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PPAR Research
Volume 2010 (2010), Article ID 584296, 16 pages
http://dx.doi.org/10.1155/2010/584296
Review Article

PPAR in Obesity: Sex Difference and Estrogen Involvement

Department of Life Sciences, Mokwon University, Taejon 302-729, Republic of Korea

Received 18 May 2010; Accepted 8 July 2010

Academic Editor: Christopher Lau

Copyright © 2010 Michung Yoon. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Peroxisome proliferator-activated receptor (PPAR ) is a member of the steroid hormone receptor superfamily and is well known to act as the molecular target for lipid-lowering drugs of the fibrate family. At the molecular level, PPAR regulates the transcription of a number of genes critical for lipid and lipoprotein metabolism. PPAR activators are further shown to reduce body weight gain and adiposity, at least in part, due to the increase of hepatic fatty acid oxidation and the decrease in levels of circulating triglycerides responsible for adipose cell hypertrophy and hyperplasia. However, these effects of the PPAR ligand fenofibrate on obesity are regulated with sexual dimorphism and seem to be influenced by the presence of functioning ovaries, suggesting the involvement of ovarian steroids in the control of obesity by PPAR . In female ovariectomized mice, 17 -estradiol inhibits the actions of fenofibrate on obesity through its suppressive effects on the expression of PPAR target genes, and these processes may be mediated by inhibiting the coactivator recruitment of PPAR . Thus, it is likely that PPAR functions on obesity may be enhanced in estrogen-deficient states.