Role of AMP-Activated Protein Kinase in the Control of Glucose Homeostasis

Author(s): B. R. Barnes, J. R. Zierath.

Journal Name: Current Molecular Medicine

Volume 5 , Issue 3 , 2005

Become EABM
Become Reviewer


Skeletal muscle insulin resistance is a hallmark feature of Type 2 diabetes. Physical exercise/muscle contraction elicits an insulin-independent increase in glucose transport and perturbation of this pathway may bypass defective insulin signaling. To date, the exercise-responsive signaling molecules governing glucose metabolism in skeletal muscle are largely unknown. AMPactivated protein kinase (AMPK) has been suggested as one of the exercise-responsive signaling molecules involved in glucose homeostasis and consequently it has been heavily explored as a pharmacological target for the treatment of Type 2 diabetes. AMPK exists in heterotrimeric complexes composed of a catalytic α-subunit and regulatory β- and γ-subunits. The γ3-isoform of AMPK is expressed specifically in skeletal muscle of humans and rodents and this tissue specific expression pattern offers selectivity in AMPK action. Furthermore, mutations in the AMPK γ3-isoform may provide protection from diet-induced insulin resistance by increasing lipid oxidation in the presence of increased lipid supply. This review highlights the current understanding of the role of the regulatory AMPK γ3-isoform in the control of skeletal muscle metabolism.

Keywords: skeletal muscle, amp-activated protein kinase, exercise, type diabetes, insulin resistance, metabolism

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2005
Page: [341 - 348]
Pages: 8
DOI: 10.2174/1566524053766103
Price: $58

Article Metrics

PDF: 7