{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T08:19:44Z","timestamp":1792657184480,"version":"4.5.0"},"reference-count":40,"publisher":"Wiley","issue":"17","license":[{"start":{"date-parts":[[2011,8,2]],"date-time":"2011-08-02T00:00:00Z","timestamp":1312243200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The FEBS Journal"],"published-print":{"date-parts":[[2011,9]]},"abstract":"<jats:p>Apolipoprotein\u2003E (apoE) mediates the efficient catabolism of the chylomicron remnants very low\u2010density lipoprotein and low\u2010density lipoprotein from the circulation, and the <jats:italic>de\u2003novo<\/jats:italic> biogenesis of high\u2010density lipoprotein. Lipid\u2010bound apoE is the natural ligand for the low\u2010density lipoprotein receptor (LDLr), LDLr\u2010related protein\u20031 and other scavenger receptors. Recently, we have established that deficiency in apoE renders mice resistant to diet\u2010induced obesity. In the light of these well\u2010documented properties of apoE, we sought to investigate its role in the development of diet\u2010induced nonalcoholic fatty liver disease (NAFLD). apoE\u2010deficient, LDLr\u2010deficient and control C57BL\/6 mice were fed a western\u2010type diet (17.3% protein, 48.5% carbohydrate, 21.2% fat, 0.2% cholesterol, 4.5\u2003kcal\u00b7g<jats:sup>\u2212<\/jats:sup>) for 24\u2003weeks and their sensitivity to NAFLD was assessed by histological and biochemical methods. apoE\u2010deficient mice were less sensitive than control C57BL\/6 mice to diet\u2010induced NAFLD. In an attempt to identify the molecular basis for this phenomenon, biochemical and kinetic analyses revealed that apoE\u2010deficient mice displayed a significantly delayed post\u2010prandial triglyceride clearance from their plasma. In contrast with apoE\u2010deficient mice, LDLr\u2010deficient mice fed a western\u2010type diet for 24\u2003weeks developed significant accumulation of hepatic triglycerides and NAFLD, suggesting that apoE\u2010mediated hepatic triglyceride accumulation in mice is independent of LDLr. Our findings suggest a new role of apoE as a key peripheral contributor to hepatic lipid homeostasis and the development of diet\u2010induced NAFLD.<\/jats:p>","DOI":"10.1111\/j.1742-4658.2011.08238.x","type":"journal-article","created":{"date-parts":[[2011,7,9]],"date-time":"2011-07-09T05:47:16Z","timestamp":1310190436000},"page":"3119-3129","source":"Crossref","is-referenced-by-count":39,"title":["Deficiency in apolipoprotein\u2003E has a protective effect on diet\u2010induced nonalcoholic fatty liver disease in mice"],"prefix":"10.1111","volume":"278","author":[{"given":"Eleni A.","family":"Karavia","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dionysios 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