated_internal_url":"","created_at":"2015-05-19T13:56:32.644-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31309978,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":31309978,"first_name":"Alain","middle_initials":null,"last_name":"Montoudis","page_name":"AlainMontoudis","domain_name":"independent","created_at":"2015-05-19T13:55:47.683-07:00","display_name":"Alain Montoudis","url":"https://independent.academia.edu/AlainMontoudis"},"attachments":[],"research_interests":[{"id":524,"name":"Analytical Chemistry","url":"https://www.academia.edu/Documents/in/Analytical_Chemistry"},{"id":5769,"name":"Mass Spectrometry","url":"https://www.academia.edu/Documents/in/Mass_Spectrometry"},{"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":246560,"name":"High Pressure Liquid Chromatography","url":"https://www.academia.edu/Documents/in/High_Pressure_Liquid_Chromatography"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":549972,"name":"Microchemistry","url":"https://www.academia.edu/Documents/in/Microchemistry"},{"id":788677,"name":"Rabbits","url":"https://www.academia.edu/Documents/in/Rabbits"},{"id":806387,"name":"Analytical Biochemistry","url":"https://www.academia.edu/Documents/in/Analytical_Biochemistry"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"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="12472805"><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/12472805/Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7alpha_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites"><img alt="Research paper thumbnail of Evaluation of 3-hydroxy-3-methylglutaryl-COA-reductase, cholesterol-7alpha-hydroxylase and acyl-COA:cholesterol acyltransferase activities: alternative chromatographic methods to separate metabolites" 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/12472805/Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7alpha_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites">Evaluation of 3-hydroxy-3-methylglutaryl-COA-reductase, cholesterol-7alpha-hydroxylase and acyl-COA:cholesterol acyltransferase activities: alternative chromatographic methods to separate metabolites</a></div><div class="wp-workCard_item"><span>Biomedical chromatography : BMC</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites...</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">Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites of enzymes involved in cholesterol metabolism in rabbit liver microsomes: hydroxyl-methylglutaryl-CoA reductase, cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase. A comparison method of thin-layer chromatography and solid-phase extraction column were assayed to separate substrate and metabolite of hydroxy-methylglutaryl-CoA reductase, whereas for cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase, this comparison was done between thin layer chromatography and HPLC. The results obtained by the new analytical chromatographic methods are not significantly different than those observed in literature. Moreover a larger percentage recovery was obtained for analysed metabolites. Our results demonstrate the reliability of these alternative chromatographic techniques and showed that they are valuable tools to precisely and rapidly measure the activity ...</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="12472805"><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="12472805"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472805; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472805]").text(description); $(".js-view-count[data-work-id=12472805]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472805; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472805']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472805, 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" } } $('.js-work-strip[data-work-id=12472805]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472805,"title":"Evaluation of 3-hydroxy-3-methylglutaryl-COA-reductase, cholesterol-7alpha-hydroxylase and acyl-COA:cholesterol acyltransferase activities: alternative chromatographic methods to separate metabolites","translated_title":"","metadata":{"abstract":"Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites of enzymes involved in cholesterol metabolism in rabbit liver microsomes: hydroxyl-methylglutaryl-CoA reductase, cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase. A comparison method of thin-layer chromatography and solid-phase extraction column were assayed to separate substrate and metabolite of hydroxy-methylglutaryl-CoA reductase, whereas for cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase, this comparison was done between thin layer chromatography and HPLC. The results obtained by the new analytical chromatographic methods are not significantly different than those observed in literature. Moreover a larger percentage recovery was obtained for analysed metabolites. Our results demonstrate the reliability of these alternative chromatographic techniques and showed that they are valuable tools to precisely and rapidly measure the activity ...","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Biomedical chromatography : BMC"},"translated_abstract":"Alternative HPLC and solid-phase extraction column methods were developed to separate metabolites of enzymes involved in cholesterol metabolism in rabbit liver microsomes: hydroxyl-methylglutaryl-CoA reductase, cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase. A comparison method of thin-layer chromatography and solid-phase extraction column were assayed to separate substrate and metabolite of hydroxy-methylglutaryl-CoA reductase, whereas for cholesterol-7alpha-hydroxylase and acyl-CoA:cholesterol acyltransferase, this comparison was done between thin layer chromatography and HPLC. The results obtained by the new analytical chromatographic methods are not significantly different than those observed in literature. Moreover a larger percentage recovery was obtained for analysed metabolites. Our results demonstrate the reliability of these alternative chromatographic techniques and showed that they are valuable tools to precisely and rapidly measure the activity ...","internal_url":"https://www.academia.edu/12472805/Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7alpha_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites","translated_internal_url":"","created_at":"2015-05-19T13:56:27.691-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31309978,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Evaluation_of_3_hydroxy_3_methylglutaryl_COA_reductase_cholesterol_7alpha_hydroxylase_and_acyl_COA_cholesterol_acyltransferase_activities_alternative_chromatographic_methods_to_separate_metabolites","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":31309978,"first_name":"Alain","middle_initials":null,"last_name":"Montoudis","page_name":"AlainMontoudis","domain_name":"independent","created_at":"2015-05-19T13:55:47.683-07:00","display_name":"Alain