Effect of treadmill exercise on skeletal muscle autophagy in rats with obesity induced by a high-fat diet

Abstract

[Purpose]This study aimed to investigate the effects of treadmill exercise on body weight, blood biochemistry, and autophagy.[Methods]Triglyceride, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, insulin, and glucose levels were measured, the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) score was calculated, and the soleus muscle was analyzed for autophagy-related factors (Beclin-1, p62, LC3, Lamp-2) in rats with obesity induced by a high-fat diet. Eight-week-old Sprague Dawley rats were fed a high-fat diet for 35 weeks and then subjected to 10 weeks of treadmill exercise. The experimental group was divided into a Normal Diet-Sedentary (ND-SED, n=8) group, an (High-Fat Diet-Sedentary (HF-SED, n=8) group, and an High-Fat Diet + Treadmill Exercise (HF-TE, n=8) group. The intensity of treadmill exercise was set as 8 m/min for 5 min, 11 m/min for 5 min, 15 m/min for 20 min, and 11 m/min for the last 5 minutes. A glucose tolerance test was performed at the 2nd and 8th week of exercise by sampling of tail blood.[Results]With endurance exercise, the HFTE group showed a significant decrease in body weight, with improved blood biochemical indices and HOMA-IR scores, in comparison with the HF-SED group. However, there was no significant difference in Beclin-1, p62, LC3, and Lamp-2 proteins as measured by autophagic flux in the soleus muscle.[Conclusion]Treadmill exercise induced improvements in body weight, body fat, and biochemical indicators of obesity and Type 2 diabetes, but had no effect on autophagy in soleus muscle.

Type 2 diabetes causes skeletal muscle atrophy but does not impair resistance training‐mediated myonuclear accretion and muscle mass gain in rats

“…In this study, changes in LC3 and p62 were measured to evaluate the progression of autophagy (Sakuma et al, 2016); T2DM rats did not show any change in their levels as compared with those in healthy control rats in the resting state and after RT. These observations were consistent with previous studies (Cho, Choi, & Cho, 2017;Turpin et al, 2009). p62 expression is known to increase in skeletal muscle at an early period of RT (Ulbricht et al, 2015).…”

Effects of propofol on LC3II and mTOR/p‑mTOR expression during ischemia‑reperfusion myocardium injury in rats with type 2 diabetes mellitus

“…The degree of injury in myocardial cells and mitochondria in the LP and HP group was between the CI and MP group (Figs. [5][6][7][8][9].…”

“…A previous study in rats demonstrated that autophagy is closely associated with T2DM (5,6) and myocardial ischemia reperfusion injury (MIRI) (7). Mammalian target of rapamycin (mTOR) is a key regulator of cell growth, autophagy, translation and survival (8).…”

Mitochondrial destiny in type 2 diabetes: the effects of oxidative stress on the dynamics and biogenesis of mitochondria

“…Because dysfunctional mitochondria contribute to the development of IR, autophagy is essential to maintain the normal functioning of mitochondria and glucose metabolism. It has been shown that, against the background of IR, skeletal muscle and liver cells suppress the autophagy of organelles (Cho, Choi & Cho, 2017).…”