مشخصات پژوهش

صفحه نخست /High-intensity interval ...
عنوان High-intensity interval training prevents high-fat diet-induced hepatic steatosis by modulating miRNA-34a, miRNA-467b, and their primary target proteins in male rats
نوع پژوهش مقاله چاپ‌شده
کلیدواژه‌ها Non-alcoholic fatty liver disease – High-intensity intermittent training – microRNA-34a – microRNA-467b – Obesity
چکیده Aims: High-fat diet (HFD) consumption contributes to obesity and liver damage, while exercise training may counteract these effects. Given the regulatory role of microRNAs in lipid metabolism, this study investigates the impact of high-intensity interval training (HIIT) and HFD on hepatic fat accumulation, as well as the expression of miRNA-34a, miRNA-467b, and their associated proteins. Main methods: Twenty-four male rats were randomly assigned to four groups: (1) CON, (2) HIIT, (3) HFD, and (4) HIIT+HFD. The HFD groups received a 60% fat diet, while the rats in the HIIT groups performed high-intensity interval training (3 sessions/week, 2.5minutes high-intensity running × 90% maximal running capacity (MRC) with 2.5minutes active rest × 50% MRC, for ten weeks). Forty-eight hours post-intervention, blood and liver samples were collected to assess histopathology, liver enzymes, and the expression of miRNA-34a, miRNA-467b, SIRT1, PPAR-ɑ, and LPL proteins. Key findings: The HFD group exhibited excessive hepatic lipid accumulation, whereas HIIT significantly prevented HFD-induced hepatic steatosis, as confirmed by histopathological examinations. Liver enzyme levels (AST, ALT, and ALP) were significantly higher in the HFD group and significantly lower in both the HIIT and HIIT+HFD groups. Additionally, HIIT significantly increased miRNA-467b, SIRT1, and PPAR-ɑ expression while significantly decreasing miRNA-34a and LPL expression, preventing the effects of HFD. Significance: Our findings identified a novel molecular mechanism confirming that HIIT is beneficial to prevent hepatic steatosis and hepatic damage induced by HFD, likely due to the modulation of miRNA-467b, miRNA-34a, and their main target proteins.
پژوهشگران محمد پرستش (نفر پنجم)، حسن کردی (نفر دوم)، رضا قراخانلو (نفر سوم)، حمید رضا خالونجاد (نفر چهارم)، امیر محمد محمدی حاجی وند (نفر اول)