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

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. 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. 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. 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.