Abstract
Diabetic myopathy refers to the manifestations in the skeletal muscle as a result of altered glucose homeostasis which reflects as fibrosis. Since physical exercise has been indicated a protective strategy for improving glucose metabolism in skeletal muscle, we tested a hypothesis under which the endurance exercise training could reverse the produced skeletal muscle fibrosis by diabetes. Eight-week-old male Wistar rats were randomly assigned into four groups including healthy control (HC), healthy trained (HT), diabetic control (DC), and diabetic trained (DT) groups. Diabetes was induced by a single intraperitoneal injection of streptozotocin (STZ; 45 mg/kg). Rats in the HT and DT groups carried out an exercise program on a motorized treadmill for five days a week over six weeks. Skeletal muscle levels of NRG1and ErbB2 were measured by the Western blot method. Exercise training decreased blood glucose levels in the DT group. Induction of diabetes increased skeletal muscle fibrosis in both the fast extensor digitorum longus (EDL) and slow soleus muscles, while endurance training modified it in diabetic trained rats. Moreover, muscle NRG1and ErbB2 levels were increased in diabetic rats, while training modified muscle NRG1and ErbB2 levels in diabetic trained rats. Our study provides novel evidence that endurance training could modify skeletal muscle fibrosis through NRG1/ErbB2 modification in STZ-induced diabetic rats.
Highlights
According to the International Diabetes Federation (IDF), there were approximately 425 million people living with diabetes worldwide in 2017, out of which 5% to 10% are estimated to have T1DM (42.5 to 95 million) [1]
Diabetic myopathy, which is characterized by decreased muscle capacity, strength, and mass [4], is a complication of diabetes mellitus and directly affects the mortality rate due to the fact that the skeletal muscle is the largest source of glucose consumption, and any changes in its health can affect the metabolism of whole-body glucose [5]
Before starting the training protocol, the blood glucose level of the diabetic control (DC) group had a significant difference from healthy control (HC) (P = 0:001), and the significant difference was maintained at the end of six weeks
Summary
According to the International Diabetes Federation (IDF), there were approximately 425 million people living with diabetes worldwide in 2017, out of which 5% to 10% are estimated to have T1DM (42.5 to 95 million) [1]. Skeletal muscle responds to many stimuli through changes in muscle size, distribution of fiber types, or metabolism [2]. Diabetic myopathy, which is characterized by decreased muscle capacity, strength, and mass [4], is a complication of diabetes mellitus and directly affects the mortality rate due to the fact that the skeletal muscle is the largest source of glucose consumption, and any changes in its health can affect the metabolism of whole-body glucose [5]. GLUT4 is an important component in the transfer of glucose into the muscle cell. It can enter the cell surface through exercise and cause glucose to enter the cell (independent of insulin) and neuregulin 1 (NRG1) can facilitate the above process [6]
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