Montoudis","url":"https://independent.academia.edu/AlainMontoudis"},"attachments":[],"research_interests":[{"id":524,"name":"Analytical Chemistry","url":"https://www.academia.edu/Documents/in/Analytical_Chemistry"},{"id":5769,"name":"Mass Spectrometry","url":"https://www.academia.edu/Documents/in/Mass_Spectrometry"},{"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":246560,"name":"High Pressure Liquid Chromatography","url":"https://www.academia.edu/Documents/in/High_Pressure_Liquid_Chromatography"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":549972,"name":"Microchemistry","url":"https://www.academia.edu/Documents/in/Microchemistry"},{"id":788677,"name":"Rabbits","url":"https://www.academia.edu/Documents/in/Rabbits"},{"id":806387,"name":"Analytical Biochemistry","url":"https://www.academia.edu/Documents/in/Analytical_Biochemistry"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"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="12472804"><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/12472804/Influence_of_a_maternal_cholesterol_enriched_diet_on_1_14C_linoleic_acid_and_L_4_5_3H_leucine_entry_in_plasma_of_rabbit_offspring"><img alt="Research paper thumbnail of Influence of a maternal cholesterol-enriched diet on [1-14C]-linoleic acid and L-[4, 5-3H]-leucine entry in plasma of rabbit offspring" class="work-thumbnail" src="https://attachments.academia-assets.com/46157157/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/12472804/Influence_of_a_maternal_cholesterol_enriched_diet_on_1_14C_linoleic_acid_and_L_4_5_3H_leucine_entry_in_plasma_of_rabbit_offspring">Influence of a maternal cholesterol-enriched diet on [1-14C]-linoleic acid and L-[4, 5-3H]-leucine entry in plasma of rabbit offspring</a></div><div class="wp-workCard_item"><span>Life sciences</span><span>, Jan 20, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Fetal development requires an important entry of essential free fatty acids (EFFA) and essential ...</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">Fetal development requires an important entry of essential free fatty acids (EFFA) and essential amino acids (EAA) into the fetal circulation. We have reported that a 0.2% enriched-cholesterol diet (ECD) during rabbit gestation significantly reduces fetus weight compared to control diet. It is known that dietary linoleic acid deficiency, an EFFA, during the fetal development induces an important impair to the somatic development. Moreover, intrauterine growth retardation induced a reduction of the flux of leucine, an EAA, from maternal to fetal circulation. Therefore, we hypothesized that the administration of an ECD induces modifications of placental lipid composition concomitant alterations of the transfer of linoleic acid and leucine in fetal circulation. Quantification of placental lipids revealed that in the ECD group a reduction of total-cholesterol (TC) and free-cholesterol (FC) is observed, however an increased in FFA and phospholipids is noticed when compared to the control...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b011f6ac7a41651cca17e40019719970" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{&quot;attachment_id&quot;:46157157,&quot;asset_id&quot;:12472804,&quot;asset_type&quot;:&quot;Work&quot;,&quot;button_location&quot;:&quot;profile&quot;}" href="https://www.academia.edu/attachments/46157157/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&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="12472804"><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="12472804"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472804; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472804]").text(description); $(".js-view-count[data-work-id=12472804]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472804; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472804']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472804, 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: "b011f6ac7a41651cca17e40019719970" } } $('.js-work-strip[data-work-id=12472804]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472804,"title":"Influence of a maternal cholesterol-enriched diet on [1-14C]-linoleic acid and L-[4, 5-3H]-leucine entry in plasma of rabbit offspring","translated_title":"","metadata":{"abstract":"Fetal development requires an important entry of essential free fatty acids (EFFA) and essential amino acids (EAA) into the fetal circulation. We have reported that a 0.2% enriched-cholesterol diet (ECD) during rabbit gestation significantly reduces fetus weight compared to control diet. It is known that dietary linoleic acid deficiency, an EFFA, during the fetal development induces an important impair to the somatic development. Moreover, intrauterine growth retardation induced a reduction of the flux of leucine, an EAA, from maternal to fetal circulation. Therefore, we hypothesized that the administration of an ECD induces modifications of placental lipid composition concomitant alterations of the transfer of linoleic acid and leucine in fetal circulation. Quantification of placental lipids revealed that in the ECD group a reduction of total-cholesterol (TC) and free-cholesterol (FC) is observed, however an increased in FFA and phospholipids is noticed when compared to the control...","publication_date":{"day":20,"month":1,"year":2004,"errors":{}},"publication_name":"Life sciences"},"translated_abstract":"Fetal development requires an important entry of essential free fatty acids (EFFA) and essential amino acids (EAA) into the fetal circulation. We have reported that a 0.2% enriched-cholesterol diet (ECD) during rabbit gestation significantly reduces fetus weight compared to control diet. It is known that dietary linoleic acid deficiency, an EFFA, during the fetal development induces an important impair to the somatic development. Moreover, intrauterine growth retardation induced a reduction of the flux of leucine, an EAA, from maternal to fetal circulation. Therefore, we hypothesized that the administration of an ECD induces modifications of placental lipid composition concomitant alterations of the transfer of linoleic acid and leucine in fetal circulation. Quantification of placental lipids revealed that in the ECD group a reduction of total-cholesterol (TC) and free-cholesterol (FC) is observed, however an increased in FFA and phospholipids is noticed when compared to the 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hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/12472803/Impact_of_an_enriched_cholesterol_diet_on_enzymatic_cholesterol_metabolism_during_rabbit_gestation"><img alt="Research paper thumbnail of Impact of an enriched-cholesterol diet on enzymatic cholesterol metabolism during rabbit gestation" class="work-thumbnail" src="https://attachments.academia-assets.com/46157152/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/12472803/Impact_of_an_enriched_cholesterol_diet_on_enzymatic_cholesterol_metabolism_during_rabbit_gestation">Impact of an enriched-cholesterol diet on enzymatic cholesterol metabolism during rabbit gestation</a></div><div class="wp-workCard_item"><span>Life sciences</span><span>, 2003</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">An appropriate cholesterol homeostasis is vital for the maintenance and the optimal fetal develop...