Type II diabetes is characterized by defects in insulin action on peripheral tissues, such as skeletal muscle, adipose tissue and liver and pancreatic β-cell defects. Since the skeletal muscle accounts for approx. 75% of whole body insulin-stimulated glucose uptake, defects in this tissue play a major role in the impaired glucose homoeostasis in Type II diabetic patients. Thus identifying defective steps in this process may reveal attractive targets for drug development to combat insulin resistance and Type II diabetes. This review will describe the effects of insulin on glucose transport and other metabolic events in skeletal muscle that are mediated by intracellular signalling cascades. Evidence for impaired activation of the insulin receptor signalling cascade and defective glucose transporter 4 translocation in the skeletal muscle from Type II diabetic patients will be presented. Through the identification of the intracellular defects in insulin action that control glucose homoeostasis, a better understanding of the disease pathogenesis can be gained and strategies for intervention may be developed.
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Conference Article|
April 01 2005
Insulin signal transduction in human skeletal muscle: identifying the defects in Type II diabetes
M. Björnholm;
M. Björnholm
1Department of Surgical Sciences, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden
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J.R. Zierath
J.R. Zierath
1
1Department of Surgical Sciences, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden
1To whom correspondence should be addressed (email Juleen.Zierath@fyfa.ki.se).
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Publisher: Portland Press Ltd
Received:
November 01 2004
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2005 The Biochemical Society
2005
Biochem Soc Trans (2005) 33 (2): 354–357.
Article history
Received:
November 01 2004
Citation
M. Björnholm, J.R. Zierath; Insulin signal transduction in human skeletal muscle: identifying the defects in Type II diabetes. Biochem Soc Trans 1 April 2005; 33 (2): 354–357. doi: https://doi.org/10.1042/BST0330354
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