مجله علوم پزشکی پارس

تاثیر تمرین تناوبی شدید بر بیان ژن عوامل درگیر در متابولیسم عضله اسکلتی موش های دیابتی

نویسندگان

1 کارشناسی ارشدفیزیولوژی ورزشی، واحدیادگارامام خمینی(ره) شهر ری،دانشگاه آزاد اسلامی،تهران، ایران

2 استادیارفیزیولوژی ورزشی،گروه تربیت بدنی وعلوم ورزشی، واحدیادگارامام خمینی(ره)شهرری، دانشگاه آزاداسلامی،تهران،ایران

3 استادیار فیزیولوژی ورزشی، گروه تربیت بدنی وعلوم ورزشی، واحدیادگارامام خمینی(ره)شهرری،دانشگاه آزاداسلامی،تهران،ایران

چکیده

مقدمه‌: بهبود متابولیسم عضلات اسکتی یکی از سازوکارهای مهم برای درمان دیابت نوع 2 است. هدف از این پژوهش، تاثیر تمرین تناوبی شدید بر بیان ژن عوامل درگیر در متابولیسم عضله اسکلتی موش­ های دیابتی بود.
روش کار: در این مطالعه تجربی، ۶۰ سر رت نر ویستار با میانگین وزنی 20±220 گرم به طور تصادفی در 4 گروه شامل کنترل، دیابت، تمرین و دیابت-تمرین قرار گرفتند. در این مطالعه، موش ­ها با استفاده از تزریق درون صفاقی نیکوتین، آمید-استرپتوزوتوسین، دیابتی نوع 2 شدند. تمرین تناوبی شدید با شدت 85-80 درصد VO2max،  پنج روز در هفته و به مدت ۸ هفته اجرا شد. میزان بیان ژن­ های GLUT4 وPGC-1α به روش Real Time PCR اندازه ­گیری شد. برای تجزیه و تحلیل داده­ ها از تحلیل واریانس یک طرفه و آزمون تعقیبی توکی در سطح 0.05>P  استفاده شد.
یافته ­ها: نتایج نشان داد بین میانگین بیان ژن GLUT4 و PGC-1α  عضله اسکلتی موش­ های دیابتی در گروه های مختلف تفاوت وجود دارد (p<0.001). تغییرات بیان این ژن ها در گروه دیابت نسبت به گروه­ کنترل به طور معناداری کمتر بود (p=0.036). تمرین تناوبی شدید موجب افزایش معنا­دار بیان ژن های مذکور  شد (p<0.001).
نتیجه‌گیری: با توجه به یافته های پژوهش حاضر، تمرین تناوبی شدید احتمالا می تواند از طریق افزایش بیان ژن PGC-1α و GLUT4 در عضله اسکلتی به بهبود سطوح انرژی سلولی طی دیابت کمک کند.

کلیدواژه‌ها

عنوان مقاله [English]

The effect of high-intensity interval training (HIIT) on gene expression of the factors involved in the skeletal muscle metabolism of diabetic rats

نویسندگان [English]

  • Mona Bostan manesh nik javan 1
  • Saeedeh Shadmehri 2
  • Mozhgan Ahmadi 3

1 Department of Physical Education and Sport Science Yadegar-e-Imam Khomeini (RAH) Shahre-rey Branch, Islamic Azad University, Tehran, Iran

2 Assistant Professor, Department of Physical Education and Sport Science Yadegar-e-Imam Khomeini (RAH) Shahre-rey Branch, Islamic Azad University, Tehran, Iran

3 Assistant Professor, Department of Physical Education and Sport Science Yadegar-e-Imam Khomeini (RAH) Shahre-rey Branch, Islamic Azad University, Tehran, Iran

چکیده [English]

Introduction: Improving the metabolism of skeletal muscle is one of the important mechanisms for the treatment of
type 2 diabetes. The aim of this study was to evaluate the effect of high-intensity interval training (HIIT) on gene expression of the factors involved in the skeletal muscle metabolism of diabetic rats.
Materials and Methods: To implementation of this experimental research, 48 male Wistar rats weighing 220 ± 20 gr randomly were divided into 4 groups including control, diabetes, training and diabetes-training. In this study, the
rats become diabetes type 2 using peritoneal injection nicotinamide-STZ. High-intensity interval training performed with intensity of 80-85% VO2max, 5 days a week and for 8 weeks. The expression of GLUT4 and PGC-1α genes were measured by Real Time PCR. Data were analyzed by One-way ANOVA and Tukey post hoc test at the P<0.05.
Results: The results showed a significant difference between the mean expression of GLUT4 and PGC-1α of skeletal muscle in diabetic rats in different groups (P< 0.001). The changes in the expression of GLUT4 and PGC-1α of the skeletal muscle in the diabetes group were significantly lower than the control group (P=0.036). High-intensity interval training significantly caused higher the expression of GLUT4 and PGC-1α (P< 0.001).
Conclusion: According to the findings of the present study, high-intensity interval training can help to improve cellular energy levels during diabetes as a result of increasing the expression of PGC-1α and GLUT4 in skeletal muscle.

