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Endogenous ApoE Expression Modulates Adipocyte Triglyceride Content and Turnover

¹ Department of Medicine, University of Illinois, Chicago, Illinois
² Department of Pathology, University of Chicago, Chicago, Illinois
³ Departments of Medicine and Pharmacology, University of Illinois at Chicago, Chicago, Illinois

Address correspondence and reprint requests to Theodore Mazzone, MD, Section of Endocrinology, Diabetes and Metabolism (MC 797), University of Illinois, 1819 W. Polk St., Chicago, IL 60612. E-mail: tmazzone{at}uic.edu

Abbreviations: apo, apolipoprotein; CEBP, CCAAT/enhancer binding protein; DMEM, Dulbecco’s modified Eagle’s medium; FBS, fetal bovine serum; IFP, inguinal fat pad; PID, post-induction day; PPAR, peroxisome proliferator–activated receptor; TGRL, triglyceride-rich lipoprotein

Apolipoprotein E (apoE) is highly expressed in adipose tissue and adipocytes in which its expression is regulated by peroxisome proliferator–activated receptor (PPAR)- agonists and tumor necrosis factor–. There is, however, no information regarding a role for endogenous apoE in differentiated adipocyte function. In this report, we define a novel role for apoE in modulating adipocyte lipid metabolism. ApoE^–/– mice have less body fat and smaller adipocytes compared with wild-type controls. Freshly isolated adipose tissue from apoE^–/– mice contains lower levels of triglyceride and free fatty acid, and these differences are maintained in cultured adipocytes derived from preadipocytes. Adenoviral expression of apoE in apoE^–/–-cultured adipocytes increases triglyceride and fatty acid content. During incubation with apoE-containing triglyceride-rich lipoproteins, apoE^–/– adipose tissue accumulates less triglyceride than wild type. The absence of apoE expression in primary cultured adipocytes also leads to changes in the expression of genes involved in the metabolism/turnover of fatty acids and the triglyceride droplet. Markers of adipocyte differentiation were lower in freshly isolated and cultured apoE^–/– adipocytes. Importantly, PPAR-–mediated changes in lipid content and gene expression are markedly altered in cultured apoE^–/– adipocytes. These results establish a novel role for endogenous apoE in adipocyte lipid metabolism and have implications for constructing an integrated model of adipocyte physiology in health and disease.

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