Investigating the effect of Resistance Training on the Axis / IGF-1 PI3K in Skeletal Muscle and Insulin Sensitivity in Type 2 Diabetic Rats

IGF-1 is a polypeptide hormone that plays a vital role in the development and regeneration of skeletal muscles.IGF-1 activates anabolic pathways such as PI3K and IRS-1/2 to activate a series of intracellular anabolic signals. The purpose of this study was to investigate the effect of 8 weeks resistance training on IGF1, PI3K and insulin sensitivity in neural muscle in type 2 diabetic rats.

In this experimental study, 14 male Wistar mice aged 8 to 10 weeks and induction of type 2 diabetes (type 2 diabetes was induced by intraperitoneal injection of nicotinamide and STZ in diabetic groups) and were divided into two groups of resistance training and control groups. The mice in the control group did not exercise during the study, while the resistance group performed 8 weeks of training for 5 sessions per week. Resistance exercises in each session were performed in the form of 10 repetitions with 90-second rest intervals in the form of climbing a 26-step ladder to a height of one meter with a vertical slope of 85%, and weight was applied to the base of the rat's tail. 48 hours after the last training session, blood samples were taken from the heart and neural muscle tissue was extracted. Real Time-PCR method was used to determine the genes and one-way ANOVA test was used to compare the variables. All statistical studies were done using SPSS version 16 software.

The results of this study showed that expression of IGF-1 and PI3K in the duodenal axis of diabetic rats in resistance training group was significantly higher than that of the control group (P = 0.001) (P = 0.11). Serum insulin sensitivity in diabetic rats was not significantly different in diabetic rats compared to the diabetic rats (P=0.778).

It seems that eight weeks of resistance training can be a strong stimulus on IGF-1 and PI3K gene expression and no change in insulin sensitivity in neural muscle in type 2 diabetic rats.