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Molecular Endocrinology, doi:10.1210/me.2003-0151
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Molecular Endocrinology 17 (12): 2477-2493
Copyright © 2003 by The Endocrine Society

The Peroxisome Proliferator-Activated Receptor ß/{delta} Agonist, GW501516, Regulates the Expression of Genes Involved in Lipid Catabolism and Energy Uncoupling in Skeletal Muscle Cells

Uwe Dressel, Tamara L. Allen, Jyotsna B. Pippal, Paul R. Rohde, Patrick Lau and George E. O. Muscat

Institute for Molecular Bioscience, The University of Queensland, St. Lucia, Queensland 4072, Australia

Address all correspondence and requests for reprints to: George Muscat, Institute Molecular Bioscience, St. Lucia, Queensland 4072, Australia. E-mail: G.Muscat{at}imb.uq.edu.au.

Lipid homeostasis is controlled by the peroxisome proliferator-activated receptors (PPAR{alpha}, -ß/{delta}, and -{gamma}) that function as fatty acid-dependent DNA-binding proteins that regulate lipid metabolism. In vitro and in vivo genetic and pharmacological studies have demonstrated PPAR{alpha} regulates lipid catabolism. In contrast, PPAR{gamma} regulates the conflicting process of lipid storage. However, relatively little is known about PPARß/{delta} in the context of target tissues, target genes, lipid homeostasis, and functional overlap with PPAR{alpha} and -{gamma}. PPARß/{delta}, a very low-density lipoprotein sensor, is abundantly expressed in skeletal muscle, a major mass peripheral tissue that accounts for approximately 40% of total body weight. Skeletal muscle is a metabolically active tissue, and a primary site of glucose metabolism, fatty acid oxidation, and cholesterol efflux. Consequently, it has a significant role in insulin sensitivity, the blood-lipid profile, and lipid homeostasis. Surprisingly, the role of PPARß/{delta} in skeletal muscle has not been investigated. We utilize selective PPAR{alpha}, -ß/{delta}, -{gamma}, and liver X receptor agonists in skeletal muscle cells to understand the functional role of PPARß/{delta}, and the complementary and/or contrasting roles of PPARs in this major mass peripheral tissue. Activation of PPARß/{delta} by GW501516 in skeletal muscle cells induces the expression of genes involved in preferential lipid utilization, ß-oxidation, cholesterol efflux, and energy uncoupling. Furthermore, we show that treatment of muscle cells with GW501516 increases apolipoprotein-A1 specific efflux of intracellular cholesterol, thus identifying this tissue as an important target of PPARß/{delta} agonists. Interestingly, fenofibrate induces genes involved in fructose uptake, and glycogen formation. In contrast, rosiglitazone-mediated activation of PPAR{gamma} induces gene expression associated with glucose uptake, fatty acid synthesis, and lipid storage. Furthermore, we show that the PPAR-dependent reporter in the muscle carnitine palmitoyl-transferase-1 promoter is directly regulated by PPARß/{delta}, and not PPAR{alpha} in skeletal muscle cells in a PPAR{gamma} coactivator-1-dependent manner. This study demonstrates that PPARs have distinct roles in skeletal muscle cells with respect to the regulation of lipid, carbohydrate, and energy homeostasis. Moreover, we surmise that PPARß/{delta} agonists would increase fatty acid catabolism, cholesterol efflux, and energy expenditure in muscle, and speculate selective activators of PPARß/{delta} may have therapeutic utility in the treatment of hyperlipidemia, atherosclerosis, and obesity.

NURSA Molecule Pages Link:

Nuclear Receptors:   PPARα  |  PPARδ  |  PPARγ
Coregulators:   PGC-1  |  p300  |  GRIP1
Ligands:   Rosiglitazone



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