Protective effects of HIIT vs. CET exercise training on high-fat-high-fructose diet-induced hyperglycemia, hyperlipidemia, and histopathology of liver in rats: regulation of SIRT1/PGC-1α

Background Disruption of the function of sirtuin1 (SIRT1) has been reported to link with diabetes and metabolic disorders. Aim The aim of this study was to investigate the effect of a modified high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) or continuous endurance training (CET) program on Sirt1 and PGC-1 alpha mRNA gene expression in hepatocytes of high-fat/high-fructose diet-induced diabetes in rats. Methods Twenty-eight male Wistar rats (220 +/- 20 g) were randomly divided into four groups of non-diabetic (NDC), diabetic control (received high fat high-fructose diet (HFHFD-DC)), CET (HFHFD-CET), and HIIT (HFHFD-HIIT). Diabetes was induced by feeding rats a high-fat (30%) high-fructose (20%) diet for 25 weeks. Following confirmed hyperglycemia, both HFHFD-CET (60-65% Vo2max) and HFHFD-HIIT (85-90% Vo2max) rats underwent treadmill exercise for 30 min, 5 days/week at 10 m/min for 8 weeks. Thereafter, blood and liver samples were obtained for biochemical studies. For histological analysis, the liver was fixed in 10% formalin, embedded in paraffin, and sectioned (5 mu m thickness) for H&E staining. SIRT-1 and PGC-1 alpha mRNA expression were measured by RT-PCR from the liver sample (frizzed sample). All data were presented as mean +/- standard error mean and compared the differences by one-way analysis of variances. The alpha level was set at 0.05 (p < 0.05) for statistical difference. Results The results show that HIIT was more effective than CET to reduce vesicular steatosis. HIIT significantly enhanced the expression of SIRT-1 compared to the HFHFD-DC group (fold change: 1.47, p < 0.047). However, HIIT decreased PGC-1 alpha expression compared to the HFHFD-DC group, but it was not significant (fold change: 1.32 and p < 0.247). Conclusions HIIT was more effective than CET in SIRT-1 expression augmentation in high-fat, high-fructose diabetic rats which suggests a possible treatment strategy in the context of type 2 diabetes.