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Diabetes 52:2338-2345, 2003
© 2003 by the American Diabetes Association, Inc.

Intramuscular Heat Shock Protein 72 and Heme Oxygenase-1 mRNA Are Reduced in Patients With Type 2 Diabetes

Evidence That Insulin Resistance Is Associated With a Disturbed Antioxidant Defense Mechanism

Clinton R. Bruce1, Andrew L. Carey2, John A. Hawley1, and Mark A. Febbraio2

1 Exercise Metabolism Group, School of Medical Sciences, RMIT University, Bundoora, Victoria, Australia
2 Skeletal Muscle Research Laboratory, School of Medical Sciences, RMIT University, Bundoora, Victoria, Australia

To examine whether genes associated with cellular defense against oxidative stress are associated with insulin sensitivity, patients with type 2 diabetes (n = 7) and age-matched (n = 5) and young (n = 9) control subjects underwent a euglycemic-hyperinsulinemic clamp for 120 min. Muscle samples were obtained before and after the clamp and analyzed for heat shock protein (HSP)72 and heme oxygenase (HO)-1 mRNA, intramuscular triglyceride content, and the maximal activities of ß-hyroxyacyl-CoA dehydrogenase (ß-HAD) and citrate synthase (CS). Basal expression of both HSP72 and HO-1 mRNA were lower (P < 0.05) by 33 and 55%, respectively, when comparing diabetic patients with age-matched and young control subjects, with no differences between the latter groups. Both basal HSP72 (r = 0.75, P < 0.001) and HO-1 (r = 0.50, P < 0.05) mRNA expression correlated with the glucose infusion rate during the clamp. Significant correlations were also observed between HSP72 mRNA and both ß-HAD (r = 0.61, P < 0.01) and CS (r = 0.65, P < 0.01). HSP72 mRNA was induced (P < 0.05) by the clamp in all groups. Although HO-1 mRNA was unaffected by the clamp in both the young and age-matched control subjects, it was increased (P < 0.05) ~70-fold in the diabetic patients after the clamp. These data demonstrate that genes involved in providing cellular protection against oxidative stress are defective in patients with type 2 diabetes and correlate with insulin-stimulated glucose disposal and markers of muscle oxidative capacity. The data provide new evidence that the pathogenesis of type 2 diabetes involves perturbations to the antioxidant defense mechanism within skeletal muscle.

Address correspondence and reprint requests to Mark A. Febbraio, PhD, Associate Professor Research, Skeletal Muscle Research Laboratory, School of Medical Sciences, RMIT University, P.O. Box 71, Bundoora 3083, Victoria, Australia. E-mail: mark.febbraio{at}rmit.edu.au


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