PGC-1α is Dispensable for Exercise-Induced Mitochondrial Biogenesis in Skeletal Muscle
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CitationRowe, Glenn C., Riyad El-Khoury, Ian S. Patten, Pierre Rustin, and Zolt Arany. 2012. Pgc-1α is dispensable for exercise-induced mitochondrial biogenesis in skeletal muscle. PLoS ONE 7(7).
AbstractExercise confers numerous health benefits, many of which are thought to stem from exercise-induced mitochondrial biogenesis (EIMB) in skeletal muscle. The transcriptional coactivator PGC-1α, a potent regulator of metabolism in numerous tissues, is widely believed to be required for EIMB. We show here that this is not the case. Mice engineered to lack PGC-1α specifically in skeletal muscle (Myo-PGC-1αKO mice) retained intact EIMB. The exercise capacity of these mice was comparable to littermate controls. Induction of metabolic genes after 2 weeks of in-cage voluntary wheel running was intact. Electron microscopy revealed no gross abnormalities in mitochondria, and the mitochondrial biogenic response to endurance exercise was as robust in Myo-PGC-1αKO mice as in wildtype mice. The induction of enzymatic activity of the electron transport chain by exercise was likewise unperturbed in Myo-PGC-1αKO mice. These data demonstrate that PGC-1α is dispensable for exercise-induced mitochondrial biogenesis in skeletal muscle, in sharp contrast to the prevalent assumption in the field.
Citable link to this pagehttp://nrs.harvard.edu/urn-3:HUL.InstRepos:10436255
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