تاثیر تمرین تناوبی با شدت بالا و روزه‌داری متناوب بر SIRT1/PGC-1α بافت کبد در رت های نر تحت رژیم غذایی پرچرب و پرفروکتوز

نوع مقاله : مقاله های پژوهشی

نویسندگان

گروه علوم ورزشی، دانشکده علوم انسانی، دانشگاه کاشان، کاشان ایران

10.48305/jims.v43.i818.0632

چکیده

مقاله پژوهشی




مقدمه: هدف از مطالعه‌ی حاضر، بررسی تأثیر تمرین تناوبی با شدت بالا (High-Intensity Interval Training) HIIT و روزه‌داری متناوب (Intermittent Fasting) ADF بر بیوژنز میتوکندری کبد در رت‌های نر تحت رژیم غذایی پرچرب و پرفروکتوز (HFD+HF) می‌باشد.
روش‌ها: 30 سر رت نر، نژاد اسپراگ‌-دولی (8 هفته‌ای)، به‌طور تصادفی به پنج گروه تقسیم شدند: رژیم غذایی استاندارد (ND)، رژیم غذایی پرچرب و پرفروکتوز (HFD+HF)، رژیم غذایی پرچرب و پرفروکتوز همراه با تمرین ورزشی (HFD+HF+HIIT)، رژیم غذایی پرچرب و پرفروکتوز همراه با روزه‌داری متناوب (HFD+HF+ADF) و رژیم غذایی پرچرب و پرفروکتوز همراه با تمرین ورزشی و روزه‌داری متناوب (HFD+HF+HIIT+ADF). پروتکل HIIT (5 روز در هفته) و رژیم ADF (یک روز در میان خوردن و ناشتایی) به مدت 12 هفته اجرا شدند. مقادیر پروتئینی PGC-1α و SIRT1 در بافت کبد با روش وسترن بلات اندازه‌گیری شد.
یافته‌ها: رژیم غذایی پرچرب و پرفروکتوز منجر به کاهش معنی‌داری در مقادیر پروتئینی PGC-1α و SIRT1 کبدی نسبت به ND شد (0/001 > P). همچنین، هر سه گروه HFD+HF+ADF، HFD+HF+HIIT و HFD+HF+HIIT+ADF افزایش معنی‌داری در PGC-1α نسبت به گروه HFD+HF نشان دادند (0/05 > P). همچنین، دو گروه HFD+HF+ADF وHFD+HF+HIIT+ADF  منجر به افزایش معنی‌داری در SIRT1 نسبت به گروه HFD+HF شد (0/05 > P). همچنین، گروه HFD+HF+HIIT+ADF افزایش معنی‌داری را در SIRT1 نسبت به هر کدام از گروه‌ها به تنهایی HFD+HF+ADF و HFD+HF+HIIT نشان داد (0/05 > P).
نتیجه‌گیری: ترکیب HIIT و روزه‌داری می‌تواند به‌طور مؤثری منجر افزایش بیوژنز میتوکندری شود و احتمالاً با افزایش عملکرد میتوکندری می‌تواند اثرات منفی رژیم پرچرب و پرفروکتوز را معکوس کند و راهبرد مؤثرتری برای بهبود محتوی چربی کبد باشد.

تازه های تحقیق

موسی خلفی: Google Scholar 

کیوان شریف مرادی: Google Scholar 

کلیدواژه‌ها

موضوعات


عنوان مقاله [English]

The Effect of High Intensity Interval Training and Intermittent Fasting on SIRT1/PGC-1α of Liver Tissue in Rat Fed with a High-Fat and High-Fructose Diet

نویسندگان [English]

  • Mahdi Hosseinkhah
  • Mousa Khalafi
  • Keywan Sharifmoradi
Department of Sport Sciences, Faculty of Humanities, University of Kashan, Kashan, Iran
چکیده [English]

Background: The aim of the present study was to investigate the effect of high-intensity interval training (HIIT) and intermittent fasting (ADF) on liver mitochondrial biogenesis in male rats fed a high-fat, high-fructose diet (HFD+HF).
Methods: Thirty male Sprague-Dawley rats (8 weeks old) were randomly divided into five groups: standard diet (ND), high-fat and high-fructose diet (HFD+HF), high-fat and high-fructose diet with exercise (HFD+HF+HIIT), high-fat and high-fructose diet with intermittent fasting (HFD+HF+ADF), and high-fat and high-fructose diet with exercise and intermittent fasting (HFD+HF+HIIT+ADF). The HIIT protocol (5 days per week) and the ADF diet (every other day eating and fasting) were performed for 12 weeks. The protein levels of PGC-1α and SIRT1 in liver tissue were measured by Western blotting.
Findings: High-fat and high-fructose diet resulted in a significant decrease in hepatic PGC-1α and SIRT1 protein levels compared to ND (P<0.001). Also, all three groups HFD+HF+ADF, HFD+HF+HIIT and HFD+HF+HIIT+ADF showed a significant increase in PGC-1α compared to the HFD+HF group (P<0.05). Also, the two groups HFD+HF+ADF and HFD+HF+HIIT+ADF resulted in a significant increase in SIRT1 compared to the HFD+HF group (P<0.05). Also, the HFD+HF+HIIT+ADF group showed a significant increase in SIRT1 compared to each of the groups HFD+HF+ADF and HFD+HF+HIIT alone (P<0.05).
Conclusion: The combination of HIIT and ADF can effectively increase mitochondrial biogenesis and possibly reverse the negative effects of a high-fat, high-fructose diet by improving mitochondrial function and be a more effective strategy for improving liver fat content.

کلیدواژه‌ها [English]

  • High-intensity interval training
  • High-fat
  • high-fructose diet
  • Intermittent fasting
  • Mitochondrial biogenesis
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