Exercise training benefits pancreatic islet by modulating the insulin-like growth factor 1/phosphatidylinositol...

Diabetes is characterized by insulin resistance as well as impaired insulin production, with β-cell dysfunction playing a critical role in disease progression. Exercise is known to improve insulin sensitivity, but its effects on pancreatic islet quality and function remain poorly understood. This work hypothesized that swimming training enhances glycemic control and insulin secretion by upregulating the insulin-like growth factor 1 (IGF-1)/phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway in streptozotocin (STZ)-induced diabetic rats.

To investigate the effects of swimming on pancreatic islet quality and function in STZ-induced diabetic rats via the IGF-1/PI3K/AKT pathway.

Twenty-six Sprague-Dawley rats were grouped into diabetic and control groups, with each group further split into exercise and sedentary subgroups. Diabetic rats were induced with STZ. The exercise groups underwent swimming training for 60 minutes/day, 5 days/week, for 8 weeks. Body weight, food intake, blood glucose, insulin, lipids, and muscle glycogen were measured. Pancreatic islet morphology and the protein expression levels of IGF-1, PI3K, and AKT were analyzed. Data were analyzed using two-way repeated-measure ANOVA, followed by Tukey's post-hoc test.

Exercise training significantly improved body weight [diabetic exercise group (D-Ex): 390.66 ± 50.14 g vs diabetic sedentary group (D-Sed): 315.89 ± 50.12 g, P < 0.05], reduced blood glucose (D-Ex: 12.21 ± 4.43 mmol/L vs D-Sed: 17.79 ± 2.05 mmol/L, P < 0.05), and increased insulin levels (D-Ex: 53.50 ± 15.31 pmol/L vs D-Sed: 25.31 ± 10.23 pmol/L, P < 0.05) in diabetic rats. It also enhanced islet morphology, increased IGF-1 expression, and activated the PI3K/AKT pathway (P < 0.05). In-vitro experiments confirmed that IGF-1 positively regulated insulin expression and inhibited β-cell apoptosis via the PI3K/AKT pathway.

Exercise training improves pancreatic islet quality and function in diabetic rats by modulating the IGF-1/PI3K/AKT pathway, highlighting its therapeutic potential for diabetes management.