کلیدواژه‌ها [English]

  • Diabetes
  • High-Intensity Interval Training
  • GLUT4
  • PGC-1α
  • Rats
1. Fujimaki S, Kuwabara T. Diabetes-Induced Dysfunction of Mitochondria and Stem Cells in Skeletal Muscle and the Nervous System. Int J Mol Sci. 2017; 18(10):2147-2169. 2. D’Souza D.M., Al-Sajee D., Hawke T.J. Diabetic myopathy: Impact of diabetes mellitus on skeletal muscle progenitor cells. Front. Physiol. 2013; 4(379):1-7. 3. Gispen W.H., Biessels G.J. Cognition and synaptic plasticity in diabetes mellitus. Trends Neurosci. 2000; 23(11):542-9. 4. Egan, B. Zierath, J. R. Exercise metabolism and the molecular regulation of skeletal muscle adaptation. Cell Metab. 2013; 17(2):162-84. 5. Oberbach A., Bossenz Y., Lehmann S., Niebauer J., Adams V., Paschke R., Schon M.R., Bluher M., Punkt K. Altered fiber distribution and fiber-specific glycolytic and oxidative enzyme activity in skeletal muscle of patients with type 2 diabetes. Diabetes Care. 2006; 29(4):895-900. 6. Cho K, Kim YB. Molecular mechanism of insulin resistance in obesity and type 2 diabetes. Korean J Intern Med. 2010; 25(2): 119–129. 7. Esfarjani F, Rashidi F, Marandi S M. The Effect of Aerobic Exercise on Blood Glucose, Lipid Profile and Apo. J Ardabil Univ Med Sci. 2013; 13(2):132-141 8. Liang H, Ward WF. PGC-1alpha: a key regulator of energy metabolism. Adv Physiol Educ. 2006; 30(4):145-51. 9. Wende AR, Schaeffer PJ, Parker GJ, Zechner C, Han DH, Chen MM, and Kelly DP. A role for the transcriptional coactivator PGC-1α in muscle refueling. J Biol Chem. 2007; 282(50):36642-51 10. Jung S, Kim K. Exercise-induced PGC-1α transcriptional factors in skeletal muscle. Integr Med Res. 2014; 3(4):155–160. 11. Brandt N, Dethlefsen MM, Bangsbo J, Pilegaard H. PGC-1α and exercise intensity dependent adaptations in mouse skeletal muscle. PLoS ONE 2017; 12(10):231-252. 12. Safdar A, Little JP, Stokl AJ, Hettinga BP, Akhtar M, Tarnopolsky MA, et al. Exercise increases mitochondrial PGC-1α content and promotes nuclear-mitochondrial cross-talk to coordinate mitochondrial biogenesis. J Biol Chem. 2011; 286(12):10605-17. 13. Hussey SE, McGee SL, Garnham A, McConell GK, Hargreaves M. Exercise increases skeletal muscle GLUT4 gene expression in patients with type 2 diabetes. Diabetes Obes Metab. 2012; 14(8):768-71. 14. Tadaishi M, Miura S, Kai Y, Kano Y, Oishi Y, Ezaki O. Skeletal muscle-specific expression of PGC-1α-b, an exercise-responsive isoform, increases exercise capacity and peak oxygen uptake. PLoS ONE, 2011; 6(12): 341-357. 15. Handschin C, Choi CS, Chin S, Kim S, Kawamori D, Kurpad AJ, et al. Abnormal glucose homeostasis in skeletal muscle-specific PGC-1alpha knockout mice. J Clin Invest. 2007; 117(11):3463-74. 16. Chan MC, Arany Z. The many roles of PGC-1α in muscle-recent developments. Metabolism. 2014; 63(4):441-51 17. Adhihetty PJ, Irrcher I, Joseph AM, Ljubicic V, Hood DA. Plasticity of skeletal muscle mitochondria in response to contractile activity. Exp Physiol. 2003; 88(1):99-107 18. Taylor CW, Ingham SA, Hunt JE, Martin NR, Pringle JS, Ferguson RA. Exercise duration‑matched interval and continuous sprint cycling induce similar increases in AMPK phosphorylation, PGC‑1α and VEGF mRNA expression in trained individuals. Eur J Appl Physiol. 2016; 116(8):1445-54. 19. Engel FA, Ackermann A, Chtourou H, Sperlich B. High-Intensity Interval Training Performed by Young Athletes: A Systematic Review and Meta-Analysis. Front Physiol. 2018; 9:1012-30. 20. Cassidy S, Thoma C, Houghton D, Trenell MI. High-intensity interval training: a review of its impact on glucose control and cardiometabolic health. Diabetologia. 2017; 60(1):7-23. 21. Wormgoor SG, Dalleck LC, Zinn C, Harris NK. Effects of High-Intensity Interval Training on People Living with Type 2 Diabetes: A Narrative Review. Can J Diabetes. 2017; 41(5):536-547. 22. Francois ME, Little JP. Effectiveness and safety of high-intensity interval training in patients with type 2 diabetes. Diabetes Spectr. 