</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">An appropriate cholesterol homeostasis is vital for the maintenance and the optimal fetal development. The cholesterol is essential for the synthesis of progesterone and 17beta-estradiol, hormones that actively participate to sustain gestation. However, the administration of 0.2% enriched cholesterol diet (ECD) during rabbit gestation significantly increased the cholesterol blood profile (total-cholesterol, LDL, HDL, esterified-cholesterol and free-cholesterol) of dams and offspring, and induced a reduction of the offspring weight of 15% as compared to the control group. Enzymes involved in cholesterol metabolism (ACAT, HMG-CoA-reductase and cholesterol-7alpha-hydroxylase) are greatly influenced by cholesterol profile. We hypothesized that the administration of an ECD during rabbit gestation modifies the activity of those enzymes. Female rabbits (pregnant or not) were fed with a standard diet or an ECD. At term, livers (dams and offspring) and placentas were collected and ACAT, HMG-...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="e82f990b6b2c7ff9f0931b46e464636d" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{&quot;attachment_id&quot;:46157152,&quot;asset_id&quot;:12472803,&quot;asset_type&quot;:&quot;Work&quot;,&quot;button_location&quot;:&quot;profile&quot;}" href="https://www.academia.edu/attachments/46157152/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&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="12472803"><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="12472803"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472803; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472803]").text(description); $(".js-view-count[data-work-id=12472803]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472803; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472803']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472803, 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: "e82f990b6b2c7ff9f0931b46e464636d" } } $('.js-work-strip[data-work-id=12472803]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472803,"title":"Impact of an enriched-cholesterol diet on enzymatic cholesterol metabolism during rabbit gestation","translated_title":"","metadata":{"abstract":"An appropriate cholesterol homeostasis is vital for the maintenance and the optimal fetal development. The cholesterol is essential for the synthesis of progesterone and 17beta-estradiol, hormones that actively participate to sustain gestation. However, the administration of 0.2% enriched cholesterol diet (ECD) during rabbit gestation significantly increased the cholesterol blood profile (total-cholesterol, LDL, HDL, esterified-cholesterol and free-cholesterol) of dams and offspring, and induced a reduction of the offspring weight of 15% as compared to the control group. Enzymes involved in cholesterol metabolism (ACAT, HMG-CoA-reductase and cholesterol-7alpha-hydroxylase) are greatly influenced by cholesterol profile. We hypothesized that the administration of an ECD during rabbit gestation modifies the activity of those enzymes. Female rabbits (pregnant or not) were fed with a standard diet or an ECD. At term, livers (dams and offspring) and placentas were collected and ACAT, HMG-...","publication_date":{"day":null,"month":null,"year":2003,"errors":{}},"publication_name":"Life sciences"},"translated_abstract":"An appropriate cholesterol homeostasis is vital for the maintenance and the optimal fetal development. The cholesterol is essential for the synthesis of progesterone and 17beta-estradiol, hormones that actively participate to sustain gestation. However, the administration of 0.2% enriched cholesterol diet (ECD) during rabbit gestation significantly increased the cholesterol blood profile (total-cholesterol, LDL, HDL, esterified-cholesterol and free-cholesterol) of dams and offspring, and induced a reduction of the offspring weight of 15% as compared to the control group. Enzymes involved in cholesterol metabolism (ACAT, HMG-CoA-reductase and cholesterol-7alpha-hydroxylase) are greatly influenced by cholesterol profile. We hypothesized that the administration of an ECD during rabbit gestation modifies the activity of those enzymes. Female rabbits (pregnant or not) were fed with a standard diet or an ECD. At term, livers (dams and offspring) and placentas were collected and ACAT, HMG-...","internal_url":"https://www.academia.edu/12472803/Impact_of_an_enriched_cholesterol_diet_on_enzymatic_cholesterol_metabolism_during_rabbit_gestation","translated_internal_url":"","created_at":"2015-05-19T13:56:27.447-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31309978,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":46157152,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/46157152/thumbnails/1.jpg","file_name":"s0024-3205_2803_2900436-320160602-6801-1dkpxnv.pdf","download_url":"https://www.academia.edu/attachments/46157152/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Impact_of_an_enriched_cholesterol_diet_o.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/46157152/s0024-3205_2803_2900436-320160602-6801-1dkpxnv-libre.pdf?1464855341=\u0026response-content-disposition=attachment%3B+filename%3DImpact_of_an_enriched_cholesterol_diet_o.pdf\u0026Expires=1732126075\u0026Signature=GBF5of-sgoIt7caHvhoxKHXS~31J5t48fAFHjlQV3-IineH-iWNYXodewbCeaX0V~7XKF68RdPx7DvEZMQpfbp5YlkiYDtmdVLyv5-CDqlGj5hC1H7xR8CNKRpgXj5J7LoJHOY~0qNcuKWAaDmuLDTLeVeLYL9KglGbqd8C68HKZkCdotQrwkk7THlouxSnR6k7Ow9~zHFS2AGIqihrzgyONHv9n~HqQOocfb10B9w6aUjVtxgy5Rf2ztkk~zuF6dDJIkNI1BB62cajgI5CI4KOfjD77sTy3b7~4M7sNFxTJTCMabbSFt4~O7zkOsjqtRdPXXExPQ-gXsBimjJgR7A__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Impact_of_an_enriched_cholesterol_diet_on_enzymatic_cholesterol_metabolism_during_rabbit_gestation","translated_slug":"","page_count":15,"language":"en","content_type":"Work","owner":{"id":31309978,"first_name":"Alain","middle_initials":null,"last_name":"Montoudis","page_name":"AlainMontoudis","domain_name":"independent","created_at":"2015-05-19T13:55:47.683-07:00","display_name":"Alain Montoudis","url":"https://independent.academia.edu/AlainMontoudis"},"attachments":[{"id":46157152,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/46157152/thumbnails/1.jpg","file_name":"s0024-3205_2803_2900436-320160602-6801-1dkpxnv.pdf","download_url":"https://www.academia.edu/attachments/46157152/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Impact_of_an_enriched_cholesterol_diet_o.