Abstract
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
Current Molecular Medicine
Title: Role of AMP-Activated Protein Kinase in the Control of Glucose Homeostasis
Volume: 5 Issue: 3
Author(s): B. R. Barnes and J. R. Zierath
Affiliation:
Keywords: skeletal muscle, amp-activated protein kinase, exercise, type diabetes, insulin resistance, metabolism
Abstract: 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.
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Cite this article as:
Barnes R. B. and Zierath R. J., Role of AMP-Activated Protein Kinase in the Control of Glucose Homeostasis, Current Molecular Medicine 2005; 5 (3) . https://dx.doi.org/10.2174/1566524053766103
DOI https://dx.doi.org/10.2174/1566524053766103 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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