The Effects of Exercise on Cerebellar Growth-Associated Protein 43 and Adenylyl Cyclase- Associated Protein 1 Gene Expression and Proteins in Diabetic-Induced Neuropathy and Healthy Male Wistar Rats

BACKGROUND: The effect of exercise on the cerebellum cells in diabetic-induced neuropathy and healthy situations is not clear yet. Growth-associated protein 43 (GAP-43) and adenylyl cyclase-associated protein 1 (CAP-1) proteins can restore nerve cells. This study aimed to investigate the effect of aerobic exercise on GAP-43 and CAP-1 and their mRNA in the cerebellar tissue of diabetic-induced neuropathy and healthy Wistar rats. METHODS: Around 40 healthy male Wistar rats with a mean weight of 271 ± 11.2 g were divided randomly into four groups; healthy aerobic exercise, diabetic-aerobic exercise, healthy-control, and diabetic-control. The exercise group performed aerobic exercise 5 days per week for 6 weeks. RESULTS: Exercise increased CAP1 protein in the cerebellum tissue of healthy (P = 0.002) and diabetic (P = 0.002) groups compared with matched control groups. The effect of exercise on CAP1 was greater in diabetic compared with the healthy group (P = 0.002). The expression of CAP1 mRNA in the cerebellum was higher in the healthy exercise compared with the healthy control group (P = 0.002) and in the healthy exercise compared with the diabetic exercise group (P = 0.026). GAP43 protein was lower in the healthy exercise compared with the healthy control group (P = 0.002) while it was higher in diabetic exercise compared to the healthy exercise group (P = 0.002). Expression of GAP43 mRNA in the cerebellum was higher in the healthy (P = 0.002) and diabetic (P = 0.002) exercise groups compared to non-exercise matched groups and in the diabetic control group compared with the healthy control group (P = 0.002). Exercise improved latency in diabetic (P = 0.001) and healthy exercise groups (P = 0.02). No significant difference was found in blood glucose between exercise and control groups (P > 0.05). CONCLUSION: Exercise improved cerebellar functions in healthy and diabetic rats, probably mediating by CAP1 protein, even without changing blood glucose.