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/46157152/s0024-3205_2803_2900436-320160602-6801-1dkpxnv-libre.pdf?1464855341=\u0026response-content-disposition=attachment%3B+filename%3DImpact_of_an_enriched_cholesterol_diet_o.pdf\u0026Expires=1732126075\u0026Signature=GBF5of-sgoIt7caHvhoxKHXS~31J5t48fAFHjlQV3-IineH-iWNYXodewbCeaX0V~7XKF68RdPx7DvEZMQpfbp5YlkiYDtmdVLyv5-CDqlGj5hC1H7xR8CNKRpgXj5J7LoJHOY~0qNcuKWAaDmuLDTLeVeLYL9KglGbqd8C68HKZkCdotQrwkk7THlouxSnR6k7Ow9~zHFS2AGIqihrzgyONHv9n~HqQOocfb10B9w6aUjVtxgy5Rf2ztkk~zuF6dDJIkNI1BB62cajgI5CI4KOfjD77sTy3b7~4M7sNFxTJTCMabbSFt4~O7zkOsjqtRdPXXExPQ-gXsBimjJgR7A__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":8014,"name":"Life Sciences","url":"https://www.academia.edu/Documents/in/Life_Sciences"},{"id":43162,"name":"Fetal development","url":"https://www.academia.edu/Documents/in/Fetal_development"},{"id":62550,"name":"Pregnancy","url":"https://www.academia.edu/Documents/in/Pregnancy"},{"id":71437,"name":"Liver","url":"https://www.academia.edu/Documents/in/Liver"},{"id":76061,"name":"Placenta","url":"https://www.academia.edu/Documents/in/Placenta"},{"id":90514,"name":"Cholesterol","url":"https://www.academia.edu/Documents/in/Cholesterol"},{"id":98925,"name":"Female","url":"https://www.academia.edu/Documents/in/Female"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":231661,"name":"Enzyme","url":"https://www.academia.edu/Documents/in/Enzyme"},{"id":788677,"name":"Rabbits","url":"https://www.academia.edu/Documents/in/Rabbits"},{"id":1274497,"name":"Total Cholesterol","url":"https://www.academia.edu/Documents/in/Total_Cholesterol"},{"id":1631043,"name":"Control Group","url":"https://www.academia.edu/Documents/in/Control_Group"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"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="12472802"><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/12472802/Influence_of_a_maternal_cholesterol_enriched_diet_on_1_14C_linoleic_acid_and_L_4_5_3H_leucine_entry_in_plasma_of_rabbit_offspring"><img alt="Research paper thumbnail of Influence of a maternal cholesterol-enriched diet on [1-14C]-linoleic acid and L-[4, 5-3H]-leucine entry in plasma of rabbit offspring" class="work-thumbnail" src="https://attachments.academia-assets.com/46157158/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/12472802/Influence_of_a_maternal_cholesterol_enriched_diet_on_1_14C_linoleic_acid_and_L_4_5_3H_leucine_entry_in_plasma_of_rabbit_offspring">Influence of a maternal cholesterol-enriched diet on [1-14C]-linoleic acid and L-[4, 5-3H]-leucine entry in plasma of rabbit offspring</a></div><div class="wp-workCard_item"><span>Life Sciences</span><span>, 2004</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f62095d7d3b3885fc8b7c8a50a30265b" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{&quot;attachment_id&quot;:46157158,&quot;asset_id&quot;:12472802,&quot;asset_type&quot;:&quot;Work&quot;,&quot;button_location&quot;:&quot;profile&quot;}" href="https://www.academia.edu/attachments/46157158/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&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="12472802"><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="12472802"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472802; 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We have reported that a 0.2% enriched-cholesterol diet (ECD) during rabbit gestation significantly reduces fetus weight compared to control diet. It is known that dietary linoleic acid deficiency, an EFFA, during the fetal development induces an important impair to the somatic development. Moreover, intrauterine growth retardation induced a reduction of the flux of leucine, an EAA, from maternal to fetal circulation. Therefore, we hypothesized that the administration of an ECD induces modifications of placental lipid composition concomitant alterations of the transfer of linoleic acid and leucine in fetal circulation. Quantification of placental lipids revealed that in the ECD group a reduction of total-cholesterol (TC) and free-cholesterol (FC) is observed, however an increased in FFA and phospholipids is noticed when compared to the control group. In placenta from the ECD group, the FC/ TC ratio is significantly reduced compared to the control group. In the ECD group, the liver shows an increase of TC, FC and FFA compared to the control group. However, the quantity of triacylglycerol present in the liver from the ECD is significantly reduced compared to the control group. To evaluate the placental transfer of some essential nutrients, intravenous injection of [1-14 C]-linoleic acid or L-[4, 5-3 H]-leucine to term rabbit (control and ECD group) were done. Two hours later, rabbits were euthanized and we collected placenta, livers and blood from dams and offspring. The concentrations of both radiolabeled molecules (linoleic acid and its esterified form or leucine) were higher in the plasma of ECD offspring than those found in offspring from control diet. Despite 0024-3205/$ -see front matter D (J. 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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/46157167/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/12472800/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. 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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="12472799"><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/12472799/Intestinal_fatty_acid_binding_protein_and_lipid_transport_in_human_intestinal_epithelial_cells"><img alt="Research paper thumbnail of Intestinal-fatty acid binding protein and lipid transport in human intestinal epithelial cells" class="work-thumbnail" src="https://attachments.academia-assets.com/46157159/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/12472799/Intestinal_fatty_acid_binding_protein_and_lipid_transport_in_human_intestinal_epithelial_cells">Intestinal-fatty acid binding protein and lipid transport in human intestinal epithelial cells</a></div><div class="wp-workCard_item"><span>Biochemical and biophysical research communications</span><span>, Jan 6, 2006</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Intestinal-fatty acid binding protein (I-FABP) is a 14-15 kDa cytoplasmic molecule highly express...