TAILIEUCHUNG - Báo cáo khoa học: Deficiency in apolipoprotein E has a protective effect on diet-induced nonalcoholic fatty liver disease in mice

Apolipoprotein E (apoE) mediates the efficient catabolism of the chylomicron remnants very low-density lipoprotein and low-density lipo-protein from the circulation, and thede novo biogenesis of high-density lipoprotein. Lipid-bound apoE is the natural ligand for the low-density lipoprotein receptor (LDLr), LDLr-related protein 1 and other scavenger receptors. | IFEBS Journal Deficiency in apolipoprotein E has a protective effect on diet-induced nonalcoholic fatty liver disease in mice Eleni A. Karavia1 Dionysios J. Papachristou2 Ioanna Kotsikogianni2 Ioanna Giopanou2 and Kyriakos E. Kypreos1 1 Department of Medicine Pharmacology Unit University of Patras Schoolof Health Sciences Rio-Achaias Greece 2 Department of Medicine Anatomy Histology and Embryology Unit University of Patras Schoolof Health Sciences Rio-Achaias Greece Keywords apoE-deficient mice apolipoprotein E low density lipoprotein receptor lipoproteins nonalcoholic fatty liver disease Correspondence K. E. Kypreos Department of Medicine University of Patras Schoolof Health Sciences Panepistimioupolis Rio TK 26500 Greece Fax 302610994720 Tel 302610969120 E-mail kkypreos@ Received 21 March 2011 revised 7 June 2011 accepted 6 July 2011 doi Apolipoprotein E apoE mediates the efficient catabolism of the chylomicron remnants very low-density lipoprotein and low-density lipoprotein from the circulation and the de novo biogenesis of high-density lipoprotein. Lipid-bound apoE is the natural ligand for the low-density lipoprotein receptor LDLr LDLr-related protein 1 and other scavenger receptors. Recently we have established that deficiency in apoE renders mice resistant to diet-induced obesity. In the light of these well-documented properties of apoE we sought to investigate its role in the development of diet-induced nonalcoholic fatty liver disease NAFLD . apoE-deficient LDLr-deficient and control C57BL 6 mice were fed a western-type diet protein carbohydrate fat cholesterol kca-l-g-1 for 24 weeks and their sensitivity to NAFLD was assessed by histological and biochemical methods. apoE-deficient mice were less sensitive than control C57BL 6 mice to diet-induced NAFLD. In an attempt to identify the molecular basis for this phenomenon biochemical and kinetic analyses revealed that apoE-deficient mice .

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