Meghan Kelly

TL;DR: It is reported here that incubation with IL-6 increases the phosphorylation of AMPK and that of its target molecule, acetyl CoA carboxylase, in both extensor digitorum longus muscle and cultured F422a adipocytes, and that this contributes to, but does not fully account for, the increase in AMPK activity in these tissues in response to exercise.

TL;DR: The results indicate that TZDs can act within minutes to activate AMPK in mammalian tissues and suggest that this effect is associated with a change in cellular energy state and that it is not dependent on PPARgamma-mediated gene transcription.

TL;DR: It is found that AMPK activity is diminished in muscle and adipose tissue of 3-month-old IL-6 knockout (KO) mice at rest and that the absolute increases in AM PK activity in these tissues caused by exercise is diminished compared with control mice.

TL;DR: The findings indicate the retention of dysfunctional mitochondria in MERKO muscle and implicate ERα in the preservation of mitochondrial health and insulin sensitivity as a defense against metabolic disease in women.

TL;DR: Findings raise the possibility that glucose-induced changes in AMPK are linked to alterations in SIRT1 abundance and activity and possibly cellular redox state.