</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">Intestinal-fatty acid binding protein (I-FABP) is a 14-15 kDa cytoplasmic molecule highly expressed in the enterocyte. Although different functions have been proposed for various FABP family members, the specific function of I-FABP in human intestine remains unclear. Here, we studied the role of I-FABP in molecularly modified normal human intestinal epithelial cells (HIEC-6). cDNA transfection resulted in 90-fold I-FABP overexpression compared to cells treated with empty pQCXIP vector. The high-resolution immunogold technique revealed labeling mainly in the cytosol and confirmed the marked phenotype abundance of I-FABP in cDNA transfected cells. I-FABP overexpression was not associated with alterations in cell proliferation and viability. Studies using these transfected cells cultured with [14C]oleic acid did not reveal higher efficiency in de novo synthesis or secretion of triglycerides, phospholipids, and cholesteryl esters compared to cells treated with empty pQCXIP vector only. ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c60d4cf177d28699409d5b910f9a7c4c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{&quot;attachment_id&quot;:46157159,&quot;asset_id&quot;:12472799,&quot;asset_type&quot;:&quot;Work&quot;,&quot;button_location&quot;:&quot;profile&quot;}" href="https://www.academia.edu/attachments/46157159/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&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="12472799"><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="12472799"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472799; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472799]").text(description); $(".js-view-count[data-work-id=12472799]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472799; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472799']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472799, 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: "c60d4cf177d28699409d5b910f9a7c4c" } } $('.js-work-strip[data-work-id=12472799]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472799,"title":"Intestinal-fatty acid binding protein and lipid transport in human intestinal epithelial cells","translated_title":"","metadata":{"abstract":"Intestinal-fatty acid binding protein (I-FABP) is a 14-15 kDa cytoplasmic molecule highly expressed in the enterocyte. 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The high-resolution immunogold technique revealed labeling mainly in the cytosol and confirmed the marked phenotype abundance of I-FABP in cDNA transfected cells. I-FABP overexpression was not associated with alterations in cell proliferation and viability. 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hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/12472798/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" rel="nofollow" href="https://www.academia.edu/12472798/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;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="12472798"><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="12472798"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472798; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472798]").text(description); $(".js-view-count[data-work-id=12472798]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472798; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472798']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472798, 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" } } $('.js-work-strip[data-work-id=12472798]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472798,"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;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;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/12472798/Prevention_of_oxidative_stress_inflammation_and_mitochondrial_dysfunction_in_the_intestine_by_different_cranberry_phenolic_fractions","translated_internal_url":"","created_at":"2015-05-19T13:56:26.889-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31309978,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"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":31309978,"first_name":"Alain","middle_initials":null,"last_name":"Montoudis","page_name":"AlainMontoudis","domain_name":"independent","created_at":"2015-05-19T13:55:47.683-07:00","display_name":"Alain Montoudis","url":"https://independent.academia.edu/AlainMontoudis"},"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="12472797"><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/12472797/Impact_of_an_enriched_cholesterol_diet_on_enzymatic_cholesterol_metabolism_during_rabbit_gestation"><img alt="Research paper thumbnail of Impact of an enriched-cholesterol diet on enzymatic cholesterol metabolism during rabbit gestation" class="work-thumbnail" src="https://attachments.academia-assets.com/46157153/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/12472797/Impact_of_an_enriched_cholesterol_diet_on_enzymatic_cholesterol_metabolism_during_rabbit_gestation">Impact of an enriched-cholesterol diet on enzymatic cholesterol metabolism during rabbit gestation</a></div><div class="wp-workCard_item"><span>Life Sciences</span><span>, 2003</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="658f64e3bdc92b834024aea4e28c1e3d" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{&quot;attachment_id&quot;:46157153,&quot;asset_id&quot;:12472797,&quot;asset_type&quot;:&quot;Work&quot;,&quot;button_location&quot;:&quot;profile&quot;}" href="https://www.academia.edu/attachments/46157153/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&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="12472797"><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="12472797"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472797; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "658f64e3bdc92b834024aea4e28c1e3d" } } $('.js-work-strip[data-work-id=12472797]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472797,"title":"Impact of an enriched-cholesterol diet on enzymatic cholesterol metabolism during rabbit gestation","translated_title":"","metadata":{"grobid_abstract":"An appropriate cholesterol homeostasis is vital for the maintenance and the optimal fetal development. The cholesterol is essential for the synthesis of progesterone and 17h-estradiol, hormones that actively participate to sustain gestation. However, the administration of 0.2% enriched cholesterol diet (ECD) during rabbit gestation significantly increased the cholesterol blood profile (total-cholesterol, LDL, HDL, esterified-cholesterol and freecholesterol) of dams and offspring, and induced a reduction of the offspring weight of 15% as compared to the control group. Enzymes involved in cholesterol metabolism (ACAT, HMG-CoA-reductase and cholesterol-7ahydroxylase) are greatly influenced by cholesterol profile. We hypothesized that the