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muscle is a major site to regulate whole-body fatty-acid and glucose metabolism. We show that mice with increased oxidative fibers are resistant to high-fat-induced obesity and glucose intolerance. Moreover, ligand studies provide compelling evidence that activation of endogenous PPARδ can produce similar effects. Might PPARδ have any beneficial effects on glucose metabolism in the lean condition? This has not been explored; however, insulin resistance in the elderly is confined mostly to skeletal muscle and may be due to reduction of mitochondrial number and/or function (Petersen et al. 2003). The ability of PPARδ to stimulate mitochondrial biogenesis and oxidative function suggests that PPARδ could be important for control of insulin resistance during normal aging. Together, these data indicate that PPARδ and its ligands comprise a key molecular switch to regulate muscle fiber specification, obesity resistance, insulin sensitivity, and, most surprisingly, physical endurance. This work demonstrates that complex physiologic properties such as fatigue, endurance, and running capacity can be genetically manipulated."}

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