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M707006200v1
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Papers In Press, published online ahead of print October 11, 2007
J. Biol. Chem, 10.1074/jbc.M707006200
Submitted on August 21, 2007
Revised on October 9, 2007
Accepted on October 11, 2007

A role for the transcriptional coactivator PGC-1alpha in muscle refueling

Adam R. Wende, Paul J. Schaeffer, Glendon J. Parker, Christoph Zechner, Dong-Ho Han, May M. Chen, Chad R. Hancock, John J. Lehman, Janice M. Huss, Donald A. McClain, John O. Holloszy, and Daniel P. Kelly

Cardiology, Washington University School of Medicine, St. Louis, MO 63110

Corresponding Author: dkelly{at}im.wustl.edu

The transcriptional coactivator, PPAR coactivator-1a (PGC-1a) has been identified as an inducible regulator of mitochondrial function. Skeletal muscle PGC-1a expression is induced post-exercise. Therefore, we sought to determine its role in the regulation of muscle fuel metabolism. Studies were performed using conditional, muscle-specific, PGC-1a gain-of-function and constitutive, generalized, loss-of-function mice. Forced expression of PGC-1a increased muscle glucose uptake concomitant with augmentation of glycogen stores, a metabolic response similar to post-exercise recovery. Induction of muscle PGC-1a expression prevented muscle glycogen depletion during exercise. Conversely, PGC-1a-deficient animals exhibited reduced rates of muscle glycogen repletion post-exercise. PGC-1a was shown to increase muscle glycogen stores via several mechanisms including stimulation of glucose import, suppression of glycolytic flux, and by downregulation of the expression of glycogen phosphorylase and its activating kinase, phosphorylase kinase a. These findings identify PGC-1a as a critical regulator of skeletal muscle fuel stores.


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