2015; 28(1):39-44. 23. Ruschke K, Fishbein L, Dietrich A, Klöting N, Tönjes A, Oberbach A, et al. Gene expression of PPARg and PGC-1a in human omental and subcutaneous adipose tissues is related to insulin resistance markers and mediates beneficial effects of physical training. Eur J Endocrinol. 2010; 162(3):515-23. 24. Pasini E, Le Douairon Lahaye S, Flati V, Assanelli D, Corsetti G, Speca S, et al. Effects of treadmill exercise and training frequency on anabolic signaling pathways in the skeletal muscle of aged rats. Exp Gerontol. 2012; 47(1):23-8. 25. Erlich AT, Tryon LD, Crilly MJ, Memme JM, Moosavi ZSM, Oliveira AN, et al. Function of specialized regulatory proteins and signaling pathways in exercise-induced muscle mitochondrial biogenesis. Integr Med Res. 2016; 5(3):187–197. 26. Chinsomboon J, Ruas J, Gupta RK, Thom R, Shoag J, Rowe GC, et al., The transcriptional coactivator PGC-1alpha mediates exercise-induced angiogenesis in skeletal muscle. Proc Natl Acad Sci U S A. 2009; 106(50):21401-6. 27. Lundberg TR, Fernandez-Gonzalo R, Norrbom J, Fischer H, Tesch PA, Gustafsson T. Truncated splice variant PGC-1α4 is not associated with exercise-induced human muscle hypertrophy. Acta Physiol. 2014; 212(2):142-51. 28. Wang L, Jia Y, Rogers H, Suzuki N, Gassmann M, Wang Q, et al. Erythropoietin contributes to slow oxidative muscle fiber specification via PGC-1α and AMPK activation. Int J Biochem Cell Biol. 2013; 45(7):1155-64. 29. Park ST, Kim K, Yoon JH, Lee S. Effect of Exercise on GLUT4 Expression of Skeletal Muscle in Streptozotocin-Induced Diabetic Rats. Journal of Exercise Physiology Online. 2011; 14(3):113-122. 30. Wang Y, Wen L, Zhou S, Zhang Y, Wang XH, He YY, et al. Effects of four weeks’ intermittent hypoxia intervention on glucose homeostasis, insulin sensitivity, GLUT4 translocation, insulin receptor phosphorylation, and Akt activity in skeletal muscle of obese mice with type 2 diabetes. PLoS ONE 2018; 13(9):1-22. 31. Afzalpour ME, Yousefi MR, Eivari HA, Ilbeigi S. The comparison of continuous and intermittent training impact on glucose-4 transporter protein level and insulin sensitivity in diabetic rats. 2016. 32. Mohebbi H, Rohani H, Hassan-Nia S. The effect of 12 weeks’ endurance training at 2 different intensities on GLUT4 mRNA expression of soleus and gastrocnemius muscles in obese mice. Apunts Medicina de l" Esport (English Edition). 2016; 51(191):93-9. 33. Luk J, Kilpatrick K, Davidson L, Hudson R, Ross R. Whole-body skeletal muscle mass is not related to glucose tolerance or insulin sensitivity in overweight and obese men and women. Appl Physiol Nutr Metab. 2008; 33(4):769-74 34. Brooks N, Layne EJ, Gordon LP, Roubenoff R, Nelson EM, Castaneda SC. Strength training improves muscle quality and insulin sensitivity in Hispanic older adults with type 2 diabetes. Int J Med Sci. 2006; 4(1):19-27. 35. Ivy JL. Role of exercise training in the prevention and treatment of insulin resistance and non-insulin-dependent diabetes mellitus. Sports Med 1997; 24(5):321-36. 36. K VLM, Katch WD, Frank I. Essentials of exercise physiology. 4th eds, 2011. 37. Ku YH, Han KA, Kwon H, Koo BK, Kim HC. Resistance exercise did not alter intramuscular adipose tissue but reduced retinol binding protein 4 concentration in individuals with type 2 diabetes mellitus. J Int Med Res. 2010; 38(3):782-91. 38. Woo KS, Chook P, Chung WY, Sung RY, Qiao M, Leung SS, et al. Effects of diet and exercise on obesity-related vascular dysfunction in children. Circulation. 2004; 109(16):1981-6. 39. Zarekar M, Saghebjoo M, Foadodini M, Hedayati M. Combined effect of aerobic training and pistacia athlantica extract on GLUT-4 protein expression and muscle glycogen in diabetic rats. Iranian Journal of Endocrinology and Metabolism. 2014; 16(4):245-53.
مجله علوم پزشکی پارس
دوره 17، شماره 2 - شماره پیاپی 48
تیر 1398
صفحه 32-39