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

Bruce, C, Carey, A, Hawley, J and Febbraio, M 2003, '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', Diabetes, vol. 52, no. 9, pp. 2338-2345.


Document type: Journal Article
Collection: Journal Articles

Title 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
Author(s) Bruce, C
Carey, A
Hawley, J
Febbraio, M
Year 2003
Journal name Diabetes
Volume number 52
Issue number 9
Start page 2338
End page 2345
Total pages 8
Publisher American Diabetes Association
Abstract 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.
Subject Endocrinology
DOI - identifier 10.2337/diabetes.52.9.2338
Copyright notice © 2003 American Diabetes Association
ISSN 0012-1797
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