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Paris Sud XI University | Biochimie - Academia.edu

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var $lessLink = $(".js-mobile-nav-collapse-trigger"); var $section = $('.js-mobile-nav-expand-section'); $moreLink.click(function(ev){ ev.preventDefault(); $moreLink.hide(); $lessLink.show(); $section.collapse('show'); }); $lessLink.click(function(ev){ ev.preventDefault(); $moreLink.show(); $lessLink.hide(); $section.collapse('hide'); }); })() if ($a.is_logged_in() || false) { new Aedu.NavigationController({ el: '.js-main-nav', showHighlightedNotification: false }); } else { $(".js-header-login-url").attr("href", $a.loginUrlWithRedirect()); } Aedu.autocompleteSearch = new AutocompleteSearch({el: '.js-SiteSearch-form'});</script></div></div> <div id='site' class='fixed'> <div id="content" class="clearfix"> <script>document.addEventListener('DOMContentLoaded', function(){ var $dismissible = $(".dismissible_banner"); $dismissible.click(function(ev) { $dismissible.hide(); }); });</script> <div class="DesignSystem" style="margin-top:-40px"><div class="PageHeader"><div class="container"><div class="row"><div class="col-xs-12 clearfix"><div class="u-floatLeft u-fs24 u-tcGrayDarkest"><span class="PageHeader-title u-m0x u-fw700 u-mr5x u-pr5x u-borderColorGrayLight u-borderRight1"><a href="https://u-psud.academia.edu/"><span class="u-linkUnstyled u-tcGrayDarkest">Paris Sud XI University</span></a></span><h1 class="u-m0x u-fw300 u-fs24 u-displayInline">Biochimie</h1></div><div class="u-floatRight u-mt1x"></div></div></div></div></div><div class="TabbedNavigation"><div class="container"><div class="row"><div class="col-xs-12 clearfix"><ul class="nav u-m0x u-p0x list-inline"><li class="u-floatLeft u-pr5x u-mr5x u-borderColorGrayLight u-borderRight1"><a href="https://u-psud.academia.edu/"><span><i class="fa fa-arrow-left"></i>&nbsp;&nbsp;All Departments</span></a></li><li class="u-floatLeft active"><a href="https://u-psud.academia.edu/Departments/Biochimie/Documents">26 Papers</a></li><li class="u-floatLeft"><a href="https://u-psud.academia.edu/Departments/Biochimie">1 Researchers</a></li></ul></div></div></div></div><div class="container"><div class="row"><div class="col-xs-12"><div class="u-displayFlex"><div class="u-flexGrow1"><div class="u-ph0x"><div class="works"><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_26650128 coauthored" data-work_id="26650128" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26650128/Fibrate_treatment_induced_quantitative_and_qualitative_HDL_changes_associated_with_an_increase_of_SR_BI_cholesterol_efflux_capacities_in_rabbits">Fibrate treatment induced quantitative and qualitative HDL changes associated with an increase of SR-BI cholesterol efflux capacities in rabbits</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Fibrates are widely used as lipid lowering drugs acting as peroxisome proliferator-activated receptors a (PPARa) agonists and modulating the expression of several genes involved in lipid and lipoprotein metabolism. Much less is known on... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26650128" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Fibrates are widely used as lipid lowering drugs acting as peroxisome proliferator-activated receptors a (PPARa) agonists and modulating the expression of several genes involved in lipid and lipoprotein metabolism. Much less is known on the effect of fibrates in HDL structure and composition. Therefore, we examined whether fenofibrate induces quantitative and/or qualitative modifications in HDL metabolism in the rabbit, an animal that, contrary to rodents and similar to humans, is less sensitive to peroxisome proliferators. We first demonstrated that 3-week treatment with fenofibrate (250 mg/kg/day) induced an important increase in serum apolipoprotein A-I, HDL-cholesterol and HDL-phospholipids concentrations and a relative enrichment in HDL cholesteryl ester content. Moreover, the fatty acid profiles from fenofibrate-treated rabbits displayed a dramatic increase in the serum or HDL C18:3 u6 to C18:2 u6 ratio suggesting higher D6 desaturase activity. In addition, HDL from fenofibrate-treated animals exhibited higher relative proportions of sphingomyelin, phosphatidylinositol and phosphatidylethanolamine. We then reported that fenofibrate induced major changes in the physical characteristics of HDL, mainly a higher size and a faster mobility on agarose gel electrophoresis. Finally, serum or HDL from treated rabbits exhibited higher capacity to promote cholesterol efflux from Scavenger receptor class B type I (SR-BI)-rich Fu5AH cells compared to controls. Our findings demonstrate that fenofibrate has beneficial effects in rabbits by increasing the mass of the circulating HDL pool and by modifying their composition transforming them as better acceptors of cellular cholesterol through SR-BI pathway. These effects of fenofibrate might contribute to its benefits on the prevention and treatment of atherosclerosis.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26650128" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="56836489ddc59715eb3bf3dd2fe4d2f8" rel="nofollow" data-download="{&quot;attachment_id&quot;:46937274,&quot;asset_id&quot;:26650128,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46937274/download_file?st=MTc0MDUwMzc1MCw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span><span class="u-displayInlineBlock InlineList-item-text">&nbsp;and&nbsp;<span class="u-textDecorationUnderline u-clickable InlineList-item-text js-work-more-authors-26650128">+1</span><div class="hidden js-additional-users-26650128"><div><span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a href="https://independent.academia.edu/PatriceTh%C3%A9rond">Patrice Thérond</a></span></div></div></span><script>(function(){ var popoverSettings = { el: $('.js-work-more-authors-26650128'), placement: 'bottom', hide_delay: 200, html: true, content: function(){ return $('.js-additional-users-26650128').html(); 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Much less is known on the effect of fibrates in HDL structure and composition. Therefore, we examined whether fenofibrate induces quantitative and/or qualitative modifications in HDL metabolism in the rabbit, an animal that, contrary to rodents and similar to humans, is less sensitive to peroxisome proliferators. We first demonstrated that 3-week treatment with fenofibrate (250 mg/kg/day) induced an important increase in serum apolipoprotein A-I, HDL-cholesterol and HDL-phospholipids concentrations and a relative enrichment in HDL cholesteryl ester content. Moreover, the fatty acid profiles from fenofibrate-treated rabbits displayed a dramatic increase in the serum or HDL C18:3 u6 to C18:2 u6 ratio suggesting higher D6 desaturase activity. In addition, HDL from fenofibrate-treated animals exhibited higher relative proportions of sphingomyelin, phosphatidylinositol and phosphatidylethanolamine. We then reported that fenofibrate induced major changes in the physical characteristics of HDL, mainly a higher size and a faster mobility on agarose gel electrophoresis. Finally, serum or HDL from treated rabbits exhibited higher capacity to promote cholesterol efflux from Scavenger receptor class B type I (SR-BI)-rich Fu5AH cells compared to controls. Our findings demonstrate that fenofibrate has beneficial effects in rabbits by increasing the mass of the circulating HDL pool and by modifying their composition transforming them as better acceptors of cellular cholesterol through SR-BI pathway. These effects of fenofibrate might contribute to its benefits on the prevention and treatment of atherosclerosis.","publication":"Biochimie","publication_with_fallback":"Biochimie","downloadable_attachments":[{"id":46937274,"asset_id":26650128,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/46937274/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/46937274/j.biochi.2013.02.00120160701-8147-1errv99-libre.pdf?1467410123=\u0026response-content-disposition=attachment%3B+filename%3DFibrate_treatment_induced_quantitative_a.pdf\u0026Expires=1740507350\u0026Signature=Cok5MUL1NTKx3OTUBXD6MiX4GOjqJLGBtaKCCEC6Oz9EKUW3NULEWNdmeSNdAt3Skm6K-XUAMv93NNBjLA2KxgPzOTL1~fKqqvYKKgfceDyqSBTJz09ikth94FZtHP4-CCRj1j2VgMxia1SmZiyOT~rnn~vZWUvFawVaLESk8Zs8mMuhKDq6cULwcUJFcz~7kuQpgYXDOXyCQsvz2DAc2CbgAdZUzpLcdoy3gxMl-KOEeLtEf~TVMXWMWkyonKHkrtAoTkl2Cj5T4iIxC5G7A1SGijWIKjVz2Xk7VxXjG2dbCYBG8XAIc7Xcbvx6gyK-Szr8DsbxE3fhHCK3pZcfvw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/46937274/download_file?st=MTc0MDUwMzc1MCw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/46937274/mini_magick20190208-25089-elt7wu.png?1549638217"}],"downloadable_attachments_with_full_thumbnails":[{"id":46937274,"asset_id":26650128,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/46937274/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/46937274/j.biochi.2013.02.00120160701-8147-1errv99-libre.pdf?1467410123=\u0026response-content-disposition=attachment%3B+filename%3DFibrate_treatment_induced_quantitative_a.pdf\u0026Expires=1740507350\u0026Signature=Cok5MUL1NTKx3OTUBXD6MiX4GOjqJLGBtaKCCEC6Oz9EKUW3NULEWNdmeSNdAt3Skm6K-XUAMv93NNBjLA2KxgPzOTL1~fKqqvYKKgfceDyqSBTJz09ikth94FZtHP4-CCRj1j2VgMxia1SmZiyOT~rnn~vZWUvFawVaLESk8Zs8mMuhKDq6cULwcUJFcz~7kuQpgYXDOXyCQsvz2DAc2CbgAdZUzpLcdoy3gxMl-KOEeLtEf~TVMXWMWkyonKHkrtAoTkl2Cj5T4iIxC5G7A1SGijWIKjVz2Xk7VxXjG2dbCYBG8XAIc7Xcbvx6gyK-Szr8DsbxE3fhHCK3pZcfvw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/46937274/download_file?st=MTc0MDUwMzc1MCw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/46937274/mini_magick20190208-25089-elt7wu.png?1549638217"}],"has_pdf":true,"has_fulltext":true,"page_count":10,"ordered_authors":[{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"},{"id":50639665,"first_name":"Patrice","last_name":"Thérond","domain_name":"independent","page_name":"PatriceThérond","display_name":"Patrice Thérond","profile_url":"https://independent.academia.edu/PatriceTh%C3%A9rond","photo":"/images/s65_no_pic.png"}],"research_interests":[{"id":21732,"name":"Magnetic Resonance Spectroscopy","url":"https://www.academia.edu/Documents/in/Magnetic_Resonance_Spectroscopy","nofollow":true},{"id":76407,"name":"Circular Dichroism","url":"https://www.academia.edu/Documents/in/Circular_Dichroism","nofollow":true},{"id":90514,"name":"Cholesterol","url":"https://www.academia.edu/Documents/in/Cholesterol","nofollow":true},{"id":193464,"name":"Sodium Dodecyl Sulfate-Polyacrylamide Gel Electrophoresis","url":"https://www.academia.edu/Documents/in/Sodium_Dodecyl_Sulfate-Polyacrylamide_Gel_Electrophoresis","nofollow":true},{"id":285486,"name":"Biochimie","url":"https://www.academia.edu/Documents/in/Biochimie"},{"id":788677,"name":"Rabbits","url":"https://www.academia.edu/Documents/in/Rabbits"},{"id":1421488,"name":"#Hypolipidemic Agents","url":"https://www.academia.edu/Documents/in/_Hypolipidemic_Agents"},{"id":1523045,"name":"Fenofibrate","url":"https://www.academia.edu/Documents/in/Fenofibrate"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"publication_year":2013,"publication_year_with_fallback":2013,"paper_rank":null,"all_time_views":15,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_26703929" data-work_id="26703929" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26703929/Moderate_Alcohol_Consumption_Increases_Cholesterol_Efflux_Mediated_by_ABCA1">Moderate Alcohol Consumption Increases Cholesterol Efflux Mediated by ABCA1</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Moderate alcohol consumption increases HDL cholesterol, which is involved in reverse cholesterol transport (RCT). The aim of this study was to investigate the effect of moderate alcohol consumption on cholesterol efflux, using J774 mouse... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703929" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Moderate alcohol consumption increases HDL cholesterol, which is involved in reverse cholesterol transport (RCT). The aim of this study was to investigate the effect of moderate alcohol consumption on cholesterol efflux, using J774 mouse macrophages and Fu5AH cells, and on other parameters in the RCT pathway. Twenty-three healthy men (45-65 years) participated in a randomized, partially diet-controlled, crossover trial. They consumed four glasses of whisky (40 g of alcohol) or water daily for 17 days. After 17 days of whisky consumption, serum capacity to induce ABCA1-dependent cholesterol efflux from J774 mouse macrophages was increased by 17.5% ( P ‫؍‬ 0.027) compared with water consumption. Plasma capacity to induce cholesterol efflux from Fu5AH cells increased by 4.6% ( P ‫؍‬ 0.002). Pre ␤ -HDL, apolipoprotein A-I (apoA-I), and lipoprotein A-I:A-II also increased by 31.6, 6.2, and 5.7% ( P Ͻ 0.05), respectively, after whisky consumption compared with water consumption. Changes of cAMP-stimulated cholesterol efflux correlated ( r ‫؍‬ 0.65, P Ͻ 0.05) with changes of apoA-I but not with changes of pre ␤ -HDL ( r ‫؍‬ 0.30, P ‫؍‬ 0.18). Cholesterol efflux capacities from serum of lean men were higher than those from overweight men.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703929" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="71c85788984c8991b8636f061f7fc5d4" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985669,&quot;asset_id&quot;:26703929,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985669/download_file?st=MTc0MDUwMzc1MCw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span></li><li class="js-paper-rank-work_26703929 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="26703929"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 26703929, container: ".js-paper-rank-work_26703929", }); 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The aim of this study was to investigate the effect of moderate alcohol consumption on cholesterol efflux, using J774 mouse macrophages and Fu5AH cells, and on other parameters in the RCT pathway. Twenty-three healthy men (45-65 years) participated in a randomized, partially diet-controlled, crossover trial. They consumed four glasses of whisky (40 g of alcohol) or water daily for 17 days. After 17 days of whisky consumption, serum capacity to induce ABCA1-dependent cholesterol efflux from J774 mouse macrophages was increased by 17.5% ( P ‫؍‬ 0.027) compared with water consumption. Plasma capacity to induce cholesterol efflux from Fu5AH cells increased by 4.6% ( P ‫؍‬ 0.002). Pre ␤ -HDL, apolipoprotein A-I (apoA-I), and lipoprotein A-I:A-II also increased by 31.6, 6.2, and 5.7% ( P Ͻ 0.05), respectively, after whisky consumption compared with water consumption. Changes of cAMP-stimulated cholesterol efflux correlated ( r ‫؍‬ 0.65, P Ͻ 0.05) with changes of apoA-I but not with changes of pre ␤ -HDL ( r ‫؍‬ 0.30, P ‫؍‬ 0.18). Cholesterol efflux capacities from serum of lean men were higher than those from overweight men.","publication":"Alcoholism: Clinical \u0026 Experimental Research","publication_with_fallback":"Alcoholism: Clinical \u0026 Experimental 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Studies","url":"https://www.academia.edu/Documents/in/Cross-Over_Studies"},{"id":1239755,"name":"Neurosciences","url":"https://www.academia.edu/Documents/in/Neurosciences"},{"id":1371154,"name":"Lipoprotein a","url":"https://www.academia.edu/Documents/in/Lipoprotein_a"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"publication_year":2004,"publication_year_with_fallback":2004,"paper_rank":null,"all_time_views":87,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_26703930" data-work_id="26703930" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26703930/Human_ApoA_IV_Overexpression_in_Transgenic_Mice_Induces_cAMP_Stimulated_Cholesterol_Efflux_From_J774_Macrophages_to_Whole_Serum">Human ApoA-IV Overexpression in Transgenic Mice Induces cAMP-Stimulated Cholesterol Efflux From J774 Macrophages to Whole Serum</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">The role of apolipoprotein A-IV (apoA-IV) in lipoprotein metabolism has not been established. The aim of the present study was to investigate the role of apoA-IV in reverse cholesterol transport by comparing cellular cholesterol efflux to... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703930" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">The role of apolipoprotein A-IV (apoA-IV) in lipoprotein metabolism has not been established. The aim of the present study was to investigate the role of apoA-IV in reverse cholesterol transport by comparing cellular cholesterol efflux to serum or serum fractions from control mice and from mice transgenic for human apoA-IV (HuA-IVTg mice). When Fu5AH hepatoma cells were used, the cholesterol efflux to serum from either control or transgenic mice was similar. When control J774 macrophage cells were used, a comparison of efflux to serum or lipoprotein-deficient serum (LPDS) failed to demonstrate any differences between control and transgenic mice. In contrast, when the J774 cells were pretreated with cAMP, there was a stimulation of efflux to whole serum or LPDS from HuA-IVTg mice. cAMP treatment had no effect on efflux to serum or LPDS from control mice. Pretreatment of the cells with cAMP did not enhance the efflux response to high density lipoprotein isolated from HuA-IVTg mouse serum. Our results suggest that apoA-IV, unassociated with high density lipoprotein particles, is responsible for enhanced cholesterol efflux. This study illustrates the role of lipid-free apolipoproteins in mediating cellular cholesterol efflux with use of a biological fluid and is potentially of physiological relevance, especially in apolipoprotein-rich extravascular fluids. (Arterioscler Thromb</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703930" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="a285dd6473548a00725e122f0d3cfd4a" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985662,&quot;asset_id&quot;:26703930,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985662/download_file?st=MTc0MDUwMzc1MSw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span></li><li class="js-paper-rank-work_26703930 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="26703930"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 26703930, container: ".js-paper-rank-work_26703930", }); 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Relations between serum components and efflux, esterification, and transfer</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">A cell culture system was employed to test a large number of samples of human serum for the ability to stimulate the efflux of cell cholesterol. The extent of efflux obtained with each specimen was correlated with the serum concentrations... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703933" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">A cell culture system was employed to test a large number of samples of human serum for the ability to stimulate the efflux of cell cholesterol. The extent of efflux obtained with each specimen was correlated with the serum concentrations of cholesterol, triglycerides, apoprotein (apo) B, apo A-I, apo A-II, and lipoprotein subfractions (ie, high-density lipoprotein 2 [HDL 2 ], HDL 3 , lipoprotein [Lp] A-I, and LpA-I:A-II). In addition, the subsequent esterification of the released cholesterol and the distribution of the synthesized exogenous cholesteryl esters between HDL and low-density lipoprotein/ very-low-density lipoprotein provided estimates of the lecithin:cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP) activities of each serum. The values for these activities were analyzed for correlations with cell efflux and the various serum parameters. Cell cholesterol efflux best correlated with serum total HDL cholesterol values. HDL 2 and HDL 3 correlated about equally well with efflux, whereas LpA-I demonstrated a much greater association with</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703933" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="61251d6c88c30e138f7d04a3ebc899f3" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985673,&quot;asset_id&quot;:26703933,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985673/download_file?st=MTc0MDUwMzc1MSw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span><span class="u-displayInlineBlock InlineList-item-text">&nbsp;and&nbsp;<span class="u-textDecorationUnderline u-clickable InlineList-item-text js-work-more-authors-26703933">+1</span><div class="hidden js-additional-users-26703933"><div><span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a href="https://independent.academia.edu/VeroniqueAtger">Véronique Atger</a></span></div></div></span><script>(function(){ var popoverSettings = { el: $('.js-work-more-authors-26703933'), placement: 'bottom', hide_delay: 200, html: true, content: function(){ return $('.js-additional-users-26703933').html(); 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The extent of efflux obtained with each specimen was correlated with the serum concentrations of cholesterol, triglycerides, apoprotein (apo) B, apo A-I, apo A-II, and lipoprotein subfractions (ie, high-density lipoprotein 2 [HDL 2 ], HDL 3 , lipoprotein [Lp] A-I, and LpA-I:A-II). In addition, the subsequent esterification of the released cholesterol and the distribution of the synthesized exogenous cholesteryl esters between HDL and low-density lipoprotein/ very-low-density lipoprotein provided estimates of the lecithin:cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP) activities of each serum. The values for these activities were analyzed for correlations with cell efflux and the various serum parameters. Cell cholesterol efflux best correlated with serum total HDL cholesterol values. 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Concrete","url":"https://www.academia.edu/Documents/in/High_Density_Concrete"},{"id":1274496,"name":"Low Density Lipoprotein (LDL)","url":"https://www.academia.edu/Documents/in/Low_Density_Lipoprotein_LDL_"},{"id":1371154,"name":"Lipoprotein a","url":"https://www.academia.edu/Documents/in/Lipoprotein_a"},{"id":1984565,"name":"Apoproteins","url":"https://www.academia.edu/Documents/in/Apoproteins"}],"publication_year":1994,"publication_year_with_fallback":1994,"paper_rank":null,"all_time_views":42,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_26703934 coauthored" data-work_id="26703934" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26703934/Opposite_Effects_of_Plasma_From_Human_Apolipoprotein_A_II_Transgenic_Mice_on_Cholesterol_Efflux_From_J774_Macrophages_and_Fu5AH_Hepatoma_Cells">Opposite Effects of Plasma From Human Apolipoprotein A-II Transgenic Mice on Cholesterol Efflux From J774 Macrophages and Fu5AH Hepatoma Cells</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Overexpression of human apolipoprotein A-II (hapo A-II) in transgenic mice (hAIItg mice) induced marked hypertriglyceridemia and low levels of plasma high density lipoprotein (HDL) with a high hapo A-II content. We sought to determine... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703934" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Overexpression of human apolipoprotein A-II (hapo A-II) in transgenic mice (hAIItg mice) induced marked hypertriglyceridemia and low levels of plasma high density lipoprotein (HDL) with a high hapo A-II content. We sought to determine whether cholesterol efflux to plasma and HDL from these mice would be affected. In the Fu5AH cell system, plasma from hAIItg mice induced a markedly lower cholesterol efflux than did control plasma, in accordance with the dependence of efflux on HDL concentration. Moreover, HDLs from hAIItg mice were less effective acceptors than were control HDLs. In the J774 macrophage cell system, pretreatment with cAMP, which upregulates ATP binding cassette transporter 1, induced a marked increase in the efflux to hAIItg plasma as well as to purified hapo A-I and hapo A-II, whereas it had no effect on cholesterol efflux to control plasma. A strong positive correlation was established between percent cAMP stimulation of efflux and plasma hapo A-II concentration. The cAMP stimulation of efflux to hAIItg mouse plasma may be linked to the presence of pre-␤ migrating HDL containing hapo A-II. Thus, despite lower HDL and apolipoprotein A-I contents, the increased ability of plasma from hAIItg mice to extract cholesterol from macrophage-like cells may have an antiatherogenic influence. (Arterioscler Thromb Vasc Biol. 2002;22:638-643.)</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703934" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="487e72ea6d0dbdc10ef0c91a3ea2d62a" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985661,&quot;asset_id&quot;:26703934,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985661/download_file?st=MTc0MDUwMzc1MSw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span><span class="u-displayInlineBlock InlineList-item-text">&nbsp;and&nbsp;<span class="u-textDecorationUnderline u-clickable InlineList-item-text js-work-more-authors-26703934">+1</span><div class="hidden js-additional-users-26703934"><div><span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a href="https://independent.academia.edu/DominiqueGoudouneche">Dominique Goudouneche</a></span></div></div></span><script>(function(){ var popoverSettings = { el: $('.js-work-more-authors-26703934'), placement: 'bottom', hide_delay: 200, html: true, content: function(){ return $('.js-additional-users-26703934').html(); 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We sought to determine whether cholesterol efflux to plasma and HDL from these mice would be affected. In the Fu5AH cell system, plasma from hAIItg mice induced a markedly lower cholesterol efflux than did control plasma, in accordance with the dependence of efflux on HDL concentration. Moreover, HDLs from hAIItg mice were less effective acceptors than were control HDLs. In the J774 macrophage cell system, pretreatment with cAMP, which upregulates ATP binding cassette transporter 1, induced a marked increase in the efflux to hAIItg plasma as well as to purified hapo A-I and hapo A-II, whereas it had no effect on cholesterol efflux to control plasma. A strong positive correlation was established between percent cAMP stimulation of efflux and plasma hapo A-II concentration. The cAMP stimulation of efflux to hAIItg mouse plasma may be linked to the presence of pre-␤ migrating HDL containing hapo A-II. 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itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26703935/Atheroprotective_Reverse_Cholesterol_Transport_Pathway_Is_Defective_in_Familial_Hypercholesterolemia">Atheroprotective Reverse Cholesterol Transport Pathway Is Defective in Familial Hypercholesterolemia</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Objective-Low high-density lipoprotein (HDL) cholesterol levels are frequently observed in familial hypercholesterolemia (FH) and might be associated with functional alterations of HDL particles that may influence their efficaciousness in... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703935" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Objective-Low high-density lipoprotein (HDL) cholesterol levels are frequently observed in familial hypercholesterolemia (FH) and might be associated with functional alterations of HDL particles that may influence their efficaciousness in the reverse cholesterol transport pathway.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703935" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="d1ec01b5d2655817648340e36897c0e6" rel="nofollow" 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el: $('*[data-has-card-for-ri-list=26703935]'), work: {"id":26703935,"title":"Atheroprotective Reverse Cholesterol Transport Pathway Is Defective in Familial Hypercholesterolemia","created_at":"2016-07-03T15:33:46.744-07:00","owner_id":50697757,"url":"https://www.academia.edu/26703935/Atheroprotective_Reverse_Cholesterol_Transport_Pathway_Is_Defective_in_Familial_Hypercholesterolemia","slug":"Atheroprotective_Reverse_Cholesterol_Transport_Pathway_Is_Defective_in_Familial_Hypercholesterolemia","dom_id":"work_26703935","summary":"Objective-Low high-density lipoprotein (HDL) cholesterol levels are frequently observed in familial hypercholesterolemia (FH) and might be associated with functional alterations of HDL particles that may influence their efficaciousness in the reverse cholesterol transport pathway.","publication":"Arteriosclerosis, Thrombosis, and Vascular Biology","publication_with_fallback":"Arteriosclerosis, Thrombosis, and Vascular 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Studies","url":"https://www.academia.edu/Documents/in/Case_Control_Studies"},{"id":2460249,"name":"Femoral Artery","url":"https://www.academia.edu/Documents/in/Femoral_Artery"}],"publication_year":2011,"publication_year_with_fallback":2011,"paper_rank":null,"all_time_views":14,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_26703936" data-work_id="26703936" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26703936/Enhanced_efflux_of_cholesterol_from_ABCA1_expressing_macrophages_to_serum_from_type_IV_hypertriglyceridemic_subjects">Enhanced efflux of cholesterol from ABCA1-expressing macrophages to serum from type IV hypertriglyceridemic subjects</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Since elevated plasma triglycerides (TGs) are an independent cardiovascular risk factor, we have compared the cholesterol efflux potential of sera from asymptomatic hypertriglyceridemic (HTG) type IIb, type IV or normolipidemic (NLP)... