{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,4,24]],"date-time":"2025-04-24T16:27:00Z","timestamp":1745512020357},"reference-count":46,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2016,6,1]],"date-time":"2016-06-01T00:00:00Z","timestamp":1464739200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100002661","name":"Fonds De La Recherche Scientifique - FNRS","doi-asserted-by":"publisher","award":["CDR J.0122.15"],"award-info":[{"award-number":["CDR J.0122.15"]}],"id":[{"id":"10.13039\/501100002661","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Nutrition Food Res"],"published-print":{"date-parts":[[2016,10]]},"abstract":"<jats:sec><jats:title>Scope<\/jats:title><jats:p>Western diets are characterized by low intake of <jats:italic>n<\/jats:italic>\u20103 PUFA compensated by constant amounts of <jats:italic>n<\/jats:italic>\u20106 PUFA. Reduced intake of <jats:italic>n<\/jats:italic>\u20103 PUFA is associated with increased cardiovascular risk, as observed in nonalcoholic fatty liver disease patients. The study aimed to evaluating the impact of dietary <jats:italic>n<\/jats:italic>\u20103 PUFA depletion on endothelial function, an early key event of cardiovascular diseases.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods and results<\/jats:title><jats:p>C57Bl\/6J or apolipoprotein E knock\u2010out (apoE<jats:sup>\u2212\/\u2212<\/jats:sup>) were fed control (CT) or <jats:italic>n<\/jats:italic>\u20103 PUFA\u2010depleted diets (DEF) for 12 wks. Mice fed <jats:italic>n<\/jats:italic>\u20103 DEF diet developed a hepatic steatosis, linked to changes in hepatic expression of genes controlled by Sterol Regulatory Element Binding Protein\u20101 and \u20102. Vascular function was assessed on second\u2010 and third\u2010order mesenteric arteries and <jats:italic>n<\/jats:italic>\u20103 PUFA\u2010depleted apoE<jats:sup>\u2212\/\u2212<\/jats:sup> mice presented endothelial dysfunction characterized by decreased vasorelaxation in response of acetylcholine. The presence of a nitric oxide synthase (NOS) inhibitor blunted the relaxation in each groups and heme\u2010nitrosylated hemoglobin blood (Hb\u2010NO) level was significantly lower in <jats:italic>n<\/jats:italic>\u20103 PUFA\u2010depleted apoE<jats:sup>\u2212\/\u2212<\/jats:sup> mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Twelve weeks of <jats:italic>n<\/jats:italic>\u20103 DEF diet promote steatosis and accelerate the process of endothelial dysfunction in apoE<jats:sup>\u2212\/\u2212<\/jats:sup> mice by a mechanism involving the NOS\/NO pathway. We propose <jats:italic>n<\/jats:italic>\u20103 PUFA\u2010depleted apoE<jats:sup>\u2212\/\u2212<\/jats:sup> mice as a new model to study endothelial dysfunction related to hepatic steatosis independently of obesity.<\/jats:p><\/jats:sec>","DOI":"10.1002\/mnfr.201500930","type":"journal-article","created":{"date-parts":[[2016,5,2]],"date-time":"2016-05-02T16:25:31Z","timestamp":1462206331000},"page":"2198-2207","source":"Crossref","is-referenced-by-count":5,"title":["Nutritional depletion in <i>n<\/i>\u20103 PUFA in apoE knock\u2010out mice: A new model of endothelial dysfunction associated with fatty liver disease"],"prefix":"10.1002","volume":"60","author":[{"given":"Emilie","family":"Catry","sequence":"first","affiliation":[{"name":"Metabolism and Nutrition Research Group, Louvain Drug Research Institute Universit\u00e9 catholique de Louvain  Brussels Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Audrey M.","family":"Neyrinck","sequence":"additional","affiliation":[{"name":"Metabolism and Nutrition Research Group, Louvain Drug Research Institute Universit\u00e9 catholique de Louvain  Brussels Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Irina","family":"Lobysheva","sequence":"additional","affiliation":[{"name":"P\u00f4le de Pharmacologie et Th\u00e9rapeutique, Institut de Recherche Exp\u00e9rimentale et Clinique Universit\u00e9 catholique de Louvain  Brussels Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Barbara D.","family":"Pachikian","sequence":"additional","affiliation":[{"name":"Metabolism and Nutrition Research Group, Louvain Drug Research Institute Universit\u00e9 catholique de Louvain  Brussels Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthias","family":"Van Hul","sequence":"additional","affiliation":[{"name":"Metabolism and Nutrition Research Group, Louvain Drug Research Institute Universit\u00e9 catholique de Louvain  Brussels Belgium"},{"name":"Walloon Excellence in Life sciences and Biotechnology (WELBIO)  Wavre Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patrice D.","family":"Cani","sequence":"additional","affiliation":[{"name":"Metabolism and Nutrition Research Group, Louvain Drug Research Institute Universit\u00e9 catholique de Louvain  Brussels Belgium"},{"name":"Walloon Excellence in Life sciences and Biotechnology (WELBIO)  Wavre Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chantal","family":"Dessy","sequence":"additional","affiliation":[{"name":"P\u00f4le de Pharmacologie et Th\u00e9rapeutique, Institut de Recherche Exp\u00e9rimentale et Clinique Universit\u00e9 catholique de Louvain  Brussels Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nathalie M.","family":"Delzenne","sequence":"additional","affiliation":[{"name":"Metabolism and Nutrition Research Group, Louvain Drug Research Institute Universit\u00e9 catholique de Louvain  Brussels Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2016,6]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1161\/circ.131.suppl_2.o29"},{"key":"e_1_2_8_3_1","unstructured":"WHO Fact sheet2015 World Health Organization Geneva Switzerland."},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1093\/ajcn\/73.4.673"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1093\/jn\/137.4.945"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.3945\/ajcn.110.006643"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1155\/2011\/364040"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pmed.1000058"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.3109\/10715762.2010.485992"},{"key":"e_1_2_8_10_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0023365"},{"key":"e_1_2_8_11_1","first-page":"330","article-title":"Progression of NAFLD to diabetes mellitus, cardiovascular disease or cirrhosis","volume":"10","author":"Anstee Q. 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