administration of an ECD during rabbit gestation modifies the activity of those enzymes. Female rabbits (pregnant or not) were fed with a standard diet or an ECD. At term, livers (dams and offspring) and placentas were collected and ACAT, HMG-CoA-reductase and cholesterol-7a-hydroxylase activities were assayed. Our results demonstrate that gestation induced a reduction of ACAT activity (48.9%) in dam's liver and, an augmentation of HMG-CoA-reductase activity (142.4%) whereas it has no effect on cholesterol-7a-hydroxylase activity. The administration of the ECD has no additive effect on ACAT, but significantly reduced the HMG-CoA-reductase activity and cholesterol-7a-hydroxylase activity as compared with the pregnant control group. In placentas the ECD supplementation has an influence for HMG-CoA-reductase activity, where a 43% increased in observed. Any ACAT activity was detected in placenta and the ECD has no influence on the cholesterol-7a-hydroxylase activity. Whereas their offspring's liver present a reduction of ACAT and HMG-CoA-reductase activity. Gestation associated with ECD reduces significantly the HMG-CoA-reductase activity, decreasing the 0024-3205/03/$ -see front matter D cholesterol synthesis, but placenta seems to compensate this effect by increasing its HMG-CoA-reductase activity. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="12472796"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/12472796/Intestinal_fatty_acid_binding_protein_regulates_mitochondrion_oxidation_and_cholesterol_uptake"><img alt="Research paper thumbnail of Intestinal fatty acid binding protein regulates mitochondrion 聽-oxidation and cholesterol uptake" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/12472796/Intestinal_fatty_acid_binding_protein_regulates_mitochondrion_oxidation_and_cholesterol_uptake">Intestinal fatty acid binding protein regulates mitochondrion 聽-oxidation and cholesterol uptake</a></div><div class="wp-workCard_item"><span>The Journal of Lipid Research</span><span>, 2008</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="12472796"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="12472796"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472796; 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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="12472795"><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/12472795/Localization_function_and_regulation_of_the_two_intestinal_fatty_acid_binding_protein_types"><img alt="Research paper thumbnail of Localization, function and regulation of the two intestinal fatty acid-binding protein types" 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/12472795/Localization_function_and_regulation_of_the_two_intestinal_fatty_acid_binding_protein_types">Localization, function and regulation of the two intestinal fatty acid-binding protein types</a></div><div class="wp-workCard_item"><span>Histochemistry and Cell Biology</span><span>, 2009</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Although intestinal (I) and liver (L) fatty acid binding proteins (FABP) have been widely studied...</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">Although intestinal (I) and liver (L) fatty acid binding proteins (FABP) have been widely studied, the physiological significance of the presence of the two FABP forms (I- and L-FABP) in absorptive cells remains unknown as do the differences related to their distribution along the crypt-villus axis, regional expression, ontogeny and regulation in the human intestine. Our morphological experiments supported the expression of I- and L-FABP as early as 13 weeks of gestation. Whereas cytoplasmic immunofluorescence staining of L-FABP was barely detectable in the lower half of the villus and in the crypt epithelial cells, I-FABP was visualized in epithelial cells of the crypt-villus axis in all intestinal segments until the adult period in which the staining was maximized in the upper part of the villus. Immunoelectron microscopy revealed more intense labeling of L-FABP compared with I-FABP, accompanied with a heterogeneous distribution in the cytoplasm, microvilli and basolateral membranes. By western blot analysis, I- and L-FABP at 15 weeks of gestation appeared predominant in jejunum compared with duodenum, ileum, proximal and distal colon. Exploration of the maturation aspect documented a rise in L-FABP in adult tissues. Permanent transfections of Caco-2 cells with I-FABP cDNA resulted in decreased lipid export, apolipoprotein (apo) biogenesis and chylomicron secretion. Additionally, supplementation of Caco-2 with insulin, hydrocortisone and epidermal growth factor differentially modulated the expression of I- and L-FABP, apo B-48 and microsomal triglyceride transfer protein (MTP), emphasizing that these key proteins do not exhibit a parallel modulation. Overall, our findings indicate that the two FABPs display differences in localization, regulation and developmental pattern.</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="12472795"><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="12472795"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472795; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472795]").text(description); $(".js-view-count[data-work-id=12472795]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472795; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472795']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472795, 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" } } $('.js-work-strip[data-work-id=12472795]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472795,"title":"Localization, function and regulation of the two intestinal fatty acid-binding protein types","translated_title":"","metadata":{"abstract":"Although intestinal (I) and liver (L) fatty acid binding proteins (FABP) have been widely studied, the physiological significance of the presence of the two FABP forms (I- and L-FABP) in absorptive cells remains unknown as do the differences related to their distribution along the crypt-villus axis, regional expression, ontogeny and regulation in the human intestine. Our morphological experiments supported the expression of I- and L-FABP as early as 13 weeks of gestation. Whereas cytoplasmic immunofluorescence staining of L-FABP was barely detectable in the lower half of the villus and in the crypt epithelial cells, I-FABP was visualized in epithelial cells of the crypt-villus axis in all intestinal segments until the adult period in which the staining was maximized in the upper part of the villus. Immunoelectron microscopy revealed more intense labeling of L-FABP compared with I-FABP, accompanied with a heterogeneous distribution in the cytoplasm, microvilli and basolateral membranes. By western blot analysis, I- and L-FABP at 15 weeks of gestation appeared predominant in jejunum compared with duodenum, ileum, proximal and distal colon. Exploration of the maturation aspect documented a rise in L-FABP in adult tissues. Permanent transfections of Caco-2 cells with I-FABP cDNA resulted in decreased lipid export, apolipoprotein (apo) biogenesis and chylomicron secretion. Additionally, supplementation of Caco-2 with insulin, hydrocortisone and epidermal growth factor differentially modulated the expression of I- and L-FABP, apo B-48 and microsomal triglyceride transfer protein (MTP), emphasizing that these key proteins do not exhibit a parallel modulation. 