Journal
CELL METABOLISM
Volume 12, Issue 6, Pages 633-642Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2010.11.008
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Funding
- NIH [DK45416, HL58427]
- Neuroscience Blueprint Interdisciplinary [P30 NS057105]
- American Diabetes Association [AR050429]
- Deutsche Forschungsgemeinschaft [ZE 796/2-1]
- Digestive Diseases Research Center at Washington University School of Medicine (WUSM) [P30 DK052574]
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Evidence is emerging that the PGC-1 coactivators serve a critical role in skeletal muscle metabolism, function, and disease. Mice with total PGC-1 deficiency in skeletal muscle (PGC-1 alpha(-/-)beta(f/f/MLC-Cre) mice) were generated and characterized. PGC-1 alpha(-/-)beta(f/f/MLC-Cre) mice exhibit a dramatic reduction in exercise performance compared to single PGC-1 alpha- or PGC-1 beta-deficient mice and wild-type controls. The exercise phenotype of the PGC-1 alpha(-/-)beta(f/f/MLC-Cre) mice was associated with a marked diminution in muscle oxidative capacity, together with rapid depletion of muscle glycogen stores. In addition, the PGC-1 alpha/beta-deficient muscle exhibited mitochondrial structural derangements consistent with fusion/fission and biogenic defects. Surprisingly, the proportion of oxidative muscle fiber types (I, IIa) was not reduced in the PGC-1 alpha(-/-)beta(f/f/MLC-Cre) mice. Moreover, insulin sensitivity and glucose tolerance were not altered in the PGC-1 alpha(-/-)beta(f/f/MLC-Cre) mice. Taken together, we conclude that PGC-1 coactivators are necessary for the oxidative and mitochondrial programs of skeletal muscle but are dispensable for fundamental fiber type determination and insulin sensitivity.
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