the effect of resistance training on pi3k/mtorc1 signaling in left ventricle of diabetic rats

Background: clinical evidence supports the influential role of genetic factors and intracellularsignaling pathways in physiological cardiac hypertrophy. this study aimed to assess the response ofthe pi3k/mtorc1 signaling pathway in cardiac tissue to resistance training in obese rats with type2 diabetes (t2d).materials and methods: a total of 21 male wistar rats (mean±sd weight: 220±20 g) were obeseby 6 weeks high-fat diet (hfd) and randomly assigned to 1) non-diabetic, 2) control t2d, and 3)exercise diabetic groups. t2d was induced by intraperitoneal injection of streptozotocin (30 mg/kg)for diabetic groups. the exercise group did the resistance exercise program (5 times per week for 6weeks). after exercise training, pi3k and mtorc1 expression in the left ventricle and the ratio of theleft ventricle to heart and heart to body weight were compared between groups. the obtained datawere compared by 1-way analysis of variance (anova) (p<0.05).results: induction of diabetes resulted in significant decrease in all mentioned variables in controldiabetic to non-diabetic rats (pi3k; p=0.021, mtorc1; p=0.004, left ventricle/heart weight; p=0.045,heart/body weight; p=0.035). significant increase was observed in all variables (pi3k; p=0.028,mtorc1; p=0.015, left ventricular/heart weight; p=0.002, heart/body weight; p=0.001) in responseto resistance training compared to the control rat.conclusion: based on our results, cardiac hypertrophy in studied diabetic rats can be attributed toimproved pi3k/mtorc1 signaling in response to resistance training. exploring the exact mechanismsresponsible for these changes in response to exercise requires further molecular-cellular studies.