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Whereas cytoplasmic immunofluorescence staining of L-FABP was barely detectable in the lower half of the villus and in the crypt epithelial cells, I-FABP was visualized in epithelial cells of the crypt-villus axis in all intestinal segments until the adult period in which the staining was maximized in the upper part of the villus. Immunoelectron microscopy revealed more intense labeling of L-FABP compared with I-FABP, accompanied with a heterogeneous distribution in the cytoplasm, microvilli and basolateral membranes. By western blot analysis, I- and L-FABP at 15 weeks of gestation appeared predominant in jejunum compared with duodenum, ileum, proximal and distal colon. Exploration of the maturation aspect documented a rise in L-FABP in adult tissues. Permanent transfections of Caco-2 cells with I-FABP cDNA resulted in decreased lipid export, apolipoprotein (apo) biogenesis and chylomicron secretion. Additionally, supplementation of Caco-2 with insulin, hydrocortisone and epidermal growth factor differentially modulated the expression of I- and L-FABP, apo B-48 and microsomal triglyceride transfer protein (MTP), emphasizing that these key proteins do not exhibit a parallel modulation. Overall, our findings indicate that the two FABPs display differences in localization, regulation and developmental pattern.","internal_url":"https://www.academia.edu/12472795/Localization_function_and_regulation_of_the_two_intestinal_fatty_acid_binding_protein_types","translated_internal_url":"","created_at":"2015-05-19T13:56:26.603-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31309978,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Localization_function_and_regulation_of_the_two_intestinal_fatty_acid_binding_protein_types","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":31309978,"first_name":"Alain","middle_initials":null,"last_name":"Montoudis","page_name":"AlainMontoudis","domain_name":"independent","created_at":"2015-05-19T13:55:47.683-07:00","display_name":"Alain Montoudis","url":"https://independent.academia.edu/AlainMontoudis"},"attachments":[],"research_interests":[{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":104853,"name":"Hormones","url":"https://www.academia.edu/Documents/in/Hormones"},{"id":134346,"name":"Infant","url":"https://www.academia.edu/Documents/in/Infant"},{"id":176898,"name":"Jejunum","url":"https://www.academia.edu/Documents/in/Jejunum"},{"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":329263,"name":"Epidermal Growth Factor","url":"https://www.academia.edu/Documents/in/Epidermal_Growth_Factor"},{"id":458879,"name":"Lipoproteins","url":"https://www.academia.edu/Documents/in/Lipoproteins"},{"id":462111,"name":"Western blot","url":"https://www.academia.edu/Documents/in/Western_blot"},{"id":829416,"name":"Colon","url":"https://www.academia.edu/Documents/in/Colon"},{"id":989723,"name":"Caco 2 Cell","url":"https://www.academia.edu/Documents/in/Caco_2_Cell"},{"id":1509323,"name":"Fatty Acid Binding Protein","url":"https://www.academia.edu/Documents/in/Fatty_Acid_Binding_Protein"}],"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="12472794"><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/12472794/Hepatocyte_specific_Ptpn6_deletion_promotes_hepatic_lipid_accretion_but_reduces_NAFLD_in_diet_induced_obesity_Potential_role_of_PPAR%CE%B3"><img alt="Research paper thumbnail of Hepatocyte-specific Ptpn6 deletion promotes hepatic lipid accretion, but reduces NAFLD in diet-induced obesity: Potential role of PPAR纬" 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/12472794/Hepatocyte_specific_Ptpn6_deletion_promotes_hepatic_lipid_accretion_but_reduces_NAFLD_in_diet_induced_obesity_Potential_role_of_PPAR%CE%B3">Hepatocyte-specific Ptpn6 deletion promotes hepatic lipid accretion, but reduces NAFLD in diet-induced obesity: Potential role of PPAR纬</a></div><div class="wp-workCard_item"><span>Hepatology</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Hepatocyte-specific Shp1 knockout mice (Ptpn6(H-KO)) are protected from hepatic insulin resistanc...</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">Hepatocyte-specific Shp1 knockout mice (Ptpn6(H-KO)) are protected from hepatic insulin resistance evoked by high-fat diet (HFD) feeding for 8 weeks. Unexpectedly, we report herein that Ptpn6(H-KO) mice fed an HFD for up to 16 weeks are still protected from insulin resistance, but are more prone to hepatic steatosis, as compared with their HFD-fed Ptpn6(f/f) counterparts. The livers from HFD-fed Ptpn6(H-KO) mice displayed 1) augmented lipogenesis, marked by increased expression of several hepatic genes involved in fatty acid biosynthesis, 2) elevated postprandial fatty acid uptake, and 3) significantly reduced lipid export with enhanced degradation of apolipoprotein B (ApoB). Despite more extensive hepatic steatosis, the inflammatory profile of the HFD-fed Ptpn6(H-KO) liver was similar (8 weeks) or even improved (16 weeks) as compared to their HFD-fed Ptpn6(f/f) littermates, along with reduced hepatocellular damage as revealed by serum levels of hepatic enzymes. Interestingly, comparative microarray analysis revealed a significant up-regulation of peroxisome proliferator-activated receptor gamma (PPAR纬) gene expression, confirmed by quantitative polymerase chain reaction. Elevated PPAR纬 nuclear activity also was observed and found to be directly regulated by Shp1 in a cell-autonomous manner. These findings highlight a novel role for hepatocyte Shp1 in the regulation of PPAR纬 and hepatic lipid metabolism. Shp1 deficiency prevents the development of severe hepatic inflammation and hepatocellular damage in steatotic livers, presenting hepatocyte Shp1 as a potential novel mediator of nonalcoholic fatty liver diseases in obesity.