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703936" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Since elevated plasma triglycerides (TGs) are an independent cardiovascular risk factor, we have compared the cholesterol efflux potential of sera from asymptomatic hypertriglyceridemic (HTG) type IIb, type IV or normolipidemic (NLP) individuals using two different cell systems. In both type IIb and IV HTG, the efflux of cholesterol from SR-BI-rich Fu5AH cells was similar to that obtained with NLP. The maintenance of efflux efficiency in spite of reduced HDL-cholesterol levels can be mainly attributed to the relative enrichment of HDL with phospholipid. In the J774 macrophage cell system, pretreatment with cAMP, which upregulates ABCA1, induced a markedly higher increase in efflux to type IV sera compared with type IIb or NLP. In addition, type IV sera exhibited two-fold higher pre-␤ HDL relative concentration (percentage of total apo AI) compared with NLP. Moreover, positive correlations were established between ABCA1-mediated efflux and the serum pre-␤ HDL levels or TG concentrations. Thus, the hyperTGemia is associated with a higher fraction of apo AI recovered as pre-␤ HDL which appear to be partly responsible for enhanced efflux obtained upon the cAMP stimulation of J774 cells. In conclusion, we demonstrated for the first time that the ABCA1-expressing J774 cell system is responsive to the percent of apo AI present in human serum as pre-␤ HDL. Our results suggest that high-plasma TG, accompanied by low HDL may not result in an impaired cholesterol efflux capacity.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703936" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="ba23bffe51c0293b827698985d9adc4f" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985672,&quot;asset_id&quot;:26703936,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985672/download_file?st=MTc0MDUwMzc1MSw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span></li><li class="js-paper-rank-work_26703936 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="26703936"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 26703936, container: ".js-paper-rank-work_26703936", }); 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In both type IIb and IV HTG, the efflux of cholesterol from SR-BI-rich Fu5AH cells was similar to that obtained with NLP. The maintenance of efflux efficiency in spite of reduced HDL-cholesterol levels can be mainly attributed to the relative enrichment of HDL with phospholipid. In the J774 macrophage cell system, pretreatment with cAMP, which upregulates ABCA1, induced a markedly higher increase in efflux to type IV sera compared with type IIb or NLP. In addition, type IV sera exhibited two-fold higher pre-␤ HDL relative concentration (percentage of total apo AI) compared with NLP. Moreover, positive correlations were established between ABCA1-mediated efflux and the serum pre-␤ HDL levels or TG concentrations. Thus, the hyperTGemia is associated with a higher fraction of apo AI recovered as pre-␤ HDL which appear to be partly responsible for enhanced efflux obtained upon the cAMP stimulation of J774 cells. In conclusion, we demonstrated for the first time that the ABCA1-expressing J774 cell system is responsive to the percent of apo AI present in human serum as pre-␤ HDL. Our results suggest that high-plasma TG, accompanied by low HDL may not result in an impaired cholesterol efflux capacity.","publication":"Atherosclerosis","publication_with_fallback":"Atherosclerosis","downloadable_attachments":[{"id":46985672,"asset_id":26703936,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/46985672/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/46985672/j.atherosclerosis.2003.08.01120160703-25928-o7intt-libre.pdf?1467585500=\u0026response-content-disposition=attachment%3B+filename%3DEnhanced_efflux_of_cholesterol_from_ABCA.pdf\u0026Expires=1740507351\u0026Signature=QWYQpfhAs-sE1ZTi75Qest9RiD6jorIOTd1z0iakF0HraWGDkcSv96cE9EGVc6KhXC6d5sFATiHWSMMwja0cU5gK9Z8-NNGxx-Pd9R8OD6~ajR-HOcAJDgZ7vqvwwpBYSTVxTBQaiSjghQAryZjprTe6IxOEiqr2MAQrEZgS6wzs3guGVEZPQRm6cLXVo~4NtmTADKPwr06n-mhEHTY9QxfUDBd0YoKDzDrYOOXjoIwsapCAN0KbQ~bLlrssPP7Gb9IVocChH7~65fcvAOajm8ec~pmk1pGuEoevq7L67NsgGE-Lajewds-kKmox2WYU95MjPvlbynMTLRpwrSmQ9Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/46985672/download_file?st=MTc0MDUwMzc1MSw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/46985672/mini_magick20190208-31644-1o6j028.png?1549625142"}],"downloadable_attachments_with_full_thumbnails":[{"id":46985672,"asset_id":26703936,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/46985672/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/46985672/j.atherosclerosis.2003.08.01120160703-25928-o7intt-libre.pdf?1467585500=\u0026response-content-disposition=attachment%3B+filename%3DEnhanced_efflux_of_cholesterol_from_ABCA.pdf\u0026Expires=1740507351\u0026Signature=QWYQpfhAs-sE1ZTi75Qest9RiD6jorIOTd1z0iakF0HraWGDkcSv96cE9EGVc6KhXC6d5sFATiHWSMMwja0cU5gK9Z8-NNGxx-Pd9R8OD6~ajR-HOcAJDgZ7vqvwwpBYSTVxTBQaiSjghQAryZjprTe6IxOEiqr2MAQrEZgS6wzs3guGVEZPQRm6cLXVo~4NtmTADKPwr06n-mhEHTY9QxfUDBd0YoKDzDrYOOXjoIwsapCAN0KbQ~bLlrssPP7Gb9IVocChH7~65fcvAOajm8ec~pmk1pGuEoevq7L67NsgGE-Lajewds-kKmox2WYU95MjPvlbynMTLRpwrSmQ9Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/46985672/download_file?st=MTc0MDUwMzc1MSw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/46985672/mini_magick20190208-31644-1o6j028.png?1549625142"}],"has_pdf":true,"has_fulltext":true,"page_count":7,"ordered_authors":[{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie 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class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_26703937" data-work_id="26703937" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26703937/Fractional_efflux_and_net_change_in_cellular_cholesterol_content_mediated_by_sera_from_mice_expressing_both_human_apolipoprotein_AI_and_human_lecithin_cholesterol_acyltransferase_genes">Fractional efflux and net change in cellular cholesterol content mediated by sera from mice expressing both human apolipoprotein AI and human lecithin:cholesterol acyltransferase genes</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Human lecithin:cholesterol acyltransferase (LCAT) is a key enzyme in the metabolism of cholesterol and is postulated to participate in the physiological process called reverse cholesterol transport. We have used transgenic mice (Tgm)... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703937" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Human lecithin:cholesterol acyltransferase (LCAT) is a key enzyme in the metabolism of cholesterol and is postulated to participate in the physiological process called reverse cholesterol transport. We have used transgenic mice (Tgm) expressing either both human apolipoprotein AI (apo AI) and human LCAT genes or only the human apo AI gene (HuAILCAT or HuAI Tgm, respectively) to assess the consequences of LCAT overexpression on serum lipid and lipoprotein profiles and on the ability of each serum to promote bidirectional flux of cholesterol between serum and Fu5AH hepatoma cells. Mean serum LCAT activity of HuAILCAT Tgm was 2-fold increased compared to the HuAI group (48 9 9 vs. 24 9 5 nmol/ml per h, PB 0.01 for HuAILCAT and HuAI Tgm, respectively) and the cholesterol esterification rates were not significantly different between the two groups of animals (66911 vs. 74918 nmol/ml per h for HuAILCAT and HuAI Tgm, respectively). HuAILCAT Tgm exhibited higher total cholesterol serum values (2.3-fold) due to an increase in both HDL-cholesterol (1.9-fold) and non-HDL-cholesterol (3-fold). The HDL particles from HuAILCAT Tgm were relatively phospholipid depleted and cholesterol enriched compared to HuAI mice. When cells were incubated for six hours with the mouse serum, the fractional efflux of radiolabeled cholesterol was slightly increased with the HuAILCAT Tgm (1.2-fold) but the increase in intracellular cholesterol content was also 2-fold higher than with the HuAI Tgm. Fu5AH can be viewed as a model for the evaluation of bidirectional flux of cholesterol in SR-BI-rich cells. In this model LCAT overexpression in mice, by increasing both HDL and non-HDL-cholesterol, mostly enhances the uptake of cholesterol by the cells, which would be of benefit for the last step of reverse cholesterol transport in hepatocytes.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703937" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="10354606d37d8d7efa2eada50b7f35d2" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985677,&quot;asset_id&quot;:26703937,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985677/download_file?st=MTc0MDUwMzc1Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span></li><li class="js-paper-rank-work_26703937 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="26703937"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 26703937, container: ".js-paper-rank-work_26703937", }); 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$(".js-view-count[data-work-id=26703937]").text(description); $(".js-view-count-work_26703937").attr('title', description).tooltip(); }); });</script></span><script>$(function() { $(".js-view-count-work_26703937").removeClass('hidden') })</script></div></li><li class="InlineList-item u-positionRelative" style="max-width: 250px"><div class="u-positionAbsolute" data-has-card-for-ri-list="26703937"><i class="fa fa-tag InlineList-item-icon u-positionRelative"></i>&nbsp;&nbsp;<a class="InlineList-item-text u-positionRelative">19</a>&nbsp;&nbsp;</div><span class="InlineList-item-text u-textTruncate u-pl10x"><a class="InlineList-item-text" data-has-card-for-ri="3243" rel="nofollow" href="https://www.academia.edu/Documents/in/Nonparametric_Statistics">Nonparametric Statistics</a>,&nbsp;<script data-card-contents-for-ri="3243" type="text/json">{"id":3243,"name":"Nonparametric Statistics","url":"https://www.academia.edu/Documents/in/Nonparametric_Statistics","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="8015" rel="nofollow" href="https://www.academia.edu/Documents/in/Atherosclerosis">Atherosclerosis</a>,&nbsp;<script data-card-contents-for-ri="8015" type="text/json">{"id":8015,"name":"Atherosclerosis","url":"https://www.academia.edu/Documents/in/Atherosclerosis","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="37931" rel="nofollow" href="https://www.academia.edu/Documents/in/Transgenic_Mice">Transgenic Mice</a>,&nbsp;<script data-card-contents-for-ri="37931" type="text/json">{"id":37931,"name":"Transgenic Mice","url":"https://www.academia.edu/Documents/in/Transgenic_Mice","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="71437" rel="nofollow" href="https://www.academia.edu/Documents/in/Liver">Liver</a><script data-card-contents-for-ri="71437" type="text/json">{"id":71437,"name":"Liver","url":"https://www.academia.edu/Documents/in/Liver","nofollow":true}</script></span></li><script>(function(){ if (true) { new Aedu.ResearchInterestListCard({ el: $('*[data-has-card-for-ri-list=26703937]'), work: {"id":26703937,"title":"Fractional efflux and net change in cellular cholesterol content mediated by sera from mice expressing both human apolipoprotein AI and human lecithin:cholesterol acyltransferase genes","created_at":"2016-07-03T15:33:46.934-07:00","owner_id":50697757,"url":"https://www.academia.edu/26703937/Fractional_efflux_and_net_change_in_cellular_cholesterol_content_mediated_by_sera_from_mice_expressing_both_human_apolipoprotein_AI_and_human_lecithin_cholesterol_acyltransferase_genes","slug":"Fractional_efflux_and_net_change_in_cellular_cholesterol_content_mediated_by_sera_from_mice_expressing_both_human_apolipoprotein_AI_and_human_lecithin_cholesterol_acyltransferase_genes","dom_id":"work_26703937","summary":"Human lecithin:cholesterol acyltransferase (LCAT) is a key enzyme in the metabolism of cholesterol and is postulated to participate in the physiological process called reverse cholesterol transport. We have used transgenic mice (Tgm) expressing either both human apolipoprotein AI (apo AI) and human LCAT genes or only the human apo AI gene (HuAILCAT or HuAI Tgm, respectively) to assess the consequences of LCAT overexpression on serum lipid and lipoprotein profiles and on the ability of each serum to promote bidirectional flux of cholesterol between serum and Fu5AH hepatoma cells. Mean serum LCAT activity of HuAILCAT Tgm was 2-fold increased compared to the HuAI group (48 9 9 vs. 24 9 5 nmol/ml per h, PB 0.01 for HuAILCAT and HuAI Tgm, respectively) and the cholesterol esterification rates were not significantly different between the two groups of animals (66911 vs. 74918 nmol/ml per h for HuAILCAT and HuAI Tgm, respectively). HuAILCAT Tgm exhibited higher total cholesterol serum values (2.3-fold) due to an increase in both HDL-cholesterol (1.9-fold) and non-HDL-cholesterol (3-fold). The HDL particles from HuAILCAT Tgm were relatively phospholipid depleted and cholesterol enriched compared to HuAI mice. When cells were incubated for six hours with the mouse serum, the fractional efflux of radiolabeled cholesterol was slightly increased with the HuAILCAT Tgm (1.2-fold) but the increase in intracellular cholesterol content was also 2-fold higher than with the HuAI Tgm. Fu5AH can be viewed as a model for the evaluation of bidirectional flux of cholesterol in SR-BI-rich cells. In this model LCAT overexpression in mice, by increasing both HDL and non-HDL-cholesterol, mostly enhances the uptake of cholesterol by the cells, which would be of benefit for the last step of reverse cholesterol transport in 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Regulation","url":"https://www.academia.edu/Documents/in/Gene_Expression_Regulation"},{"id":1850893,"name":"Serum lipids","url":"https://www.academia.edu/Documents/in/Serum_lipids"}],"publication_year":1999,"publication_year_with_fallback":1999,"paper_rank":null,"all_time_views":13,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_26703938" data-work_id="26703938" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26703938/Impact_of_android_overweight_or_obesity_and_insulin_resistance_on_basal_and_postprandial_SR_BI_and_ABCA1_mediated_serum_cholesterol_efflux_capacities">Impact of android overweight or obesity and insulin resistance on basal and postprandial SR-BI and ABCA1-mediated serum cholesterol efflux capacities</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Since android overweight/obesity and insulin resistance are independent risk factors for cardiovascular disease, we investigated their impact on basal and postprandial scavenger receptor BI (SR-BI) and ATP binding cassette transporter A1... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703938" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Since android overweight/obesity and insulin resistance are independent risk factors for cardiovascular disease, we investigated their impact on basal and postprandial scavenger receptor BI (SR-BI) and ATP binding cassette transporter A1 (ABCA1)-mediated serum cholesterol efflux. Twelve android overweight to obese and 9 normal weight controls women underwent body composition analysis by dual energy X-ray absorptiometry, a euglycemic hyperinsulinemic clamp, and an oral fat load with blood sampling at initial time (T0), 4 h (T4) and 10 h (T10) after the fat load. Serum lipids and HDL-parameters, capacities of serum to promote cholesterol efflux from SR-BI expressing Fu5AH hepatoma cells or from ABCA1-expressing J774 macrophages and to abilities of serum to induce a net removal of cholesterol from macrophage foam cells were measured at T0, T4 and T10. Sera from overweight/obese exhibited moderately decreased SR-BI-mediated cholesterol efflux capacities, in accordance with reduced HDL concentrations, but importantly increased ABCA1-mediated cholesterol efflux and increased cholesterol extraction capacities over the postprandial period, partly related to higher pre␤-HDL concentrations. In multiple regression analyses, android obesity-related parameters and HDL-PL or pre␤-HDL levels remained the only independent correlates for SR-BI or ABCA1-dependent fractional cholesterol efflux while only pre␤-HDL levels remained correlated to cholesterol extraction capacities. Our results suggest that android overweight/obesity may not result in an impaired cholesterol efflux capacity.