The Effect of Six Weeks of Endurance Training on Mitochondrial Level of OPA-1 Quadriceps in Streptozotocin-induced Diabetic Rats

Mitochondrial dynamic disorders are attributed to many diseases such as diabetes. MFN2 and OPA-1 proteins are the main regulators of fusion, and DRP1 is the essential protein regulating mitochondrial fission. Increasing or decreasing the expression of relevant genes will cause an imbalance between these two processes. This study evaluated the effect of six weeks of aerobic training on mitochondrial levels of the OPA-1 quadriceps muscle in Streptozotocin-induced diabetic rats. 

In this study, 32 rats were randomly divided into four groups (n=8): healthy-control, healthy-exercise, diabetes-control, and diabetes-exercise. The animals ran on a treadmill according to the endurance training protocol five sessions per week for six weeks. Diabetes was induced by injecting Streptozotocin (50 mg/kg) solution. After the last training session, the rats were anesthetized by intraperitoneal injection of ketamine (90 mg/kg) and xylazine (10 mg/kg), and quadriceps muscle tissue was removed and maintained according to standard conditions. One-way ANOVA test was used to compare the groups at a significance level of 0.05, and the Tukey post hoc test was used to examine the differences between the means of the two groups.

Induction of diabetes significantly reduced OPA-1 levels in the quadriceps muscle tissue of the diabetic rats (p=0.012). Also, six weeks of aerobic training significantly increased the OPA-1 protein level in the quadriceps muscle of the trained diabetic rats (p=0.016).

Induced diabetes reduces the OPA-1 protein level, but aerobic exercise increases its level in diabetic rats, leading to increased fusion and thus improved mitochondrial function in the muscle tissue of rats.