Participation of AMPK in the control of skeletal muscle mass

Abstract

The skeletal muscle plays crucial roles in whole-body glucose, lipid, and energy metabolism and in locomotive functions. The maintenance of the skeletal muscle mass is regulated by protein turnover: the balance between protein synthesis and protein degradation. The metabolic sensor 5’ AMP-activated protein kinase (AMPK) has important functions in the maintenance of cellular homeostasis and modulates glucose, lipid, and protein metabolism in the skeletal muscle. Recent studies warrant consideration of AMPK as a crucial regulator of muscle mass and suggest that AMPK controls skeletal muscle hypertrophy and atrophy by suppressing protein synthesis and promoting protein degradation via various signaling pathways. In addition, AMPK may stimulate myogenesis and regeneration of the skeletal muscle from injury. Conversely, the lack of AMPK activation probably restricts protein turnover during aging, potentially contributing to muscle loss. Taken together, these data indicate that AMPK triggers accelerated muscle turnover by regulating protein metabolism and/or myogenesis and thereby facilitates muscle mass homeostasis.