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703938" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="2b7397334715eafe8dc29cb40cf6b8f1" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985676,&quot;asset_id&quot;:26703938,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985676/download_file?st=MTc0MDUwMzc1Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span></li><li class="js-paper-rank-work_26703938 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="26703938"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 26703938, container: ".js-paper-rank-work_26703938", }); 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$(".js-view-count[data-work-id=26703938]").text(description); $(".js-view-count-work_26703938").attr('title', description).tooltip(); }); });</script></span><script>$(function() { $(".js-view-count-work_26703938").removeClass('hidden') })</script></div></li><li class="InlineList-item u-positionRelative" style="max-width: 250px"><div class="u-positionAbsolute" data-has-card-for-ri-list="26703938"><i class="fa fa-tag InlineList-item-icon u-positionRelative"></i>&nbsp;&nbsp;<a class="InlineList-item-text u-positionRelative">20</a>&nbsp;&nbsp;</div><span class="InlineList-item-text u-textTruncate u-pl10x"><a class="InlineList-item-text" data-has-card-for-ri="3851" rel="nofollow" href="https://www.academia.edu/Documents/in/Obesity">Obesity</a>,&nbsp;<script data-card-contents-for-ri="3851" type="text/json">{"id":3851,"name":"Obesity","url":"https://www.academia.edu/Documents/in/Obesity","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="8015" rel="nofollow" href="https://www.academia.edu/Documents/in/Atherosclerosis">Atherosclerosis</a>,&nbsp;<script data-card-contents-for-ri="8015" type="text/json">{"id":8015,"name":"Atherosclerosis","url":"https://www.academia.edu/Documents/in/Atherosclerosis","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="17491" rel="nofollow" href="https://www.academia.edu/Documents/in/Macrophages">Macrophages</a>,&nbsp;<script data-card-contents-for-ri="17491" type="text/json">{"id":17491,"name":"Macrophages","url":"https://www.academia.edu/Documents/in/Macrophages","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="24735" rel="nofollow" href="https://www.academia.edu/Documents/in/Cardiovascular_disease">Cardiovascular disease</a><script data-card-contents-for-ri="24735" type="text/json">{"id":24735,"name":"Cardiovascular disease","url":"https://www.academia.edu/Documents/in/Cardiovascular_disease","nofollow":true}</script></span></li><script>(function(){ if (true) { new Aedu.ResearchInterestListCard({ el: $('*[data-has-card-for-ri-list=26703938]'), work: {"id":26703938,"title":"Impact of android overweight or obesity and insulin resistance on basal and postprandial SR-BI and ABCA1-mediated serum cholesterol efflux capacities","created_at":"2016-07-03T15:33:47.034-07:00","owner_id":50697757,"url":"https://www.academia.edu/26703938/Impact_of_android_overweight_or_obesity_and_insulin_resistance_on_basal_and_postprandial_SR_BI_and_ABCA1_mediated_serum_cholesterol_efflux_capacities","slug":"Impact_of_android_overweight_or_obesity_and_insulin_resistance_on_basal_and_postprandial_SR_BI_and_ABCA1_mediated_serum_cholesterol_efflux_capacities","dom_id":"work_26703938","summary":"Since android overweight/obesity and insulin resistance are independent risk factors for cardiovascular disease, we investigated their impact on basal and postprandial scavenger receptor BI (SR-BI) and ATP binding cassette transporter A1 (ABCA1)-mediated serum cholesterol efflux. Twelve android overweight to obese and 9 normal weight controls women underwent body composition analysis by dual energy X-ray absorptiometry, a euglycemic hyperinsulinemic clamp, and an oral fat load with blood sampling at initial time (T0), 4 h (T4) and 10 h (T10) after the fat load. Serum lipids and HDL-parameters, capacities of serum to promote cholesterol efflux from SR-BI expressing Fu5AH hepatoma cells or from ABCA1-expressing J774 macrophages and to abilities of serum to induce a net removal of cholesterol from macrophage foam cells were measured at T0, T4 and T10. Sera from overweight/obese exhibited moderately decreased SR-BI-mediated cholesterol efflux capacities, in accordance with reduced HDL concentrations, but importantly increased ABCA1-mediated cholesterol efflux and increased cholesterol extraction capacities over the postprandial period, partly related to higher pre␤-HDL concentrations. In multiple regression analyses, android obesity-related parameters and HDL-PL or pre␤-HDL levels remained the only independent correlates for SR-BI or ABCA1-dependent fractional cholesterol efflux while only pre␤-HDL levels remained correlated to cholesterol extraction capacities. Our results suggest that android overweight/obesity may not result in an impaired cholesterol efflux capacity.","publication":"Atherosclerosis","publication_with_fallback":"Atherosclerosis","downloadable_attachments":[{"id":46985676,"asset_id":26703938,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/46985676/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/46985676/j.atherosclerosis.2009.09.02520160703-22008-fzljs4-libre.pdf?1467585500=\u0026response-content-disposition=attachment%3B+filename%3DImpact_of_android_overweight_or_obesity.pdf\u0026Expires=1740507352\u0026Signature=UyVbvxOYCMYqIRMWd3ddECR7hOVH1WXGPmkBFZT3y9BKS0luPhHGpyyx9WfgV6ZX1xTq7rDieZu8YDdYaDnlMHmyXmhdX1QCD-N-siHLqtPHql96Ez6pq4HB6dFXH76pNtCB6zJY~ewh8SuN-bbKBS-fUMdX7NGQpMa1BIJ6ywQVh0Kjy92TgMd3fGMc7yL6R~dfHmjmtr9F2APTBQcSJ-a1C2rsDiQtXPC2GCK2tzQmqpTMC2rp~afLB-19f63O-qyAZ2rkZ5SBo6NTZI5I4lCn2S~hlmpTbvpVI3wY~JX2~kSh2xAXBNrax0QJ~SPyGqko8wJmtbOULlAPZXGaZw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/46985676/download_file?st=MTc0MDUwMzc1Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/46985676/mini_magick20190208-17115-1w40qhu.png?1549625168"}],"downloadable_attachments_with_full_thumbnails":[{"id":46985676,"asset_id":26703938,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/46985676/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/46985676/j.atherosclerosis.2009.09.02520160703-22008-fzljs4-libre.pdf?1467585500=\u0026response-content-disposition=attachment%3B+filename%3DImpact_of_android_overweight_or_obesity.pdf\u0026Expires=1740507352\u0026Signature=UyVbvxOYCMYqIRMWd3ddECR7hOVH1WXGPmkBFZT3y9BKS0luPhHGpyyx9WfgV6ZX1xTq7rDieZu8YDdYaDnlMHmyXmhdX1QCD-N-siHLqtPHql96Ez6pq4HB6dFXH76pNtCB6zJY~ewh8SuN-bbKBS-fUMdX7NGQpMa1BIJ6ywQVh0Kjy92TgMd3fGMc7yL6R~dfHmjmtr9F2APTBQcSJ-a1C2rsDiQtXPC2GCK2tzQmqpTMC2rp~afLB-19f63O-qyAZ2rkZ5SBo6NTZI5I4lCn2S~hlmpTbvpVI3wY~JX2~kSh2xAXBNrax0QJ~SPyGqko8wJmtbOULlAPZXGaZw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/46985676/download_file?st=MTc0MDUwMzc1Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/46985676/mini_magick20190208-17115-1w40qhu.png?1549625168"}],"has_pdf":true,"has_fulltext":true,"page_count":8,"ordered_authors":[{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}],"research_interests":[{"id":3851,"name":"Obesity","url":"https://www.academia.edu/Documents/in/Obesity","nofollow":true},{"id":8015,"name":"Atherosclerosis","url":"https://www.academia.edu/Documents/in/Atherosclerosis","nofollow":true},{"id":17491,"name":"Macrophages","url":"https://www.academia.edu/Documents/in/Macrophages","nofollow":true},{"id":24735,"name":"Cardiovascular disease","url":"https://www.academia.edu/Documents/in/Cardiovascular_disease","nofollow":true},{"id":51373,"name":"Insulin Resistance","url":"https://www.academia.edu/Documents/in/Insulin_Resistance"},{"id":57808,"name":"Cell line","url":"https://www.academia.edu/Documents/in/Cell_line"},{"id":63375,"name":"Overweight","url":"https://www.academia.edu/Documents/in/Overweight"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":90514,"name":"Cholesterol","url":"https://www.academia.edu/Documents/in/Cholesterol"},{"id":100336,"name":"Body Composition","url":"https://www.academia.edu/Documents/in/Body_Composition"},{"id":103298,"name":"Blood sampling","url":"https://www.academia.edu/Documents/in/Blood_sampling"},{"id":111972,"name":"Hepatocellular Carcinoma","url":"https://www.academia.edu/Documents/in/Hepatocellular_Carcinoma"},{"id":192721,"name":"Risk factors","url":"https://www.academia.edu/Documents/in/Risk_factors"},{"id":224578,"name":"Multiple Regression","url":"https://www.academia.edu/Documents/in/Multiple_Regression"},{"id":227297,"name":"Waist Circumference","url":"https://www.academia.edu/Documents/in/Waist_Circumference"},{"id":244814,"name":"Clinical 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href="https://www.academia.edu/26703939/Enhanced_removal_of_cholesterol_from_macrophage_foam_cells_to_serum_from_type_IV_hypertriglyceridemic_subjects">Enhanced removal of cholesterol from macrophage foam cells to serum from type IV hypertriglyceridemic subjects</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Hypertriglyceridemia being an independent cardiovascular risk factor, we have compared the potential of sera from asymptomatic hypertriglyceridemic (HTG) type IIb, type IV or normolipidemic (NLP) subjects to promote both fractional... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703939" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Hypertriglyceridemia being an independent cardiovascular risk factor, we have compared the potential of sera from asymptomatic hypertriglyceridemic (HTG) type IIb, type IV or normolipidemic (NLP) subjects to promote both fractional cholesterol efflux and cellular cholesterol mass changes using macrophage foam cells. The J774 cells loaded with cholesterol by incubation with acetylated LDL were incubated in the absence or presence of cAMP to upregulate ABCA1 (ATP binding cassette transporter A1) and then incubated for 24 h with 1% serum. Compared with NLP, type IV sera exhibited a major increase in ABCA1-dependent efflux while type IIb sera exhibited a moderate but not significant increased ABCA1-mediated efflux. Moreover, positive correlations were established between ABCA1-dependent efflux and the serum pre␤-HDL or TG concentrations. The major finding was that the sera from type IV induced higher total cholesterol and cholesteryl ester mass depletions from ABCA1-expressing cells compared with other groups. Moreover, negative correlations were obtained between total cholesterol or cholesteryl ester mass changes and serum pre␤-HDL levels. In conclusion, we demonstrated for the first time that the serum pre␤-HDL present in high proportions in type IV HTG subjects are not only responsible for higher cholesterol efflux potential but also for increased abilities to promote net removal of cholesterol from macrophage foam cells.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703939" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="a1a35782deed50e5400f19fd727a3a68" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985679,&quot;asset_id&quot;:26703939,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985679/download_file?st=MTc0MDUwMzc1Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span></li><li class="js-paper-rank-work_26703939 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="26703939"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 26703939, container: ".js-paper-rank-work_26703939", }); 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$(".js-view-count[data-work-id=26703939]").text(description); $(".js-view-count-work_26703939").attr('title', description).tooltip(); }); });</script></span><script>$(function() { $(".js-view-count-work_26703939").removeClass('hidden') })</script></div></li><li class="InlineList-item u-positionRelative" style="max-width: 250px"><div class="u-positionAbsolute" data-has-card-for-ri-list="26703939"><i class="fa fa-tag InlineList-item-icon u-positionRelative"></i>&nbsp;&nbsp;<a class="InlineList-item-text u-positionRelative">8</a>&nbsp;&nbsp;</div><span class="InlineList-item-text u-textTruncate u-pl9x"><a class="InlineList-item-text" data-has-card-for-ri="8015" rel="nofollow" href="https://www.academia.edu/Documents/in/Atherosclerosis">Atherosclerosis</a>,&nbsp;<script data-card-contents-for-ri="8015" type="text/json">{"id":8015,"name":"Atherosclerosis","url":"https://www.academia.edu/Documents/in/Atherosclerosis","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="84760" rel="nofollow" href="https://www.academia.edu/Documents/in/Mice">Mice</a>,&nbsp;<script data-card-contents-for-ri="84760" type="text/json">{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="227291" rel="nofollow" href="https://www.academia.edu/Documents/in/apolipoprotein_A-I">apolipoprotein A-I</a>,&nbsp;<script data-card-contents-for-ri="227291" type="text/json">{"id":227291,"name":"apolipoprotein A-I","url":"https://www.academia.edu/Documents/in/apolipoprotein_A-I","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="227299" rel="nofollow" href="https://www.academia.edu/Documents/in/Triglycerides">Triglycerides</a><script data-card-contents-for-ri="227299" type="text/json">{"id":227299,"name":"Triglycerides","url":"https://www.academia.edu/Documents/in/Triglycerides","nofollow":true}</script></span></li><script>(function(){ if (true) { new Aedu.ResearchInterestListCard({ el: $('*[data-has-card-for-ri-list=26703939]'), work: {"id":26703939,"title":"Enhanced removal of cholesterol from macrophage foam cells to serum from type IV hypertriglyceridemic subjects","created_at":"2016-07-03T15:33:47.135-07:00","owner_id":50697757,"url":"https://www.academia.edu/26703939/Enhanced_removal_of_cholesterol_from_macrophage_foam_cells_to_serum_from_type_IV_hypertriglyceridemic_subjects","slug":"Enhanced_removal_of_cholesterol_from_macrophage_foam_cells_to_serum_from_type_IV_hypertriglyceridemic_subjects","dom_id":"work_26703939","summary":"Hypertriglyceridemia being an independent cardiovascular risk factor, we have compared the potential of sera from asymptomatic hypertriglyceridemic (HTG) type IIb, type IV or normolipidemic (NLP) subjects to promote both fractional cholesterol efflux and cellular cholesterol mass changes using macrophage foam cells. The J774 cells loaded with cholesterol by incubation with acetylated LDL were incubated in the absence or presence of cAMP to upregulate