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1 Department of Physiology, University of Kuopio, Kuopio, Savo, Finland; Laboratory of Molecular Medicine, Department of Surgery, The Ohio State University Medical Center, Dorothy M. Davis Heart & Lung Research Institute, Columbus, OH, USA
2 Department of Physiology, University of Kuopio, Kuopio, Savo, Finland; Departments of Pathology and Surgery, Tampere University Hospital and Tamere University Medical School, Kuopio, Savo, Finland
3 Department of Physiology, University of Kuopio, Kuopio, Savo, Finland
4 Laboratory of Molecular Medicine, Department of Surgery, The Ohio State University Medical Center, Dorothy M. Davis Heart & Lung Research Institute, Columbus, OH, USA
* To whom correspondence should be addressed. E-mail: sen-1{at}medctr.osu.edu.
Strenuous exercise induces oxidative stress and modification of intracellular proteins. Exercise training, however, up-regulates endogenous antioxidant defenses and heat shock protein (HSP) expression. In diabetes, perturbations in the endogenous antioxidant and HSP protection have been reported. The aim of this study was to examine the effect of eight weeks of endurance training on HSP expression and oxidative stress markers in the skeletal muscle, heart and liver of streptozotocin-induced diabetic (SID) and non-diabetic control rats. Induction of diabetes decreased HSP72 expression in heart, liver and vastus lateralis (VL) muscles. SID increased heme oygenase-1 (HO-1), an oxidative stress inducible heat shock protein, in liver, red gastrocnemius (RG) and VL muscles and glucose-regulated protein 75 (GRP75) in liver. SID increased HSP90 levels in the heart, but levels decreased in the liver. Diabetes induced oxidative stress marker protein carbonyl levels and tissue inflammation. Although endurance training increased the expression of HSP72 in all the tissues examined, this induction was less pronounced in diabetic rats than in non-diabetic controls. Furthermore, endurance training induced the activation and expression of transcriptional regulator heat shock factor-1 (HSF-1) only in non-diabetic control animals. In summary, diabetes may increase susceptibility to oxidative damage and impair HSP protection but endurance training may offset some of the adverse effects of diabetes by up-regulating tissue HSP expression. Our results suggest that diabetes impairs HSP protection possibly via transcriptionally mediated mechanisms.
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