Premium
AMP‐activated protein kinase in contraction regulation of skeletal muscle metabolism: necessary and/or sufficient?
Author(s) -
Jensen T. E.,
Wojtaszewski J. F. P.,
Richter E. A.
Publication year - 2009
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2009.01979.x
Subject(s) - ampk , skeletal muscle , mitochondrial biogenesis , amp activated protein kinase , protein kinase a , myosin , anabolism , microbiology and biotechnology , glucose uptake , biology , muscle contraction , biochemistry , chemistry , endocrinology , medicine , kinase , mitochondrion , insulin
In skeletal muscle, the contraction‐activated heterotrimeric 5′‐AMP‐activated protein kinase (AMPK) protein is proposed to regulate the balance between anabolic and catabolic processes by increasing substrate uptake and turnover in addition to regulating the transcription of proteins involved in mitochondrial biogenesis and other aspects of promoting an oxidative muscle phenotype. Here, the current knowledge on the expression of AMPK subunits in human quadriceps muscle and evidence from rodent studies suggesting distinct AMPK subunit expression pattern in different muscle types is reviewed. Then, the intensity and time dependence of AMPK activation in human quadriceps and rodent muscle are evaluated. Subsequently, a major part of this review critically examines the evidence supporting a necessary and/or sufficient role of AMPK in a broad spectrum of skeletal muscle contraction‐relevant processes. These include glucose uptake, glycogen synthesis, post‐exercise insulin sensitivity, fatty acid (FA) uptake, intramuscular triacylglyceride hydrolysis, FA oxidation, suppression of protein synthesis, proteolysis, autophagy and transcriptional regulation of genes relevant to promoting an oxidative phenotype.