</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="12472794"><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="12472794"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472794; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=12472794]").text(description); $(".js-view-count[data-work-id=12472794]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 12472794; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='12472794']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 12472794, 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" } } $('.js-work-strip[data-work-id=12472794]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":12472794,"title":"Hepatocyte-specific Ptpn6 deletion promotes hepatic lipid accretion, but reduces NAFLD in diet-induced obesity: Potential role of PPAR纬","translated_title":"","metadata":{"abstract":"Hepatocyte-specific Shp1 knockout mice (Ptpn6(H-KO)) are protected from hepatic insulin resistance evoked by high-fat diet (HFD) feeding for 8 weeks. Unexpectedly, we report herein that Ptpn6(H-KO) mice fed an HFD for up to 16 weeks are still protected from insulin resistance, but are more prone to hepatic steatosis, as compared with their HFD-fed Ptpn6(f/f) counterparts. The livers from HFD-fed Ptpn6(H-KO) mice displayed 1) augmented lipogenesis, marked by increased expression of several hepatic genes involved in fatty acid biosynthesis, 2) elevated postprandial fatty acid uptake, and 3) significantly reduced lipid export with enhanced degradation of apolipoprotein B (ApoB). Despite more extensive hepatic steatosis, the inflammatory profile of the HFD-fed Ptpn6(H-KO) liver was similar (8 weeks) or even improved (16 weeks) as compared to their HFD-fed Ptpn6(f/f) littermates, along with reduced hepatocellular damage as revealed by serum levels of hepatic enzymes. Interestingly, comparative microarray analysis revealed a significant up-regulation of peroxisome proliferator-activated receptor gamma (PPAR纬) gene expression, confirmed by quantitative polymerase chain reaction. Elevated PPAR纬 nuclear activity also was observed and found to be directly regulated by Shp1 in a cell-autonomous manner. These findings highlight a novel role for hepatocyte Shp1 in the regulation of PPAR纬 and hepatic lipid metabolism. Shp1 deficiency prevents the development of severe hepatic inflammation and hepatocellular damage in steatotic livers, presenting hepatocyte Shp1 as a potential novel mediator of nonalcoholic fatty liver diseases in obesity.","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Hepatology"},"translated_abstract":"Hepatocyte-specific Shp1 knockout mice (Ptpn6(H-KO)) are protected from hepatic insulin resistance evoked by high-fat diet (HFD) feeding for 8 weeks. Unexpectedly, we report herein that Ptpn6(H-KO) mice fed an HFD for up to 16 weeks are still protected from insulin resistance, but are more prone to hepatic steatosis, as compared with their HFD-fed Ptpn6(f/f) counterparts. The livers from HFD-fed Ptpn6(H-KO) mice displayed 1) augmented lipogenesis, marked by increased expression of several hepatic genes involved in fatty acid biosynthesis, 2) elevated postprandial fatty acid uptake, and 3) significantly reduced lipid export with enhanced degradation of apolipoprotein B (ApoB). Despite more extensive hepatic steatosis, the inflammatory profile of the HFD-fed Ptpn6(H-KO) liver was similar (8 weeks) or even improved (16 weeks) as compared to their HFD-fed Ptpn6(f/f) littermates, along with reduced hepatocellular damage as revealed by serum levels of hepatic enzymes. Interestingly, comparative microarray analysis revealed a significant up-regulation of peroxisome proliferator-activated receptor gamma (PPAR纬) gene expression, confirmed by quantitative polymerase chain reaction. Elevated PPAR纬 nuclear activity also was observed and found to be directly regulated by Shp1 in a cell-autonomous manner. These findings highlight a novel role for hepatocyte Shp1 in the regulation of PPAR纬 and hepatic lipid metabolism. Shp1 deficiency prevents the development of severe hepatic inflammation and hepatocellular damage in steatotic livers, presenting hepatocyte Shp1 as a potential novel mediator of nonalcoholic fatty liver diseases in obesity.","internal_url":"https://www.academia.edu/12472794/Hepatocyte_specific_Ptpn6_deletion_promotes_hepatic_lipid_accretion_but_reduces_NAFLD_in_diet_induced_obesity_Potential_role_of_PPAR%CE%B3","translated_internal_url":"","created_at":"2015-05-19T13:56:26.493-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":31309978,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Hepatocyte_specific_Ptpn6_deletion_promotes_hepatic_lipid_accretion_but_reduces_NAFLD_in_diet_induced_obesity_Potential_role_of_PPAR纬","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":31309978,"first_name":"Alain","middle_initials":null,"last_name":"Montoudis","page_name":"AlainMontoudis","domain_name":"independent","created_at":"2015-05-19T13:55:47.683-07:00","display_name":"Alain Montoudis","url":"https://independent.academia.edu/AlainMontoudis"},"attachments":[],"research_interests":[{"id":3851,"name":"Obesity","url":"https://www.academia.edu/Documents/in/Obesity"},{"id":37773,"name":"Hepatology","url":"https://www.academia.edu/Documents/in/Hepatology"},{"id":51373,"name":"Insulin Resistance","url":"https://www.academia.edu/Documents/in/Insulin_Resistance"},{"id":71437,"name":"Liver","url":"https://www.academia.edu/Documents/in/Liver"},{"id":72314,"name":"Fatty acids","url":"https://www.academia.edu/Documents/in/Fatty_acids"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":151036,"name":"non alcoholic fatty liver disease (NAFLD)","url":"https://www.academia.edu/Documents/in/non_alcoholic_fatty_liver_disease_NAFLD_"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":295465,"name":"Fatty Liver","url":"https://www.academia.edu/Documents/in/Fatty_Liver"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="12472793"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/12472793/Prevention_of_Lipid_oxidation_in_Paediatric_Parenteral_Nutrition"><img alt="Research paper thumbnail of Prevention of Lipid oxidation in Paediatric Parenteral Nutrition" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/12472793/Prevention_of_Lipid_oxidation_in_Paediatric_Parenteral_Nutrition">Prevention of Lipid oxidation in Paediatric Parenteral Nutrition</a></div><div class="wp-workCard_item"><span>Free Radical Biology and Medicine</span><span>, 2010</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="12472793"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="12472793"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 12472793; 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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="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="{&quot;attachment_id&quot;:46182787,&quot;asset_id&quot;:12440504,&quot;asset_type&quot;:&quot;Work&quot;,&quot;button_location&quot;:&quot;profile&quot;}" href="https://www.academia.edu/attachments/46182787/download_file?st=MTczMjM4MjAxMCw4LjIyMi4yMDguMTQ2&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 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