{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Rowe GC"],"funding":["NHLBI NIH HHS"],"pagination":["e41817"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3404101"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(7)"],"pubmed_abstract":["Exercise 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."],"journal":["PloS one"],"pubmed_title":["PGC-1α is dispensable for exercise-induced mitochondrial biogenesis in skeletal muscle."],"pmcid":["PMC3404101"],"funding_grant_id":["5T32HL007374-31","5R01HL094499-02","R01 HL094499","T32 HL007374"],"pubmed_authors":["Rustin P","Rowe GC","El-Khoury R","Patten IS","Arany Z"],"additional_accession":[]},"is_claimable":false,"name":"PGC-1α is dispensable for exercise-induced mitochondrial biogenesis in skeletal muscle.","description":"Exercise 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.","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012","modification":"2025-04-21T16:34:21.483Z","creation":"2019-03-26T23:10:51Z"},"accession":"S-EPMC3404101","cross_references":{"pubmed":["22848618"],"doi":["10.1371/journal.pone.0041817"]}}