作者: Suman Das , Frederic Morvan , Benjamin Jourde , Viktor Meier , Peter Kahle
DOI: 10.1016/J.CMET.2015.05.006
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摘要: Mitochondrial dysfunction is associated with skeletal muscle pathology, including cachexia, sarcopenia, and the muscular dystrophies. ATP citrate lyase (ACL) a cytosolic enzyme that catalyzes mitochondria-derived into oxaloacetate acetyl-CoA. Here we report activation of ACL in results improved mitochondrial function. IGF1 induces an AKT-dependent fashion. This increase cardiolipin, thus increasing critical complexes supercomplex activity, resultant oxygen consumption cellular levels. Conversely, knockdown myotubes not only reduces complex I, IV, V activity but also blocks IGF1-induced increases consumption. In vivo, increased ATP. Activation this IGF1/ACL/cardiolipin pathway combines anabolic signaling induction mechanisms needed to provide required