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PPAR? Promotes Running Endurance by Preserving Glucose.


ABSTRACT: Management of energy stores is critical during endurance exercise; a shift in substrate utilization from glucose toward fat is a hallmark of trained muscle. Here we show that this key metabolic adaptation is both dependent on muscle PPAR? and stimulated by PPAR? ligand. Furthermore, we find that muscle PPAR? expression positively correlates with endurance performance in BXD mouse reference populations. In addition to stimulating fatty acid metabolism in sedentary mice, PPAR? activation potently suppresses glucose catabolism and does so without affecting either muscle fiber type or mitochondrial content. By preserving systemic glucose levels, PPAR? acts to delay the onset of hypoglycemia and extends running time by ?100 min in treated mice. Collectively, these results identify a bifurcated PPAR? program that underlies glucose sparing and highlight the potential of PPAR?-targeted exercise mimetics in the treatment of metabolic disease, dystrophies, and, unavoidably, the enhancement of athletic performance.

SUBMITTER: Fan W 

PROVIDER: S-EPMC5492977 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature

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Management of energy stores is critical during endurance exercise; a shift in substrate utilization from glucose toward fat is a hallmark of trained muscle. Here we show that this key metabolic adaptation is both dependent on muscle PPARδ and stimulated by PPARδ ligand. Furthermore, we find that muscle PPARδ expression positively correlates with endurance performance in BXD mouse reference populations. In addition to stimulating fatty acid metabolism in sedentary mice, PPARδ activation potently  ...[more]

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