تاثیر12 هفته تمرین هوازی بر میزان عملکرد سلولهای بتا و پروتئین جفت نشده ۲ پانکراس موش های چاق دیابتی

نوع مقاله : مقاله پژوهشی Released under (CC BY-NC 4.0) license I Open Access I

نویسندگان

1 دانشجوی دکتری فیزیولوژی ورزشی، گروه تربیت بدنی و علوم ورزشی، واحد بروجرد، دانشگاه آزاد اسلامی، بروجرد، ایران

2 استاد، گروه علوم پایه، دانشکده دامپزشکی، دانشگاه تهران، تهران، ایران

3 استادیار، گروه تربیت بدنی و علوم ورزشی، دانشکده علوم انسانی، دانشگاه آیت الله العظمی بروجردی (ره) ، بروجرد، ایران

10.22049/jahssp.2023.28008.1499

چکیده

هدف: تمرین ورزشی نوعی درمان غیردارویی در چاقی و دیابت نوع 2 می‌باشد. و در عین حال مکانیسم‌های مولکولی عهده­دار سازگاری‌های ژنتیکی به آن به ویژه در پانکراس کمتر شناخته شده‌اند. هدف از مطالعه حاضر تعیین اثر 12 هفته تمرین هوازی بر میزان عملکرد سلول‌های بتا و پروتئین جفت نشده ۲ پانکراس موش‌های چاق دیابتی بود. روش­ شناسی: در این مطالعه تجربی 24 سر موش صحرایی چاق دیابتی و سالم (5±220 گرم) به شیوه تصادفی به سه گروه مساوی: سالم HE ، دیابتیDI، دیابتی تمرین هوازی DI-AT تقسیم شدند. گروه DI-AT در یک برنامه تمرینات هوازی 12 هفته‌ای به تعداد 5 جلسه در هفته شرکت نموده و گروه کنترل در هیچ برنامه تمرینی شرکت نداشتند. غلظت گلوکز به روش رنگ سنجی گلوکز اکسیداز، انسولین سرم به روش الیزا و بیان ژن UCP2 با روش RT-Real time PCR اندازه‌گیری شدند. داده‌ها با استفاده از روش آماری تحلیل واریانس یک‌طرفه، در سطح معناداری 05/0 تجزیه ‌و تحلیل شدند.  نتایج: در پایان تحقیق بیان نسبی ژنUCP2  بافت پانکراس و HOMA-B گروهDI-AT به طور معنی‌داری از گروه DI کمتر (001/0= PHOMA-B : 001/0=PUCP2). و از گروه HE بیشتر (001/0= PHOMA-B : 001/0=PUCP2) بود. نتیجه گیری: تمرینات هوازی باعث بهبود نیمرخ گلیسیمی و سطح انسولین در موش‌های صحرایی دیابتی نوع 2 منجر می‌شود، احتمالا بخشی از این بهبود می‌تواند مربوط به تغییر در بیان نسبی ژنUCP2  در بافت پانکراس موش‌های دیابتی باشد.

کلیدواژه‌ها

موضوعات

عنوان مقاله [English]

The effect of 12 weeks of aerobic training on the function of beta cells and uncoupled protein 2 pancreas of diabetic obese rats

نویسندگان [English]

  • Vahideh Riyahi 1
  • Hassan Morovvati 2
  • Amir Khosravi 3
1 PHD student of Exercise Physiology, Department of Physical Education and Exercise Science, Borujard Branch, Islamic Azad University, Borujard, Iran
2 Professor, Department of Basic Sciences, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran
3 Assistant Professor, Department of Physical Education and Exercise Science, Faculty of Humanities, Ayatollah Ozma Borujerdi University, Borujerd, Iran.
چکیده [English]

Aim:   Exercise is a type of non-pharmacological treatment for obesity and type 2 diabetes, and at the same time, the molecular mechanisms responsible for genetic adaptations to it, especially in the pancreas, are less known. The aim of this study was to determine the effect of 12 weeks of aerobic training on the function of beta cells and uncoupled protein 2 of the pancreas of diabetic obese rats. Methods: In this experimental study, 24 obese diabetic and healthy rats (220 ± 5 g) were randomly divided into three equal groups: HE healthy, DI diabetic, and DI-AT aerobic training diabetic. The DI-AT group participated in a 12-week aerobic training program with 5 sessions per week, and the control group did not participate in any training program. Glucose concentration was measured by glucose oxidase colorimetric method, serum insulin by ELISA method and UCP2 gene expression by RT-Real time PCR method. The data were analyzed using the statistical method of one-way analysis of variance at a significance level of 0.05. Results: At the end of the research, the relative expression of pancreatic tissue UCP2 gene and HOMA-B of the DI-AT group was significantly lower than the DI group (PHOMA-B = 0.001: PUCP2 = 0.001). And it was more than HE group (PHOMA-B=0.001: PUCP2=0.001). Conclusion: Aerobic training improves the glycemic profile and insulin level in type 2 diabetic rats, probably part of this improvement can be related to the change in the relative expression of UCP2 gene in the pancreatic tissue of diabetic rats.

