Abstract:
:Mitochondrial dysfunction is associated with skeletal muscle pathology, including cachexia, sarcopenia, and the muscular dystrophies. ATP citrate lyase (ACL) is a cytosolic enzyme that catalyzes mitochondria-derived citrate into oxaloacetate and acetyl-CoA. Here we report that activation of ACL in skeletal muscle results in improved mitochondrial function. IGF1 induces activation of ACL in an AKT-dependent fashion. This results in an increase in cardiolipin, thus increasing critical mitochondrial complexes and supercomplex activity, and a resultant increase in oxygen consumption and cellular ATP levels. Conversely, knockdown of ACL in myotubes not only reduces mitochondrial complex I, IV, and V activity but also blocks IGF1-induced increases in oxygen consumption. In vivo, ACL activity is associated with increased ATP. Activation of this IGF1/ACL/cardiolipin pathway combines anabolic signaling with induction of mechanisms needed to provide required ATP.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Das S,Morvan F,Jourde B,Meier V,Kahle P,Brebbia P,Toussaint G,Glass DJ,Fornaro Mdoi
10.1016/j.cmet.2015.05.006subject
Has Abstractpub_date
2015-06-02 00:00:00pages
868-76issue
6eissn
1550-4131issn
1932-7420pii
S1550-4131(15)00218-1journal_volume
21pub_type
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