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A more recent version of this article appeared on December 1, 2004

Papers In Press, published online ahead of print October 16, 2004
J. Lipid Res., doi:10.1194/jlr.R400010-JLR200
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Submitted on October 5, 2004
Revised on October 16, 2004
Accepted on October 5, 2004

PPAR and LXR-dependent pathways controlling lipid metabolism and development of atherosclerosis

Andrew C. Li and Christopher K. Glass

Cellular @ Molecular Medicine, University of Califoprnia, San Diego, La Jolla, CA 92093-0651

Corresponding Author: cglass{at}ucsd.edu

The nuclear receptor superfamily is comprised of transcription factors that positively and negatively regulate gene expression in response to the binding of a diverse array of lipid-derived hormones and metabolites. Intense efforts are currently being directed at defining the biological roles and mechanisms of action Liver X receptors (LXRs) and Peroxisome Proliferator-Activated Receptors (PPARs). LXRs have been found to play essential roles in the regulation of whole body cholesterol absorption and excretion, in the efflux of cholesterol from peripheral cells, and in the biosynthesis and metabolism of very low density lipoproteins. PPARs have been found to regulate diverse aspects of lipid metabolism, including fatty acid oxidation, fat cell development, lipoprotein metabolism and glucose homeostasis. Intervention studies indicate that activation of PPARa, PPAR and LXRs by specific synthetic ligands can inhibit the development of atherosclerosis in animal models. Here we review recent studies that provide new insights into the mechanisms by which these subclasses of nuclear receptors act to systemically influence lipid and glucose metabolism and regulate gene expression within the artery wall.


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