ABCA1 (ATP binding cassette transporter A1) and then incubated for 24 h with 1% serum. Compared with NLP, type IV sera exhibited a major increase in ABCA1-dependent efflux while type IIb sera exhibited a moderate but not significant increased ABCA1-mediated efflux. Moreover, positive correlations were established between ABCA1-dependent efflux and the serum pre␤-HDL or TG concentrations. The major finding was that the sera from type IV induced higher total cholesterol and cholesteryl ester mass depletions from ABCA1-expressing cells compared with other groups. Moreover, negative correlations were obtained between total cholesterol or cholesteryl ester mass changes and serum pre␤-HDL levels. In conclusion, we demonstrated for the first time that the serum pre␤-HDL present in high proportions in type IV HTG subjects are not only responsible for higher cholesterol efflux potential but also for increased abilities to promote net removal of cholesterol from macrophage foam cells.","publication":"Atherosclerosis","publication_with_fallback":"Atherosclerosis","downloadable_attachments":[{"id":46985679,"asset_id":26703939,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/46985679/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/46985679/j.atherosclerosis.2007.09.02320160703-6262-1dw2pbe-libre.pdf?1467585500=\u0026response-content-disposition=attachment%3B+filename%3DEnhanced_removal_of_cholesterol_from_mac.pdf\u0026Expires=1740507352\u0026Signature=KVutLl7U1-CDvx8dw7gEHAuO7T67mtqOlfvPZIbYIiFsQRkAFwGYznDm6eVb5l7obKDjxEyU4EeJRsYTwO7vc1twsu83kUwRpLwWU6DGr~f8cTt0a9vONJm~FlAp1sYY8IGFFm~rLs6FCqwPuFHwpqIGai-pF0LI7p2nymMGRN15lIeVZ~k37r8q-mwuVX93Utoo14znM3D4V2XvJXElZAmHhyyfbzNcWmvqILA0XyrGT5gk3GjGcTJp1QPhE7rpZCq~Mj2wluS6r4l26DXfpyrFe8BrhH-TmUSPm7n2tIpMJ4jjtUdmu1RDp99vSj7FYN0xpxQkeeT2vJGFV0GBfw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/46985679/download_file?st=MTc0MDUwMzc1Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/46985679/mini_magick20190208-19601-1cu590g.png?1549625158"}],"downloadable_attachments_with_full_thumbnails":[{"id":46985679,"asset_id":26703939,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/46985679/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/46985679/j.atherosclerosis.2007.09.02320160703-6262-1dw2pbe-libre.pdf?1467585500=\u0026response-content-disposition=attachment%3B+filename%3DEnhanced_removal_of_cholesterol_from_mac.pdf\u0026Expires=1740507352\u0026Signature=KVutLl7U1-CDvx8dw7gEHAuO7T67mtqOlfvPZIbYIiFsQRkAFwGYznDm6eVb5l7obKDjxEyU4EeJRsYTwO7vc1twsu83kUwRpLwWU6DGr~f8cTt0a9vONJm~FlAp1sYY8IGFFm~rLs6FCqwPuFHwpqIGai-pF0LI7p2nymMGRN15lIeVZ~k37r8q-mwuVX93Utoo14znM3D4V2XvJXElZAmHhyyfbzNcWmvqILA0XyrGT5gk3GjGcTJp1QPhE7rpZCq~Mj2wluS6r4l26DXfpyrFe8BrhH-TmUSPm7n2tIpMJ4jjtUdmu1RDp99vSj7FYN0xpxQkeeT2vJGFV0GBfw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/46985679/download_file?st=MTc0MDUwMzc1Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/46985679/mini_magick20190208-19601-1cu590g.png?1549625158"}],"has_pdf":true,"has_fulltext":true,"page_count":8,"ordered_authors":[{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}],"research_interests":[{"id":8015,"name":"Atherosclerosis","url":"https://www.academia.edu/Documents/in/Atherosclerosis","nofollow":true},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice","nofollow":true},{"id":227291,"name":"apolipoprotein A-I","url":"https://www.academia.edu/Documents/in/apolipoprotein_A-I","nofollow":true},{"id":227299,"name":"Triglycerides","url":"https://www.academia.edu/Documents/in/Triglycerides","nofollow":true},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":425194,"name":"Cardiovascular Risk Factor","url":"https://www.academia.edu/Documents/in/Cardiovascular_Risk_Factor"},{"id":440014,"name":"Tritium","url":"https://www.academia.edu/Documents/in/Tritium"},{"id":1274497,"name":"Total Cholesterol","url":"https://www.academia.edu/Documents/in/Total_Cholesterol"}],"publication_year":2008,"publication_year_with_fallback":2008,"paper_rank":null,"all_time_views":15,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_26703940" data-work_id="26703940" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26703940/Analysis_of_the_relationship_between_triglyceridemia_and_HDL_phospholipid_concentrations_consequences_on_the_efflux_capacity_of_serum_in_the_Fu5AH_system">Analysis of the relationship between triglyceridemia and HDL-phospholipid concentrations: consequences on the efflux capacity of serum in the Fu5AH system</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">The high triglyceride/low HDL-cholesterol trait is a common finding in the general population. The aim of the present study was to analyze and interpret the relationships between triglycerides (TG), HDL-related parameters and serum... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703940" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">The high triglyceride/low HDL-cholesterol trait is a common finding in the general population. The aim of the present study was to analyze and interpret the relationships between triglycerides (TG), HDL-related parameters and serum cholesterol efflux potential in an asymptomatic population including both normo-and hyperlipidemic individuals. In a large sample (n= 1143) of this population, there was a negative correlation between TG and HDL-cholesterol (HDL-C) (r= −0.49, P B0.0001) whereas the negative correlation between TG and HDL-phospholipid (HDL-PL) (r= −0.29, P B 0.0001) was weaker, leading to a strong positive correlation between TG and HDL-PL/C ratio (r= 0.58, PB 0.0001). Thus, increased TG concentrations were associated with an enrichment of HDL with PL. Since we have demonstrated previously that HDL-PL is the major determinant for cholesterol efflux potential from Fu5AH rat hepatoma cells, we determined the effect of the variations in HDL lipid composition on the cholesterol efflux capacity in a subsample of 198 subjects. Compared with normolipidemic subjects (NLP) (TG 51.7 mmol/l; LDL-C54.1 mmol/l, n=58), hypertriglyceridemic subjects (HTG) (TG \1.7 mmol/l, n= 63) exhibited lower HDL-C levels (1.08 9 0.21 vs. 1.25 9 0.32, P= 0.0003) whereas they showed similar HDL-PL concentrations (1.25 90.21 vs. 1.25 92.7) and, thus, higher HDL-PL/C ratio (1.17 9 0.15 vs. 1.02 90.14, P = 0.0001). The relative efflux capacity of serum measured in the Fu5AH system (5% serum, 4 h incubation at 37°C) was on average identical in the HTG and NLP groups. Thus, this study provides evidence that despite decreased HDL concentrations, as determined routinely by the HDL-C assay, some HTG subjects maintained serum cholesterol efflux capacity thanks to the enrichment of HDL with PL.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703940" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="5a7c003273c5c7527f5d3038c7441307" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985674,&quot;asset_id&quot;:26703940,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985674/download_file?st=MTc0MDUwMzc1Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span></li><li class="js-paper-rank-work_26703940 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="26703940"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 26703940, container: ".js-paper-rank-work_26703940", }); 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$(".js-view-count[data-work-id=26703940]").text(description); $(".js-view-count-work_26703940").attr('title', description).tooltip(); }); });</script></span><script>$(function() { $(".js-view-count-work_26703940").removeClass('hidden') })</script></div></li><li class="InlineList-item u-positionRelative" style="max-width: 250px"><div class="u-positionAbsolute" data-has-card-for-ri-list="26703940"><i class="fa fa-tag InlineList-item-icon u-positionRelative"></i>&nbsp;&nbsp;<a class="InlineList-item-text u-positionRelative">15</a>&nbsp;&nbsp;</div><span class="InlineList-item-text u-textTruncate u-pl10x"><a class="InlineList-item-text" data-has-card-for-ri="8015" rel="nofollow" href="https://www.academia.edu/Documents/in/Atherosclerosis">Atherosclerosis</a>,&nbsp;<script data-card-contents-for-ri="8015" type="text/json">{"id":8015,"name":"Atherosclerosis","url":"https://www.academia.edu/Documents/in/Atherosclerosis","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="8501" rel="nofollow" href="https://www.academia.edu/Documents/in/Phospholipids">Phospholipids</a>,&nbsp;<script data-card-contents-for-ri="8501" type="text/json">{"id":8501,"name":"Phospholipids","url":"https://www.academia.edu/Documents/in/Phospholipids","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="39001" rel="nofollow" href="https://www.academia.edu/Documents/in/Pathophysiology">Pathophysiology</a>,&nbsp;<script data-card-contents-for-ri="39001" type="text/json">{"id":39001,"name":"Pathophysiology","url":"https://www.academia.edu/Documents/in/Pathophysiology","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="90514" rel="nofollow" href="https://www.academia.edu/Documents/in/Cholesterol">Cholesterol</a><script data-card-contents-for-ri="90514" type="text/json">{"id":90514,"name":"Cholesterol","url":"https://www.academia.edu/Documents/in/Cholesterol","nofollow":true}</script></span></li><script>(function(){ if (true) { new Aedu.ResearchInterestListCard({ el: $('*[data-has-card-for-ri-list=26703940]'), work: {"id":26703940,"title":"Analysis of the relationship between triglyceridemia and HDL-phospholipid concentrations: consequences on the efflux capacity of serum in the Fu5AH system","created_at":"2016-07-03T15:33:47.241-07:00","owner_id":50697757,"url":"https://www.academia.edu/26703940/Analysis_of_the_relationship_between_triglyceridemia_and_HDL_phospholipid_concentrations_consequences_on_the_efflux_capacity_of_serum_in_the_Fu5AH_system","slug":"Analysis_of_the_relationship_between_triglyceridemia_and_HDL_phospholipid_concentrations_consequences_on_the_efflux_capacity_of_serum_in_the_Fu5AH_system","dom_id":"work_26703940","summary":"The high triglyceride/low HDL-cholesterol trait is a common finding in the general population. The aim of the present study was to analyze and interpret the relationships between triglycerides (TG), HDL-related parameters and serum cholesterol efflux potential in an asymptomatic population including both normo-and hyperlipidemic individuals. In a large sample (n= 1143) of this population, there was a negative correlation between TG and HDL-cholesterol (HDL-C) (r= −0.49, P B0.0001) whereas the negative correlation between TG and HDL-phospholipid (HDL-PL) (r= −0.29, P B 0.0001) was weaker, leading to a strong positive correlation between TG and HDL-PL/C ratio (r= 0.58, PB 0.0001). Thus, increased TG concentrations were associated with an enrichment of HDL with PL. Since we have demonstrated previously that HDL-PL is the major determinant for cholesterol efflux potential from Fu5AH rat hepatoma cells, we determined the effect of the variations in HDL lipid composition on the cholesterol efflux capacity in a subsample of 198 subjects. Compared with normolipidemic subjects (NLP) (TG 51.7 mmol/l; LDL-C54.1 mmol/l, n=58), hypertriglyceridemic subjects (HTG) (TG \\1.7 mmol/l, n= 63) exhibited lower HDL-C levels (1.08 9 0.21 vs. 1.25 9 0.32, P= 0.0003) whereas they showed similar HDL-PL concentrations (1.25 90.21 vs. 1.25 92.7) and, thus, higher HDL-PL/C ratio (1.17 9 0.15 vs. 1.02 90.14, P = 0.0001). The relative efflux capacity of serum measured in the Fu5AH system (5% serum, 4 h incubation at 37°C) was on average identical in the HTG and NLP groups. Thus, this study provides evidence that despite decreased HDL concentrations, as determined routinely by the HDL-C assay, some HTG subjects maintained serum cholesterol efflux capacity thanks to the enrichment of HDL with 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Membrane","url":"https://www.academia.edu/Documents/in/Cell_Membrane"}],"publication_year":2001,"publication_year_with_fallback":2001,"paper_rank":null,"all_time_views":13,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_26703941" data-work_id="26703941" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26703941/Deleterious_impact_of_elaidic_fatty_acid_on_ABCA1_mediated_cholesterol_efflux_from_mouse_and_human_macrophages">Deleterious impact of elaidic fatty acid on ABCA1-mediated cholesterol efflux from mouse and human macrophages</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Consumption of trans fatty acids (TFA) increase cardiovascular risk more than do saturated FA, but the mechanisms explaining their atherogenicity are still unclear. We investigated the impact of membrane incorporation of TFA on... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703941" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Consumption of trans fatty acids (TFA) increase cardiovascular risk more than do saturated FA, but the mechanisms explaining their atherogenicity are still unclear. We investigated the impact of membrane incorporation of TFA on cholesterol efflux by exposing J774 mouse macrophages or human monocyte-derived macrophages (HMDM) to media enriched or not (standard medium) with industrially produced elaidic (trans-9 18:1) acid, naturally produced vaccenic (trans-11 18:1) acid (34 h, 70 μM) or palmitic acid. In J774 macrophages, elaidic and palmitic acid, but not vaccenic acid, reduced ABCA1-mediated efflux by~23% without affecting aqueous diffusion, SR-BI or ABCG1-mediated pathways, and this effect was maintained in cholesterol-loaded cells. The impact of elaidic acid on the ABCA1 pathway was weaker in cholesterolnormal HMDM, but elaidic acid induced a strong reduction of ABCA1-mediated efflux in cholesterol-loaded cells (−36%). In J774 cells, the FA supplies had no impact on cellular free cholesterol or cholesteryl ester masses, the abundance of ABCA1 mRNA or the total and plasma membrane ABCA1 protein content. Conversely, TFA or palmitic acid incorporation induced strong modifications of the membrane FA composition with a decrease in the ratio of (cis-monounsaturated FA + polyunsaturated FA):(saturated FA + TFA), with elaidic and vaccenic acids representing each 20% and 13% of the total FA composition, respectively. Moreover, we demonstrated that cellular ATP was required for the effect of elaidic acid, suggesting that it contributes to atherogenesis by impairing ABCA1-mediated cholesterol efflux in macrophages, likely by decreasing the membrane fluidity, which could thereby reduce ATPase activity and the function of the transporter.