Effects of forced swimming stress on expression and phosphorylation of PI3K/Akt signal pathway in pancreas of type 2 diabetic rats

BACKGROUND: To study the effects of forced swimming stress on blood glucose and insulin levels and the expression and phosphorylation of pancreatic PI3K/Akt signal pathway in type 2 diabetic rats. METHODS: Thirty adult SD rats (8-week-old, male) were randomly divided into three groups: control group, diabetic model group, and diabetic model stress group. The diabetic model group was established by feeding with the high-fat and high-glucose diet for four weeks, and then the rats were injected with low-dose streptozotocin (STZ, 25 mg/kg, once a day for 2 days). The rats in the diabetic model group were subjected to forced swimming stress for seven days, which was a diabetic model stress group. Twenty-four hours after the last forced swimming stress, the rats fasted, and blood samples were collected to detect blood glucose, insulin, triglycerides (TGs), free fatty acids (FFAs), high- and low-density lipoprotein cholesterol (HDLC and LDLC) levels. The western blot was applied to detect the expression of PI3K, Akt, p-Akt, and mTOR in the pancreas of rats in each group. RESULTS: Blood glucose and insulin levels in the diabetic model stress group were significantly lower than those in the diabetic model group, and the protein levels of PI3K, p-AKT, and mTOR in the pancreas of the diabetic model stress group were significantly higher than those of the diabetic model group. CONCLUSIONS: One-week swimming stress can decrease the blood glucose level and improve insulin indexes in type 2 diabetic rats and increase the expression and phosphorylation of pancreatic PI3K/Akt signal pathway proteins.