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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, Clinton R., Carey, Andrew L., Hawley, John A. and Febbraio, Mark A. 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, doi: 10.2337/diabetes.52.9.2338.

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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, Clinton R.ORCID iD for Bruce, Clinton R. orcid.org/0000-0002-0515-3343
Carey, Andrew L.
Hawley, John A.
Febbraio, Mark A.
Journal name Diabetes
Volume number 52
Issue number 9
Start page 2338
End page 2345
Total pages 8
Publisher American Diabetes Association
Place of publication Alexandria, Va
Publication date 2003
ISSN 0012-1797
1939-327X
Keyword(s) Citrate synthase
Critical threshold
Dual-energy X-ray absorptiometry
Free fatty acid
Fat-free mass
Glucose disposal rate
β-hyroxyacyl-CoA dehydrogenase
Heme oxygenase
Heat shock protein
Intramuscular triglyceride
c-Jun NH2-terminal kinase
Myeloperoxidase
Nitric oxide synthase
Peroxisome proliferator–activated receptor
Reactive oxygen species
Tumor necrosis factor
Summary 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 β-hyroxyacyl-CoA dehydrogenase (β-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 β-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.
Language eng
DOI 10.2337/diabetes.52.9.2338
Field of Research 119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Persistent URL http://hdl.handle.net/10536/DRO/DU:30067064

Document type: Journal Article
Collections: Faculty of Health
School of Exercise and Nutrition Sciences
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