کلیدواژه‌ها [English]

  • Aerobic training
  • UCP2
  • serum insulin
  • serum sugar
  • diabetes

Publisher: Azarbaijan Shahid Madani University          Copyright © The Authors   

   

 

This is an open access article distributed under the following Creative Commons license: Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)

مراجع

  1. Yaghoubpour K, Tasdighi E, Abdi H,

Bhattacharjee A, et al. β-cell uncoupling Barzin M, Mahdavi M, Valizadeh M, et al. Association of obesity phenotypes in adolescents and incidence of early adulthood type 2 diabetes mellitus: Tehran lipid and glucose study. Pediatric Diabetes. 2021;22(7):937-45. [In Persian]  

  1. Rivera-Mancilla E, Al-Hassany L, Villalón CM, MaassenVanDenBrink A. Metabolic aspects of migraine: Association with obesity and diabetes mellitus. Frontiers in neurology. 2021:835.
  2. De Franco E. From biology to genes and back again: gene discovery for monogenic forms of beta-cell dysfunction in diabetes. Journal of molecular biology. 2020;432(5):1535-50.
  3. Almaça J, Caicedo A, Landsman L. Beta cell dysfunction in diabetes: the islet microenvironment as an unusual suspect. Diabetologia. 2020;63(10(:2076-85.
  4. Levy J, Atkinson A, Bell P, McCance D, Hadden D. Beta‐cell deterioration determines the onset and rate of progression of secondary dietary failure in type 2 diabetes mellitus: the 10‐year follow‐up of the Belfast Diet Study. Diabetic Medicine. 1998;15(4):290-6.
  5. Hou G, Jin Y, Liu M, Wang C, Song G. UCP2–866G/A polymorphism is associated with prediabetes and type 2 diabetes. Archives of medical research. 2020;51(6):556-63.
  6. Esterbauer H, Schneitler C, Oberkofler H, Ebenbichler C, Paulweber B, Sandhofer F, et al. A common polymorphism in the promoter of UCP2 is associated with decreased risk of obesity in middle-aged humans. Nature genetics. 2001;28(2):178-83.
  7. Chan CB, De Leo D, Joseph JW, McQuaid TS, Ha XF, Xu F, et al. Increased uncoupling protein-2 levels in β-cells are associated with impaired glucose-stimulated insulin secretion: mechanism of action. Diabetes. 2001;50(6):1302-10.
  8. Robson-Doucette CA, Sultan S, Allister EM, Wikstrom JD, Koshkin V, protein 2 regulates reactive oxygen species production, which influences both insulin and glucagon secretion. Diabetes. 2011;60(11):2710-9.
  9. Zhang C-Y, Baffy G, Perret P, Krauss S, Peroni O, Grujic D, et al. Uncoupling protein-2 negatively regulates insulin secretion and is a major link between obesity, β cell dysfunction, and type 2 diabetes. Cell. 2001;105(6):745-55.
  10. Calegari VC, Zoppi CC, Rezende LF, Silveira LR, Carneiro EM, Boschero AC. Endurance training activates AMP-activated protein kinase, increases expression of uncoupling protein 2 and reduces insulin secretion from rat pancreatic islets. Journal of Endocrinology. 2011;208(3):257.
  11. Oh KS, Kim M, Lee J, Kim MJ, Nam YS, Ham JE, et al. Liver PPARα and UCP2 are involved in the regulation of obesity and lipid metabolism by swim training in genetically obese db/db mice. Biochemical and biophysical research communications. 2006;345(3):1232-9.
  12. Bo H, Jiang N, Ma G, Qu J, Zhang G, Cao D, et al. Regulation of mitochondrial uncoupling respiration during exercise in rat heart: role of reactive oxygen species (ROS) and uncoupling protein 2. Free Radical Biology and Medicine. 2008;44(7):1373-81.
  13. Dietrich MO, Andrews ZB, Horvath TL. Exercise-induced synaptogenesis in the hippocampus is dependent on UCP2-regulated mitochondrial adaptation. Journal of Neuroscience. 2008;28(42):10766-71.
  14. Tian XY, Ma S, Tse G, Wong WT, Huang Y. Uncoupling protein 2 in cardiovascular health and disease. Frontiers in Physiology. 2018;9:1060.
  15. Aroda VR, Ratner RE. Metformin and type 2 diabetes prevention. Diabetes Spectrum. 2018;31(4):336-42.
  16. Khosravi A, Khosravi P, Daneshyar S, Valipour Dehnou V. Interactive effect of aerobic exercise with Saffron extract on serum, tumor necrosis factor-α and C-reactive protein in rats following an aerobic exercise until exhaustion. Complementary Medicine Journal. 2022;11(4):358-71. [In Persian]
