Molecular mechanism by which AMP-activated protein kinase activation promotes glycogen accumulation in muscle.

ABSTRACT:

Objective

During energy stress, AMP-activated protein kinase (AMPK) promotes glucose transport and glycolysis for ATP production, while it is thought to inhibit anabolic glycogen synthesis by suppressing the activity of glycogen synthase (GS) to maintain the energy balance in muscle. Paradoxically, chronic activation of AMPK causes an increase in glycogen accumulation in skeletal and cardiac muscles, which in some cases is associated with cardiac dysfunction. The aim of this study was to elucidate the molecular mechanism by which AMPK activation promotes muscle glycogen accumulation.

Research design and methods

We recently generated knock-in mice in which wild-type muscle GS was replaced by a mutant (Arg582Ala) that could not be activated by glucose-6-phosphate (G6P), but po

SUBMITTER: Hunter RW 

PROVIDER: S-EPMC3046837 | biostudies-literature | 2011 Mar

REPOSITORIES: biostudies-literature