Metabolic control of muscle mitochondrial function and fatty acid oxidation through SIRT1/PGC‐1α

作者: Zachary Gerhart-Hines , Joseph T Rodgers , Olivia Bare , Carles Lerin , Seung-Hee Kim

DOI: 10.1038/SJ.EMBOJ.7601633

关键词: NicotinamideOxidative phosphorylationBiologyP300-CBP Transcription FactorsBeta oxidationSkeletal muscleBiochemistryEnoyl-CoA hydrataseMitochondrionDownregulation and upregulation

摘要: In mammals, maintenance of energy and nutrient homeostasis during food deprivation is accomplished through an increase in mitochondrial fatty acid oxidation peripheral tissues. An important component that drives this cellular oxidative process the transcriptional coactivator PGC‐1α. Here, we show fasting induced PGC‐1α deacetylation skeletal muscle SIRT1 required for activation genes. Moreover, expression acetyltransferase, GCN5, or inhibitor, nicotinamide, induces acetylation decreases target genes myotubes. Consistent with a switch from glucose to occurs states, induction response low concentrations. Thus, have identified as functional regulator metabolic gene transcription program oxidation. These results implications understanding selective adaptation how it might impact lifespan diseases such obesity diabetes.

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