Abstract

There is abundant evidence that ATP sensitive potassium (KATP) channels play cytoprotective role in cardiac myocytes, allowing the cell to couple metabolic state to electrical activity of the cell membrane. In cardiac myocytes Kir6.2/SUR2A are the major subunits expressed. However, expression or function of KATP channels has been found to be impaired in the presence of persistent hyperglycemia in diabetes mellitus (DM). While regular exercise can improve hyperglycemic status in DM, its impact on the expression of KATP channels subunits in heart is unknown. PURPOSE: To assess the effect of regular exercise on expression of KATP channel subunits in heart of streptozotocin-induced diabetic rats. METHODS: Male Wistar rats (25 days old) were randomly divided into four groups, among them: sedentary control, trained control, sedentary diabetic, trained diabetic. Diabetes was induced by a single streptozotocin injection (100 mg/kg body weight), animals with fasting blood glucose levels ≥ 300 mg/dL were considered as diabetic. Groups with training program performed exercise on a treadmill (30 minutes daily, 5 days/week) for 8 weeks. At the end of the intervention, two subunits of cardiac KATP channel (SUR2A and Kir 6.2) were analyzed as indicators and quantitative analysis of these subunits was achieved with real-time RT–PCR. RESULTS: In control conditions, the regular exercise reduced Kir6.2 subunit mRNA levels significantly (76%; p=0.045) in heart. In diabetes, reduced Kir6.2 expression was also observed, and there was no difference in expression levels between sedentary diabetic and trained diabetic groups (P > 0.05). Otherwise, relative mRNA expression of the subunit SUR2A was increased in both sedentary diabetic and trained diabetic groups (80.33% and 86.08%, respectively). CONCLUSION: Collectively, our data demonstrate that the regular exercise modifies expression of KATP channel subunits of heart only in control conditions. However, the gene expression patterns of KATP channel subunits are different during diabetes, by increased SUR2A and decreased Kir6.2, which was not modified by exercise. These results may provide an opportunity to understand mechanisms leading to diabetic cardiomyopathy during stress and exercise in DM.

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