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Am J Physiol Endocrinol Metab 293: E203-E209, 2007. First published March 27, 2007; doi:10.1152/ajpendo.00118.2007
0193-1849/07 $8.00
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Nutritional regulation of adipose tissue apolipoprotein E expression

Zhi Hua Huang,1 Raul M. Luque,1,3 Rhonda D. Kineman,1,3 and Theodore Mazzone1,2

1Department of Medicine, University of Illinois at Chicago, 2Department of Pharmacology, University of Illinois at Chicago, and 3Jesse Brown Veterans Administration Medical Center, Chicago, Illinois

Submitted 21 February 2007 ; accepted in final form 21 March 2007

Apolipoprotein E (apoE) is a multifunctional protein that is highly expressed in human and murine adipose tissue. Endogenous adipocyte apoE expression influences adipocyte triglyceride turnover and modulates the expression of genes involved in lipid synthesis and oxidation. We now demonstrate the regulation of adipose tissue apoE expression by nutritional status in lean and obese mice. Obesity induced by high-fat diet, or by hyperphagia in ob/ob mice, produces significant reduction of adipose tissue apoE expression at the protein and messenger RNA level. Fasting in C57BL/6J mice for 24 h significantly increased apoE protein and messenger RNA levels. In ob/ob mice, transplantation of adipose tissue from lean littermate controls to restore circulating leptin levels produced significant weight loss over 12 wk and also produced an increase in adipose tissue apoE expression. The increase in adipose tissue apoE expression in this model, however, did not require leptin. Adipose tissue apoE was also significantly increased in ob/ob mice after a 48-h fast or after 7 days of caloric restriction. In summary, obesity suppresses adipose tissue apoE expression, whereas fasting or weight loss increases it. From our previous observations, these changes in adipose tissue apoE expression will have significant impact on adipose tissue lipid flux and lipoprotein metabolism. Furthermore, these results suggest adipose tissue apoE participates in defending adipose tissue and organismal energy homeostasis in response to nutritional perturbation.

adipocytes; obesity


Address for reprint requests and other correspondence: T. Mazzone, Section of Endocrinology, Diabetes and Metabolism (MC 797), Univ. of Illinois at Chicago, 1819 W. Polk St., Chicago, IL 60612 (e-mail: tmazzone{at}uic.edu)






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