  17. Soori R, Fardin Sohrabi F, Choobineh S, Ravasi A-A, Baesi K, Abbasian S. The Effect of 12-Week Aerobic Training on Protein Tyrosine Phosphatase 1B Gene Expression and Insulin Resistance in Diabetic Rats. Journal of Arak University of Medical Sciences. 2017;19(11):57-67. [In Persian]
  18. Kadoglou NP, Iliadis F, Angelopoulou N, Perrea D, Ampatzidis G, Liapis CD, et al. The anti-inflammatory effects of exercise training in patients with type 2 diabetes mellitus. European Journal of Preventive Cardiology. 2007;14(6):837-43.
  19. Bai Y, Zhang J, Jiang S, Sun J, Zheng C, Wang K, et al. Effects of the body fat mass and blood sugar and plasma resistin to slim exercise prescription for overweight and obesity students. Wei sheng yan jiu= Journal of hygiene research. 2013;42(4):538-42, 49.
  20. Fluckey JD, Kraemer WJ, Farrell PA. Pancreatic islet insulin secretion is increased after resistance exercise in rats. Journal of applied physiology. 1995;79(4):1100-5.
  21. Park S, Hong SM, Sung SR. Exendin-4 and exercise promotes β-cell function and mass through IRS2 induction in islets of diabetic rats. Life sciences. 2008;82(9-10):503-11.
  22. Melo LC, Dativo-Medeiros J, Menezes-Silva CE, Barbosa FT, Sousa-Rodrigues CFd, Rabelo LA. Physical exercise on inflammatory markers in type 2 diabetes patients: a systematic review of randomized controlled trials. Oxidative medicine and cellular longevity. 2017;2017.
  23. B Chan C, Harper M-E. Uncoupling proteins: role in insulin resistance and insulin insufficiency. Current diabetes reviews. 2006;2(3):271-83.
  24. Kazemi F, Ebrahim K, Asl SZ. Effect of regular exercise-induced apelin on dyslipidemia of type 2 diabetic rats. Res Med. 2016;39(4):163-8. [In Persian]
  25. Wang H, Antinozzi PA, Hagenfeldt KA, Maechler P, Wollheim CB. Molecular targets of a human HNF1α mutation responsible for pancreatic β-cell dysfunction. The EMBO journal. 2000;19(16):4257-64.
  26. Lee F-YJ, Li Y, Yang EK, Yang SQ, Lin HZ, Trush MA, et al. Phenotypic abnormalities in macrophages from leptin-deficient, obese mice. American Journal of Physiology-Cell Physiology. 1999;276(2):C386-C94.
  27. Li L-X, Yoshikawa H, Egeberg KW, Grill V. Interleukin-1β swiftly down-regulates UCP-2 mRNA in β-cells by mechanisms not directly coupled to toxicity. Cytokine. 2003;23(4-5):101-7.
  28. Chan CB, MacDonald PE, Saleh MC, Johns DC, Marbàn E, Wheeler MB. Overexpression of uncoupling protein 2 inhibits glucose-stimulated insulin secretion from rat islets. Diabetes. 1999;48(7):1482-6.
  29. Ghahramani Dereshki M, Banaeifar AA, Arshadi S, Soheily S. Effects of aerobic training on expression of HNF-4αand G6pase genes in hepatocyte of streptozotocin-nicotinamide induced type-2 diabetic male rats. Daneshvar Medicine. 2020;28(2):14-27. [In Persian]
  30. Ropelle ER, Pauli JR, Prada PO, De Souza CT, Picardi PK, Faria MC, et al. Reversal of diet‐induced insulin resistance with a single bout of exercise in the rat: the role of PTP1B and IRS‐1 serine phosphorylation. The Journal of physiology. 2006;577(3):997-1007.
  31. Bittencourt A, Schroeder HT, Porto RR, de Lemos Muller CH, Krause M, de Bittencourt Jr PIH. Heat shock response to exercise in pancreatic islets of obese mice. Biochimie. 2020;168:28-40.
  32. Colombo M, Gregersen S, Kruhoeffer M, Agger A, Xiao J, Jeppesen PB, et al. Prevention of hyperglycemia in Zucker diabetic fatty rats by exercise training: effects on gene expression in insulin-sensitive tissues determined by high-density oligonucleotide microarray analysis. Metabolism. 2005;54(12):1571-81.

34.  Dejkam, Nasreen, Rezaian, Najmeh. (1400). The effect of six weeks of aerobic training on the response of meteorin-like factor and insulin resistance index in overweight and obese young women. Applied health studies in exercise physiology, 8(1), 28-35. doi: 10.22049/jahssp.2020.26893.1325 .[In Persian].

مطالعات کاربردی تندرستی در فیزیولوژی ورزش
دوره 10، شماره 1
فروردین 1402
صفحه 141-153

فایل ها

سابقه مقاله

  • تاریخ دریافت: 18 مهر 1401
  • تاریخ بازنگری: 07 اسفند 1401
  • تاریخ پذیرش: 11 اسفند 1401

هم رسانی

ارجاع به این مقاله

آمار