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703941" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="3eb373cdc783e97ee1c2586fcbf882df" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985665,&quot;asset_id&quot;:26703941,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985665/download_file?st=MTc0MDUwMzc1Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span></li><li class="js-paper-rank-work_26703941 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="26703941"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 26703941, container: ".js-paper-rank-work_26703941", }); 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$(".js-view-count[data-work-id=26703941]").text(description); $(".js-view-count-work_26703941").attr('title', description).tooltip(); }); });</script></span><script>$(function() { $(".js-view-count-work_26703941").removeClass('hidden') })</script></div></li><li class="InlineList-item u-positionRelative" style="max-width: 250px"><div class="u-positionAbsolute" data-has-card-for-ri-list="26703941"><i class="fa fa-tag InlineList-item-icon u-positionRelative"></i>&nbsp;&nbsp;<a class="InlineList-item-text u-positionRelative">18</a>&nbsp;&nbsp;</div><span class="InlineList-item-text u-textTruncate u-pl10x"><a class="InlineList-item-text" data-has-card-for-ri="8501" rel="nofollow" href="https://www.academia.edu/Documents/in/Phospholipids">Phospholipids</a>,&nbsp;<script data-card-contents-for-ri="8501" type="text/json">{"id":8501,"name":"Phospholipids","url":"https://www.academia.edu/Documents/in/Phospholipids","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="17491" rel="nofollow" href="https://www.academia.edu/Documents/in/Macrophages">Macrophages</a>,&nbsp;<script data-card-contents-for-ri="17491" type="text/json">{"id":17491,"name":"Macrophages","url":"https://www.academia.edu/Documents/in/Macrophages","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="29154" rel="nofollow" href="https://www.academia.edu/Documents/in/Cardiovascular_Risk">Cardiovascular Risk</a>,&nbsp;<script data-card-contents-for-ri="29154" type="text/json">{"id":29154,"name":"Cardiovascular Risk","url":"https://www.academia.edu/Documents/in/Cardiovascular_Risk","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="47884" rel="nofollow" href="https://www.academia.edu/Documents/in/Biological_Sciences">Biological Sciences</a><script data-card-contents-for-ri="47884" type="text/json">{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences","nofollow":true}</script></span></li><script>(function(){ if (true) { new Aedu.ResearchInterestListCard({ el: $('*[data-has-card-for-ri-list=26703941]'), work: {"id":26703941,"title":"Deleterious impact of elaidic fatty acid on ABCA1-mediated cholesterol efflux from mouse and human macrophages","created_at":"2016-07-03T15:33:47.337-07:00","owner_id":50697757,"url":"https://www.academia.edu/26703941/Deleterious_impact_of_elaidic_fatty_acid_on_ABCA1_mediated_cholesterol_efflux_from_mouse_and_human_macrophages","slug":"Deleterious_impact_of_elaidic_fatty_acid_on_ABCA1_mediated_cholesterol_efflux_from_mouse_and_human_macrophages","dom_id":"work_26703941","summary":"Consumption of trans fatty acids (TFA) increase cardiovascular risk more than do saturated FA, but the mechanisms explaining their atherogenicity are still unclear. 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Conversely, TFA or palmitic acid incorporation induced strong modifications of the membrane FA composition with a decrease in the ratio of (cis-monounsaturated FA + polyunsaturated FA):(saturated FA + TFA), with elaidic and vaccenic acids representing each 20% and 13% of the total FA composition, respectively. 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Triphosphate","url":"https://www.academia.edu/Documents/in/Adenosine_Triphosphate"},{"id":2468093,"name":"Cell Membrane","url":"https://www.academia.edu/Documents/in/Cell_Membrane"}],"publication_year":2012,"publication_year_with_fallback":2012,"paper_rank":null,"all_time_views":29,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_26703942 coauthored" data-work_id="26703942" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26703942/PP181_Evaluation_of_the_Interaction_Between_Methotrexate_and_Proton_Pump_Inhibitors_Using_Human_OAT1_And_OAT3_Hek_Transfected_Cells">PP181—Evaluation of the Interaction Between Methotrexate and Proton Pump Inhibitors Using Human OAT1 And OAT3 Hek Transfected Cells</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Volume 35 Number 8S accounting for 21.2% and 16.2% of total AED consumption (DDD 163.7 and 125.2, respectively). In the same year, oxcarbazepine and lamotrigine were the most used new AEDs (10.91% and 10.79% of total; DDD 84.1 and 83.2,... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703942" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Volume 35 Number 8S accounting for 21.2% and 16.2% of total AED consumption (DDD 163.7 and 125.2, respectively). In the same year, oxcarbazepine and lamotrigine were the most used new AEDs (10.91% and 10.79% of total; DDD 84.1 and 83.2, respectively), while gabapentin and pregabalin exhibited the higher incidence of use. The main indication of use was epileptic disorders for older AEDs and neuropathic pain for newer AEDs. A high number of patients treated with older AEDs, in particular carbamazepine, phenobarbital, and valproic acid, received coprescription at clinically relevant interaction risk. Among newer AEDs, lamotrigine showed a high annual rate of possible interaction. Conclusion: Significant differences were shown in the prescribing pattern of newer and older medications: older AEDs were mainly used in the treatment of epileptic disorders, while newer compounds were also preferred for conditions other than epilepsy, in particular neuropathic pain. The fall in the use of newer AEDs during 2007 agreed with revised reimbursement criteria for gabapentin and pregabalin. The coprescription should be evaluated with caution and avoided if possible. Drugs at risk of interactions should be replaced with others having same indication of use.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703942" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="2b70b42658f741e19ea6b81c08b13b20" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985667,&quot;asset_id&quot;:26703942,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985667/download_file?st=MTc0MDUwMzc1Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span><span class="u-displayInlineBlock InlineList-item-text">&nbsp;and&nbsp;<span class="u-textDecorationUnderline u-clickable InlineList-item-text js-work-more-authors-26703942">+1</span><div class="hidden js-additional-users-26703942"><div><span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a href="https://independent.academia.edu/RChioukh">R. Chioukh</a></span></div></div></span><script>(function(){ var popoverSettings = { el: $('.js-work-more-authors-26703942'), placement: 'bottom', hide_delay: 200, html: true, content: function(){ return $('.js-additional-users-26703942').html(); } } new HoverPopover(popoverSettings); })();</script></li><li class="js-paper-rank-work_26703942 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="26703942"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 26703942, container: ".js-paper-rank-work_26703942", }); });</script></li><li class="js-percentile-work_26703942 InlineList-item InlineList-item--bordered hidden u-tcGrayDark"><span class="percentile-widget hidden"><span class="u-mr2x percentile-widget" style="display: none">•</span><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 26703942; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-percentile-work_26703942"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></li><li class="js-view-count-work_26703942 InlineList-item InlineList-item--bordered hidden"><div><span><span class="js-view-count view-count u-mr2x" data-work-id="26703942"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 26703942; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=26703942]").text(description); $(".js-view-count-work_26703942").attr('title', description).tooltip(); }); });</script></span><script>$(function() { $(".js-view-count-work_26703942").removeClass('hidden') })</script></div></li></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_26703944" data-work_id="26703944" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26703944/Comparison_of_different_cellular_models_measuring_in_vitro_the_whole_human_serum_cholesterol_efflux_capacity">Comparison of different cellular models measuring in vitro the whole human serum cholesterol efflux capacity</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Background Fu5AH rat hepatoma cells and cAMP (cyclic AMP)-pretreated J774 mouse macrophages are commonly used as models for SR-BI (scavenger receptor class B type I) and ABCA1 (ATP binding cassette transporter 1)-mediated free cholesterol... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703944" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Background Fu5AH rat hepatoma cells and cAMP (cyclic AMP)-pretreated J774 mouse macrophages are commonly used as models for SR-BI (scavenger receptor class B type I) and ABCA1 (ATP binding cassette transporter 1)-mediated free cholesterol efflux to whole serum, respectively. However, the responsiveness of Fu5AH, control or cAMP pretreated J774 cells to the various lipids and HDL (high-density lipoprotein)-parameters from both normo-and dyslipidaemic subjects has never been compared within the same study.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703944" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="5f1552ee51bbe36097c63f3a891e7e82" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985666,&quot;asset_id&quot;:26703944,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985666/download_file?st=MTc0MDUwMzc1Myw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span></li><li class="js-paper-rank-work_26703944 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="26703944"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 26703944, container: ".js-paper-rank-work_26703944", }); 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$(".js-view-count[data-work-id=26703944]").text(description); $(".js-view-count-work_26703944").attr('title', description).tooltip(); }); });</script></span><script>$(function() { $(".js-view-count-work_26703944").removeClass('hidden') })</script></div></li><li class="InlineList-item u-positionRelative" style="max-width: 250px"><div class="u-positionAbsolute" data-has-card-for-ri-list="26703944"><i class="fa fa-tag InlineList-item-icon u-positionRelative"></i>&nbsp;&nbsp;<a class="InlineList-item-text u-positionRelative">11</a>&nbsp;&nbsp;</div><span class="InlineList-item-text u-textTruncate u-pl10x"><a class="InlineList-item-text" data-has-card-for-ri="17491" rel="nofollow" href="https://www.academia.edu/Documents/in/Macrophages">Macrophages</a>,&nbsp;<script data-card-contents-for-ri="17491" type="text/json">{"id":17491,"name":"Macrophages","url":"https://www.academia.edu/Documents/in/Macrophages","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="52055" rel="nofollow" href="https://www.academia.edu/Documents/in/Lipids">Lipids</a>,&nbsp;<script data-card-contents-for-ri="52055" type="text/json">{"id":52055,"name":"Lipids","url":"https://www.academia.edu/Documents/in/Lipids","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="84760" rel="nofollow" href="https://www.academia.edu/Documents/in/Mice">Mice</a>,&nbsp;<script data-card-contents-for-ri="84760" type="text/json">{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="90514" rel="nofollow" href="https://www.academia.edu/Documents/in/Cholesterol">Cholesterol</a><script data-card-contents-for-ri="90514" type="text/json">{"id":90514,"name":"Cholesterol","url":"https://www.academia.edu/Documents/in/Cholesterol","nofollow":true}</script></span></li><script>(function(){ if (true) { new Aedu.ResearchInterestListCard({ el: $('*[data-has-card-for-ri-list=26703944]'), work: {"id":26703944,"title":"Comparison of different cellular models measuring in vitro the whole human serum cholesterol efflux capacity","created_at":"2016-07-03T15:33:47.696-07:00","owner_id":50697757,"url":"https://www.academia.edu/26703944/Comparison_of_different_cellular_models_measuring_in_vitro_the_whole_human_serum_cholesterol_efflux_capacity","slug":"Comparison_of_different_cellular_models_measuring_in_vitro_the_whole_human_serum_cholesterol_efflux_capacity","dom_id":"work_26703944","summary":"Background Fu5AH rat hepatoma cells and cAMP (cyclic AMP)-pretreated J774 mouse macrophages are commonly used as models for SR-BI (scavenger receptor class B type I) and ABCA1 (ATP binding cassette transporter 1)-mediated free cholesterol efflux to whole serum, respectively. 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Model","url":"https://www.academia.edu/Documents/in/Cellular_Automaton_Model"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":563659,"name":"Human Serum","url":"https://www.academia.edu/Documents/in/Human_Serum"},{"id":2430620,"name":"Hypertriglyceridemia","url":"https://www.academia.edu/Documents/in/Hypertriglyceridemia"}],"publication_year":2006,"publication_year_with_fallback":2006,"paper_rank":null,"all_time_views":10,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_26703946" data-work_id="26703946" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26703946/The_Dynamin_Chemical_Inhibitor_Dynasore_Impairs_Cholesterol_Trafficking_and_Sterol_Sensitive_Genes_Transcription_in_Human_HeLa_Cells_and_Macrophages">The Dynamin Chemical Inhibitor Dynasore Impairs Cholesterol Trafficking and Sterol-Sensitive Genes Transcription in Human HeLa Cells and Macrophages</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Intracellular transport of cholesterol contributes to the regulation of cellular cholesterol homeostasis by mechanisms that are yet poorly defined. In this study, we characterized the impact of dynasore, a recently described drug that... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703946" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Intracellular transport of cholesterol contributes to the regulation of cellular cholesterol homeostasis by mechanisms that are yet poorly defined. In this study, we characterized the impact of dynasore, a recently described drug that specifically inhibits the enzymatic activity of dynamin, a GTPase regulating receptor endocytosis and cholesterol trafficking. Dynasore strongly inhibited the uptake of low-density lipoprotein (LDL) in HeLa cells, and to a lower extent in human macrophages. In both cell types, dynasore treatment led to the abnormal accumulation of LDL and free cholesterol (FC) within the endolysosomal network. The measure of cholesterol esters (CE) further showed that the delivery of regulatory cholesterol to the endoplasmic reticulum (ER) was deficient. This resulted in the inhibition of the transcriptional control of the three major sterol-sensitive genes, sterol-regulatory element binding protein 2 (SREBP-2), 3-hydroxy-3-methyl-coenzymeA reductase (HMGCoAR), and low-density lipoprotein receptor (LDLR). The sequestration of cholesterol in the endolysosomal compartment impaired both the active and passive cholesterol efflux in HMDM. Our data further illustrate the importance of membrane trafficking in cholesterol homeostasis and validate dynasore as a new pharmacological tool to study the intracellular transport of cholesterol.