Amino acid deprivation due to overexpression of UCP1 in skeletal muscle: signalling via FGF-21

ABSTRACT: Recent studies on mouse and human skeletal muscle (SM) demonstrated the important link between mitochondrial function and the cellular metabolic adaptation. To identify key compensatory molecular mechanisms in response to chronic mitochondrial distress, we analyzed mice with ectopic SM respiratory uncoupling in uncoupling protein 1 transgenic (UCP1-TG) mice as model of muscle-specific compromised mitochondrial function. Here we describe a detailed metabolic reprogramming profile associated with mitochondrial perturbations in SM, triggering an increased protein turnover and amino acid metabolism with induced biosynthetic serine/1-carbon/glycine pathway and the longevity-promoting polyamine spermidine as well as the trans-sulfuration pathway. This is related to an induction of NADPH-generati

ORGANISM(S): Mus musculus

SUBMITTER: Evert van Schothorst 

PROVIDER: E-GEOD-45991 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress