The effect of high intensity interval training on asprosin and oxidative stress in the heart tissue of diabetic male rats

The release of adipokines from adipose tissue depots plays a crucial role in regulating metabolic homeostasis and several other physiological processes in cardiovascular diseases caused by diabetes. In this study, we investigated the effect of high-intensity interval training (HIIT) on asprosin and oxidative stress of heart tissue type 2 diabetic male rats. 24 male Sprague-Dawley rats were divided into four groups: control (C), control training (CT), diabetes (D), and diabetes training (DT). Diabetes was induced by a high-fat diet and low-dose streptozotocin injection. The training group performed 8-week HIIT program on the treadmill. Two-way ANOVA was used to analyse data (P < 0.05). The results showed that there was no significant interaction in plasma asprosin (P = 0.34) and SOD2 (P = 0.5), but a significant interaction in heart tissue asprosin (P = 0.002) and P-ERK 1/2 (P < 0.0001) was found. Serum and heart tissue asprosin were higher in Group D than in Group C (p < 0.0001), and also decreased in Group CT compared to Group C (P < 0.0001, P = 0.03), and Group DT compared to Group D (P = 0.0004, P = 0.04). P-ERK 1/2, SOD2, GPX, and HDL-c were lower in Group D than Group C (P = 0.002, P = 0.01, P = 0.002, P = 0.01, respectively) and increased in Group CT compared to Group C (P = 0.001, P = 0.03, P = 0.03, P = 0.02, respectively), and Group DT compared to Group D (P < 0.0001, P = 0.002, P = 0.001, P = 0.02, respectively). There was no significant difference between groups in MDA, HOMA, LDL-c, and TG between Group C and Group CT, but it is lower in Group DT than Group D (P = 0.003, P < 0.0001, P = 0.01, P = 0.003, respectively). Asprosin is increased in type 2 diabetic rats, and HIIT reduces asprosin and oxidative stress in the heart and improves insulin resistance and lipid profile. Decreased asprosin may have a cardioprotective effect by activating downstream pathways, including regulating P-ERK 1/2 expression and increasing the antioxidant enzyme SOD2.