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703946" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="81484d98b96bb94f222d5612f76d74a7" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985683,&quot;asset_id&quot;:26703946,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985683/download_file?st=MTc0MDUwMzc1Myw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span></li><li class="js-paper-rank-work_26703946 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="26703946"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 26703946, container: ".js-paper-rank-work_26703946", }); 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In this study, we characterized the impact of dynasore, a recently described drug that specifically inhibits the enzymatic activity of dynamin, a GTPase regulating receptor endocytosis and cholesterol trafficking. Dynasore strongly inhibited the uptake of low-density lipoprotein (LDL) in HeLa cells, and to a lower extent in human macrophages. In both cell types, dynasore treatment led to the abnormal accumulation of LDL and free cholesterol (FC) within the endolysosomal network. The measure of cholesterol esters (CE) further showed that the delivery of regulatory cholesterol to the endoplasmic reticulum (ER) was deficient. This resulted in the inhibition of the transcriptional control of the three major sterol-sensitive genes, sterol-regulatory element binding protein 2 (SREBP-2), 3-hydroxy-3-methyl-coenzymeA reductase (HMGCoAR), and low-density lipoprotein receptor (LDLR). The sequestration of cholesterol in the endolysosomal compartment impaired both the active and passive cholesterol efflux in HMDM. Our data further illustrate the importance of membrane trafficking in cholesterol homeostasis and validate dynasore as a new pharmacological tool to study the intracellular transport of cholesterol.","publication":"PLoS ONE","publication_with_fallback":"PLoS ONE","downloadable_attachments":[{"id":46985683,"asset_id":26703946,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/46985683/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/46985683/The_dynamin_chemical_inhibitor_dynasore_20160703-25927-1l7rk71-libre.pdf?1467585501=\u0026response-content-disposition=attachment%3B+filename%3DThe_Dynamin_Chemical_Inhibitor_Dynasore.pdf\u0026Expires=1740507353\u0026Signature=VZFK8WbxXuAR0kCtqCZn~lnTKPHxMNGAYhkUJY9eLT7u4nh1oJ6qpkti3v~rzwjpnaR~dXlnDZ3dtR2OBgvvTZQGgDxw5ntFlQ5bbRuUtNCulZMxBdvDrpoMOj8Dgaa4r0WuXccU-AqwDW1xTPfNrmdgUhh-OsTTFuHOneY3DmZq3pC68CK-dDztvmDCLb~PISjo3nGxLTNIR7ea61jYDWBvYbBhB8PaGFiYBe8eVqF3rQh4NJulyPb8TnTNx4SMuHIf6nOiNYKIDV-LpAm9ZUus6jMLgsgt7dmXl4cFUYWwjZL6K1OMJRWxlGNqNvMcpbbAhcCGk23t-DvViDrX9g__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/46985683/download_file?st=MTc0MDUwMzc1Myw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/46985683/mini_magick20220703-28588-z79jc2.png?1656877456"}],"downloadable_attachments_with_full_thumbnails":[{"id":46985683,"asset_id":26703946,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/46985683/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/46985683/The_dynamin_chemical_inhibitor_dynasore_20160703-25927-1l7rk71-libre.pdf?1467585501=\u0026response-content-disposition=attachment%3B+filename%3DThe_Dynamin_Chemical_Inhibitor_Dynasore.pdf\u0026Expires=1740507353\u0026Signature=VZFK8WbxXuAR0kCtqCZn~lnTKPHxMNGAYhkUJY9eLT7u4nh1oJ6qpkti3v~rzwjpnaR~dXlnDZ3dtR2OBgvvTZQGgDxw5ntFlQ5bbRuUtNCulZMxBdvDrpoMOj8Dgaa4r0WuXccU-AqwDW1xTPfNrmdgUhh-OsTTFuHOneY3DmZq3pC68CK-dDztvmDCLb~PISjo3nGxLTNIR7ea61jYDWBvYbBhB8PaGFiYBe8eVqF3rQh4NJulyPb8TnTNx4SMuHIf6nOiNYKIDV-LpAm9ZUus6jMLgsgt7dmXl4cFUYWwjZL6K1OMJRWxlGNqNvMcpbbAhcCGk23t-DvViDrX9g__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/46985683/download_file?st=MTc0MDUwMzc1Myw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/46985683/mini_magick20220703-28588-z79jc2.png?1656877456"}],"has_pdf":true,"has_fulltext":true,"page_count":13,"ordered_authors":[{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}],"research_interests":[{"id":48,"name":"Engineering","url":"https://www.academia.edu/Documents/in/Engineering","nofollow":true},{"id":498,"name":"Physics","url":"https://www.academia.edu/Documents/in/Physics","nofollow":true},{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry","nofollow":true},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology","nofollow":true},{"id":12981,"name":"Enzyme Inhibitors","url":"https://www.academia.edu/Documents/in/Enzyme_Inhibitors"},{"id":17491,"name":"Macrophages","url":"https://www.academia.edu/Documents/in/Macrophages"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":28235,"name":"Multidisciplinary","url":"https://www.academia.edu/Documents/in/Multidisciplinary"},{"id":90514,"name":"Cholesterol","url":"https://www.academia.edu/Documents/in/Cholesterol"},{"id":198683,"name":"Esterification","url":"https://www.academia.edu/Documents/in/Esterification"},{"id":220780,"name":"PLoS one","url":"https://www.academia.edu/Documents/in/PLoS_one"},{"id":362533,"name":"Hydrazones","url":"https://www.academia.edu/Documents/in/Hydrazones"},{"id":379889,"name":"Homeostasis","url":"https://www.academia.edu/Documents/in/Homeostasis"},{"id":413195,"name":"Time Factors","url":"https://www.academia.edu/Documents/in/Time_Factors"},{"id":422325,"name":"HeLa cells","url":"https://www.academia.edu/Documents/in/HeLa_cells"},{"id":1254280,"name":"Endosomes","url":"https://www.academia.edu/Documents/in/Endosomes"},{"id":2039739,"name":"Down-Regulation","url":"https://www.academia.edu/Documents/in/Down-Regulation"}],"publication_year":2011,"publication_year_with_fallback":2011,"paper_rank":null,"all_time_views":18,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_26703947" data-work_id="26703947" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26703947/Rab7_Is_Functionally_Required_for_Selective_Cargo_Sorting_at_the_Early_Endosome">Rab7 Is Functionally Required for Selective Cargo Sorting at the Early Endosome</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">The small GTPases of the Rab family act as a molecular switch regulating various aspects of membrane trafficking through the selective recruitment of effector proteins. Whereas Rab7 has been classically involved in the regulation of... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703947" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">The small GTPases of the Rab family act as a molecular switch regulating various aspects of membrane trafficking through the selective recruitment of effector proteins. Whereas Rab7 has been classically involved in the regulation of transport within the endolysosomal network, persistent controversy remains as to whether Rab7 also plays a role in earlier steps of endosomal trafficking. In this study, we show that Rab7 depletion or inactivation results in enlargement of both early and late endosomes. Rab7 depletion led to the retention of a significant fraction of internalized low-density lipoproteins (LDL) mainly in enlarged early endosomes (EE). As a result, LDL processing and the transcriptional regulation of sterol-sensitive genes were impaired. We found that Rab7 activity was also required for the sorting of the mannose-6-phosphate receptor, the interferon alpha-receptor and the Shiga toxin B-subunit.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703947" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="e80e2f06ae6c88e4b41e52b8d008fbeb" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985684,&quot;asset_id&quot;:26703947,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985684/download_file?st=MTc0MDUwMzc1Myw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span></li><li class="js-paper-rank-work_26703947 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="26703947"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 26703947, container: ".js-paper-rank-work_26703947", }); 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Whereas Rab7 has been classically involved in the regulation of transport within the endolysosomal network, persistent controversy remains as to whether Rab7 also plays a role in earlier steps of endosomal trafficking. In this study, we show that Rab7 depletion or inactivation results in enlargement of both early and late endosomes. Rab7 depletion led to the retention of a significant fraction of internalized low-density lipoproteins (LDL) mainly in enlarged early endosomes (EE). As a result, LDL processing and the transcriptional regulation of sterol-sensitive genes were impaired. We found that Rab7 activity was also required for the sorting of the mannose-6-phosphate receptor, the interferon alpha-receptor and the Shiga toxin B-subunit.","publication":"Traffic","publication_with_fallback":"Traffic","downloadable_attachments":[{"id":46985684,"asset_id":26703947,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/46985684/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/46985684/Rab7_Is_Functionally_Required_for_Select20160703-6257-1mw8j96-libre.pdf?1467585503=\u0026response-content-disposition=attachment%3B+filename%3DRab7_Is_Functionally_Required_for_Select.pdf\u0026Expires=1740454287\u0026Signature=RuJojNewg~nQ37ZPLREXtVZEL~874TCEEzZlvADFpnGGsPfc1vB4H-rIVESaN9aVO85fONnFtMn3-d3jnP7eHxK~Vrq-6U5SxSFN1YkfICjXGsEY-x~bWHf-E7UBGk3LZImWEEo~OcoQW8l2YacirvybzBEc317JFuRAFobac3M384NqBQ1XAf8QhPcGI8IByOHiuRjWY8f0Dds1iWGe-rgwI2w88hjGEjVWTsd~uU52hh6soKnBkiPrMhPSnCKH~nlngAcn1RI9dvNnqGuU-1md5CJK0whJfbavHLoJQLlxet82611gDLxzt5jAL3NrzuTJyyDjjB2fEWU9n7IK9w__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/46985684/download_file?st=MTc0MDUwMzc1Myw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/46985684/mini_magick20190208-31641-1pt0nsu.png?1549625178"}],"downloadable_attachments_with_full_thumbnails":[{"id":46985684,"asset_id":26703947,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/46985684/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/46985684/Rab7_Is_Functionally_Required_for_Select20160703-6257-1mw8j96-libre.pdf?1467585503=\u0026response-content-disposition=attachment%3B+filename%3DRab7_Is_Functionally_Required_for_Select.pdf\u0026Expires=1740454287\u0026Signature=RuJojNewg~nQ37ZPLREXtVZEL~874TCEEzZlvADFpnGGsPfc1vB4H-rIVESaN9aVO85fONnFtMn3-d3jnP7eHxK~Vrq-6U5SxSFN1YkfICjXGsEY-x~bWHf-E7UBGk3LZImWEEo~OcoQW8l2YacirvybzBEc317JFuRAFobac3M384NqBQ1XAf8QhPcGI8IByOHiuRjWY8f0Dds1iWGe-rgwI2w88hjGEjVWTsd~uU52hh6soKnBkiPrMhPSnCKH~nlngAcn1RI9dvNnqGuU-1md5CJK0whJfbavHLoJQLlxet82611gDLxzt5jAL3NrzuTJyyDjjB2fEWU9n7IK9w__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/46985684/download_file?st=MTc0MDUwMzc1Myw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/46985684/mini_magick20190208-31641-1pt0nsu.png?1549625178"}],"has_pdf":true,"has_fulltext":true,"page_count":18,"ordered_authors":[{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}],"research_interests":[{"id":90156,"name":"Endocytosis","url":"https://www.academia.edu/Documents/in/Endocytosis","nofollow":true},{"id":90514,"name":"Cholesterol","url":"https://www.academia.edu/Documents/in/Cholesterol","nofollow":true},{"id":132887,"name":"Transferrin","url":"https://www.academia.edu/Documents/in/Transferrin","nofollow":true},{"id":157891,"name":"Traffic","url":"https://www.academia.edu/Documents/in/Traffic","nofollow":true},{"id":329263,"name":"Epidermal Growth Factor","url":"https://www.academia.edu/Documents/in/Epidermal_Growth_Factor"},{"id":422325,"name":"HeLa cells","url":"https://www.academia.edu/Documents/in/HeLa_cells"},{"id":503690,"name":"Shiga Toxin","url":"https://www.academia.edu/Documents/in/Shiga_Toxin"},{"id":1254280,"name":"Endosomes","url":"https://www.academia.edu/Documents/in/Endosomes"},{"id":1457054,"name":"Protein Transport","url":"https://www.academia.edu/Documents/in/Protein_Transport"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"publication_year":2014,"publication_year_with_fallback":2014,"paper_rank":null,"all_time_views":27,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_26703948 coauthored" data-work_id="26703948" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26703948/Proton_Pump_Inhibitors_Inhibit_Methotrexate_Transport_by_Renal_Basolateral_Organic_Anion_Transporter_hOAT3">Proton Pump Inhibitors Inhibit Methotrexate Transport by Renal Basolateral Organic Anion Transporter hOAT3</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">The coadministration of methotrexate (MTX) and proton pump inhibitors (PPIs) can result in a pharmacokinetic interaction that delays MTX elimination and subsequently increases the MTX blood concentrations. Human organic anion transporters... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703948" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">The coadministration of methotrexate (MTX) and proton pump inhibitors (PPIs) can result in a pharmacokinetic interaction that delays MTX elimination and subsequently increases the MTX blood concentrations. Human organic anion transporters (hOATs) are responsible for the renal tubular secretion of MTX and are thought to be involved in this drug interaction. The aim of this study was to evaluate the inhibitory potencies of PPIs on hOAT1 and hOAT3, which are the two isoforms of OATs predominantly expressed in kidney proximal tubules. Using stably transfected cell systems that express the uptake transporters human embryonic kidney (HEK)-hOAT1 and HEK-hOAT3, we analyzed the inhibitory potencies of omeprazole, lansoprazole, and pantoprazole on OAT-mediated [ 3 H]estrone sulfate (ES), [ 3 H] p-aminohippuric acid (PAH), and [ 3 H]MTX uptake in vitro. hOAT3 is a high affinity transporter for MTX (K m = 21.17 6 5.65 mM). Omeprazole, lansoprazole, and pantoprazole inhibited [ 3 H]MTX uptake in HEK-hOAT3 cells with an IC 50 of 6.8 6 1.16, 1.14 6 0.26, and 4.45 6 1.62 mM, respectively, and inhibited the [ 3 H]ES uptake in HEK-hOAT3 cells with an IC 50 of 20.59 6 4.07, 3.96 6 0.96, and 7.89 6 2.31 mM, respectively. Furthermore, omeprazole, lansoprazole, and pantoprazole exhibited inhibited PAH uptake on hOAT1 in a concentration-dependent manner (IC 50 = 4.32 6 1.26, 7.58 6 1.06, and 63.21 6 4.74 mM, respectively). These in vitro results suggest that PPIs inhibit [ 3 H]MTX transport via hOAT3 inhibition, which most likely explains the drug-drug interactions between MTX and PPIs and should be considered for other OATs substrates. Rym Chioukh started this work with funding from the Ecole Doctorale 425 Université Paris Sud for her Ph.D. dx.doi.org/10.1124/dmd.114.058529.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703948" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="3653eacd5535fb15fe3097e61f38a8b9" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985668,&quot;asset_id&quot;:26703948,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985668/download_file?st=MTc0MDUwMzc1Myw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span><span class="u-displayInlineBlock InlineList-item-text">&nbsp;and&nbsp;<span class="u-textDecorationUnderline u-clickable InlineList-item-text js-work-more-authors-26703948">+1</span><div class="hidden js-additional-users-26703948"><div><span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a href="https://independent.academia.edu/RChioukh">R. Chioukh</a></span></div></div></span><script>(function(){ var popoverSettings = { el: $('.js-work-more-authors-26703948'), placement: 'bottom', hide_delay: 200, html: true, content: function(){ return $('.js-additional-users-26703948').html(); } } new HoverPopover(popoverSettings); })();</script></li><li class="js-paper-rank-work_26703948 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="26703948"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 26703948, container: ".js-paper-rank-work_26703948", }); });</script></li><li class="js-percentile-work_26703948 InlineList-item InlineList-item--bordered hidden u-tcGrayDark"><span class="percentile-widget hidden"><span class="u-mr2x percentile-widget" style="display: none">•</span><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 26703948; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-percentile-work_26703948"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></li><li class="js-view-count-work_26703948 InlineList-item InlineList-item--bordered hidden"><div><span><span class="js-view-count view-count u-mr2x" data-work-id="26703948"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 26703948; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=26703948]").text(description); $(".js-view-count-work_26703948").attr('title', description).tooltip(); }); });</script></span><script>$(function() { $(".js-view-count-work_26703948").removeClass('hidden') })</script></div></li><li class="InlineList-item u-positionRelative" style="max-width: 250px"><div class="u-positionAbsolute" data-has-card-for-ri-list="26703948"><i class="fa fa-tag InlineList-item-icon u-positionRelative"></i>&nbsp;&nbsp;<a class="InlineList-item-text u-positionRelative">5</a>&nbsp;&nbsp;</div><span class="InlineList-item-text u-textTruncate u-pl9x"><a class="InlineList-item-text" data-has-card-for-ri="11558" rel="nofollow" href="https://www.academia.edu/Documents/in/Drug_interactions">Drug interactions</a>,&nbsp;<script data-card-contents-for-ri="11558" type="text/json">{"id":11558,"name":"Drug interactions","url":"https://www.academia.edu/Documents/in/Drug_interactions","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="57808" rel="nofollow" href="https://www.academia.edu/Documents/in/Cell_line">Cell line</a>,&nbsp;<script data-card-contents-for-ri="57808" type="text/json">{"id":57808,"name":"Cell line","url":"https://www.academia.edu/Documents/in/Cell_line","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="438985" rel="nofollow" href="https://www.academia.edu/Documents/in/Methotrexate">Methotrexate</a>,&nbsp;<script data-card-contents-for-ri="438985" type="text/json">{"id":438985,"name":"Methotrexate","url":"https://www.academia.edu/Documents/in/Methotrexate","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="2444858" rel="nofollow" href="https://www.academia.edu/Documents/in/estrone">estrone</a><script data-card-contents-for-ri="2444858" type="text/json">{"id":2444858,"name":"estrone","url":"https://www.academia.edu/Documents/in/estrone","nofollow":true}</script></span></li><script>(function(){ if (true) { new Aedu.ResearchInterestListCard({ el: $('*[data-has-card-for-ri-list=26703948]'), work: {"id":26703948,"title":"Proton Pump Inhibitors Inhibit Methotrexate Transport by Renal Basolateral Organic Anion Transporter hOAT3","created_at":"2016-07-03T15:33:48.086-07:00","owner_id":50697757,"url":"https://www.academia.edu/26703948/Proton_Pump_Inhibitors_Inhibit_Methotrexate_Transport_by_Renal_Basolateral_Organic_Anion_Transporter_hOAT3","slug":"Proton_Pump_Inhibitors_Inhibit_Methotrexate_Transport_by_Renal_Basolateral_Organic_Anion_Transporter_hOAT3","dom_id":"work_26703948","summary":"The coadministration of methotrexate (MTX) and proton pump inhibitors (PPIs) can result in a pharmacokinetic interaction that delays MTX elimination and subsequently increases the MTX blood concentrations. Human organic anion transporters (hOATs) are responsible for the renal tubular secretion of MTX and are thought to be involved in this drug interaction. The aim of this study was to evaluate the inhibitory potencies of PPIs on hOAT1 and hOAT3, which are the two isoforms of OATs predominantly expressed in kidney proximal tubules. Using stably transfected cell systems that express the uptake transporters human embryonic kidney (HEK)-hOAT1 and HEK-hOAT3, we analyzed the inhibitory potencies of omeprazole, lansoprazole, and pantoprazole on OAT-mediated [ 3 H]estrone sulfate (ES), [ 3 H] p-aminohippuric acid (PAH), and [ 3 H]MTX uptake in vitro. hOAT3 is a high affinity transporter for MTX (K m = 21.17 6 5.65 mM). Omeprazole, lansoprazole, and pantoprazole inhibited [ 3 H]MTX uptake in HEK-hOAT3 cells with an IC 50 of 6.8 6 1.16, 1.14 6 0.26, and 4.45 6 1.62 mM, respectively, and inhibited the [ 3 H]ES uptake in HEK-hOAT3 cells with an IC 50 of 20.59 6 4.07, 3.96 6 0.96, and 7.89 6 2.31 mM, respectively. Furthermore, omeprazole, lansoprazole, and pantoprazole exhibited inhibited PAH uptake on hOAT1 in a concentration-dependent manner (IC 50 = 4.32 6 1.26, 7.58 6 1.06, and 63.21 6 4.74 mM, respectively). These in vitro results suggest that PPIs inhibit [ 3 H]MTX transport via hOAT3 inhibition, which most likely explains the drug-drug interactions between MTX and PPIs and should be considered for other OATs substrates. Rym Chioukh started this work with funding from the Ecole Doctorale 425 Université Paris Sud for her Ph.D. dx.doi.org/10.1124/dmd.114.058529.","publication":"Drug Metabolism and Disposition","publication_with_fallback":"Drug Metabolism and Disposition","downloadable_attachments":[{"id":46985668,"asset_id":26703948,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/46985668/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/46985668/2041.full-libre.pdf?1467585501=\u0026response-content-disposition=attachment%3B+filename%3DProton_Pump_Inhibitors_Inhibit_Methotrex.pdf\u0026Expires=1740507353\u0026Signature=TVgFGahUfTmeihIVTIQGX6fBLZ1GIk4rxalocWEG8dW0ciixG7j5vnMw0T8tg~bjmCu~x5ei5a~CGLDFd6vAVM2K4J5~GUo1JzR5WnL-fvhxfyqq4MJZqKNGpwG39pg33A-cZv7cRHRTPjRGBdX5nSvrEAlWFnBP5AFpmdaiwfTn20gbLp8WXM4E5P7H7tyrvE5Od-b~gv9Ml~cEE~68giG9BRIg56BtcHsVvEA1raU2sbpWws6QCyHyqQT7UVezQMT1V0AMjTUSm5GJNQQupyNMkR-S0se1aKTXJLEaTYerThcpBXifnrgUmtUl8U~aPFq-km1rQOLD9uLkVRv0iA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/46985668/download_file?st=MTc0MDUwMzc1Myw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/46985668/mini_magick20190208-23866-2c7exm.png?1549625152"}],"downloadable_attachments_with_full_thumbnails":[{"id":46985668,"asset_id":26703948,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/46985668/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/46985668/2041.full-libre.pdf?1467585501=\u0026response-content-disposition=attachment%3B+filename%3DProton_Pump_Inhibitors_Inhibit_Methotrex.pdf\u0026Expires=1740507353\u0026Signature=TVgFGahUfTmeihIVTIQGX6fBLZ1GIk4rxalocWEG8dW0ciixG7j5vnMw0T8tg~bjmCu~x5ei5a~CGLDFd6vAVM2K4J5~GUo1JzR5WnL-fvhxfyqq4MJZqKNGpwG39pg33A-cZv7cRHRTPjRGBdX5nSvrEAlWFnBP5AFpmdaiwfTn20gbLp8WXM4E5P7H7tyrvE5Od-b~gv9Ml~cEE~68giG9BRIg56BtcHsVvEA1raU2sbpWws6QCyHyqQT7UVezQMT1V0AMjTUSm5GJNQQupyNMkR-S0se1aKTXJLEaTYerThcpBXifnrgUmtUl8U~aPFq-km1rQOLD9uLkVRv0iA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/46985668/download_file?st=MTc0MDUwMzc1Myw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/46985668/mini_magick20190208-23866-2c7exm.png?1549625152"}],"has_pdf":true,"has_fulltext":true,"page_count":8,"ordered_authors":[{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"},{"id":50707908,"first_name":"R.","last_name":"Chioukh","domain_name":"independent","page_name":"RChioukh","display_name":"R. 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The impact of meal fatty acid composition was explored by measure of serum promoted cholesterol effiux from Fu5AH cells after ingestion of 4 different fats: sunflower... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703950" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Cell cholesterol effiux to serum is stimulated after an oral fat load. The impact of meal fatty acid composition was explored by measure of serum promoted cholesterol effiux from Fu5AH cells after ingestion of 4 different fats: sunflower (SO, oleic-sunflower (O1), a mixed oil (Mx), and beef tallow (Bt). High density lipoprotein (HDL) 2 and HDL 3 were isolated and analyzed. Cholesterol effiux increased regularly after O1 (P &lt; 0.05 at 4 h and P &lt; 0.02 at 8 h), and 8 h after Mx (P &lt; 0.02) or Bt (P &lt; 0.05), but not after Sf. Percent HDL 3 phospholipids increased after O1 (P &lt; 0.05 at 6 h and P &lt; 0.01 at 8 h) and 8 h after Mx (P &lt; 0.01). After O1, variations in effiux and percent phospholipids in HDL 3 (but not HDL 2) were positively correlated (r= 0.929; P = 0.007 at 6 h). Using HDL 3, effiux increased 6 h after O1 (P &lt; 0.05) but not after Sf, and effiux was correlated with HDL 3 phospholipid concentration in medium (r=0.913; P=0.011). Thus postprandial increase in cholesterol effiux is influenced by ingested fats in relation to increased phospholipid availability on HDL 3. The protective effect of monounsaturated fatty acids against atherogenesis might be partly mediated by an enhanced ability of postprandial serum to accept cell cholesterol.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703950" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="fe4f8a6743d669365c8835fabfaab956" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985671,&quot;asset_id&quot;:26703950,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985671/download_file?st=MTc0MDUwMzc1Myw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span></li><li class="js-paper-rank-work_26703950 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="26703950"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 26703950, container: ".js-paper-rank-work_26703950", }); 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The impact of meal fatty acid composition was explored by measure of serum promoted cholesterol effiux from Fu5AH cells after ingestion of 4 different fats: sunflower (SO, oleic-sunflower (O1), a mixed oil (Mx), and beef tallow (Bt). High density lipoprotein (HDL) 2 and HDL 3 were isolated and analyzed. Cholesterol effiux increased regularly after O1 (P \u003c 0.05 at 4 h and P \u003c 0.02 at 8 h), and 8 h after Mx (P \u003c 0.02) or Bt (P \u003c 0.05), but not after Sf. Percent HDL 3 phospholipids increased after O1 (P \u003c 0.05 at 6 h and P \u003c 0.01 at 8 h) and 8 h after Mx (P \u003c 0.01). After O1, variations in effiux and percent phospholipids in HDL 3 (but not HDL 2) were positively correlated (r= 0.929; P = 0.007 at 6 h). Using HDL 3, effiux increased 6 h after O1 (P \u003c 0.05) but not after Sf, and effiux was correlated with HDL 3 phospholipid concentration in medium (r=0.913; P=0.011). Thus postprandial increase in cholesterol effiux is influenced by ingested fats in relation to increased phospholipid availability on HDL 3. The protective effect of monounsaturated fatty acids against atherogenesis might be partly mediated by an enhanced ability of postprandial serum to accept cell cholesterol.","publication":"Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism","publication_with_fallback":"Biochimica et Biophysica Acta (BBA) - Lipids and Lipid 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Acid","url":"https://www.academia.edu/Documents/in/Oleic_Acid"},{"id":856030,"name":"Monounsaturated Fatty Acid","url":"https://www.academia.edu/Documents/in/Monounsaturated_Fatty_Acid"},{"id":957051,"name":"HDL","url":"https://www.academia.edu/Documents/in/HDL"},{"id":1274497,"name":"Total Cholesterol","url":"https://www.academia.edu/Documents/in/Total_Cholesterol"},{"id":1358124,"name":"Fatty Acid Composition","url":"https://www.academia.edu/Documents/in/Fatty_Acid_Composition"}],"publication_year":1996,"publication_year_with_fallback":1996,"paper_rank":null,"all_time_views":11,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_26703954" data-work_id="26703954" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/26703954/Role_of_HDL_phospholipid_in_efflux_of_cell_cholesterol_to_whole_serum_studies_with_human_apoA_I_transgenic_rats">Role of HDL phospholipid in efflux of cell cholesterol to whole serum: studies with human apoA-I transgenic rats</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Sera of transgenic rats expressing human apoA-I were tested for their ability to stimulate efflux of radiolabeled cholesterol from Fu5AH rat hepatoma cells. Expression of human apoA-I resulted in a dose-dependent increase in HDL, as... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_26703954" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Sera of transgenic rats expressing human apoA-I were tested for their ability to stimulate efflux of radiolabeled cholesterol from Fu5AH rat hepatoma cells. Expression of human apoA-I resulted in a dose-dependent increase in HDL, as measured by both HDL-cholesterol and HDL-phospholipid, and produced a decrease in rat apoA-I. In rats expressing high concentrations of human apoA-I (TgR[hAI]high, human apoA-I &amp;gt; 250 mg/dl), the increase in HDL-phospholipid was not proportional to the increase in human apoA-I, as illustrated by a HDL-PL/total apoA-I ratio of 0.84 +/- 0.19 compared to a ratio of 1.28 +/- 0.29 for control rats and of 1.28 +/- 0.39 for rats expressing low levels of human apoA-I (TgR[hAI]low, human apoA-I &amp;lt; 250 mg/dl). Compared to sera from control animals, efflux of cell cholesterol was increased by 26% in the sera from TgR[hAI]low, and by 76% in the TgR[hAI]high. An examination of the relationships between efflux and HDL-related parameters demonstrated a hyperbolic r...</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/26703954" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="859e9a42a627d4b6156c8af69b1a2be9" rel="nofollow" data-download="{&quot;attachment_id&quot;:46985675,&quot;asset_id&quot;:26703954,&quot;asset_type&quot;:&quot;Work&quot;,&quot;always_allow_download&quot;:false,&quot;track&quot;:null,&quot;button_location&quot;:&quot;work_strip&quot;,&quot;source&quot;:null,&quot;hide_modal&quot;:null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/46985675/download_file?st=MTc0MDUwMzc1Myw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by&nbsp;<span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="50697757" href="https://u-psud.academia.edu/NatalieFournier">Natalie Fournier</a><script data-card-contents-for-user="50697757" type="text/json">{"id":50697757,"first_name":"Natalie","last_name":"Fournier","domain_name":"u-psud","page_name":"NatalieFournier","display_name":"Natalie Fournier","profile_url":"https://u-psud.academia.edu/NatalieFournier","photo":"/images/s65_no_pic.png"}</script></span></span></li><li class="js-paper-rank-work_26703954 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="26703954"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 26703954, container: ".js-paper-rank-work_26703954", }); 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