Impact of High-Intensity Interval Training on GLP-1R/ PKBα Axis in Pancreatic Tissue of Diabetic Rats Induced by High-Fat Diet and STZ

Behkar, Mehdi; Eizadi, Mojtaba; Sedaghaty, Saeid; Kazemzadeh, Yaser; Moslehi, Motahareh

doi:10.18502/ijdo.v15i4.14553

Volume 15, Issue 4 (12-2023) IJDO 2023, 15(4): 201-207 | Back to browse issues page

‎ 10.18502/ijdo.v15i4.14553

Mendeley

Zotero

RefWorks

Behkar M, Eizadi M, Sedaghaty S, Kazemzadeh Y, Moslehi M. Impact of High-Intensity Interval Training on GLP-1R/ PKBα Axis in Pancreatic Tissue of Diabetic Rats Induced by High-Fat Diet and STZ. IJDO 2023; 15 (4) :201-207
URL: http://ijdo.ssu.ac.ir/article-1-831-en.html

Impact of High-Intensity Interval Training on GLP-1R/ PKBα Axis in Pancreatic Tissue of Diabetic Rats Induced by High-Fat Diet and STZ

Mehdi Behkar

, Mojtaba Eizadi ^*

, Saeid Sedaghaty

, Yaser Kazemzadeh

, Motahareh Moslehi

Assistant Professor of Exercise Physiology, Saveh Branch, Islamic Azad University, Saveh, Iran.

Abstract: (266 Views)

Objective: Apart from hormonal factors and oxidative stress, insulin synthesis is strongly dependent on transcription factors in the pancreas. The aim of the present study was to assess the impact of high-intensity interval training (HIIT) on genes affecting insulin synthesis in diabetic obese rats.
Materials and Methods: Type 2 diabetes (T2D) was induced by a 6-week high-fat diet (HFD) and intraperitoneal injection of streptozotocin (25 mg /kg) in 14 male Wistar rats (10 week old, 220±10 g). Rats with fasting glucose levels between 400 and 150 were considered T2D. The diabetic rats were randomly assigned to exercise (HIIT: 6 weeks/5 sessions weekly, n= 7) or control (n= 7) groups. Forty-eight hours after the intervention, fasting GLP-1R and PKBα gene expression in pancreatic tissue and plasma insulin and glucose levels were compared between the groups. Data were compared by independent t-test used to compare variables, version 22 between groups. A P< 0.05 was considered significant.
Results: HIIT led to significant increase in PKBα gene expression (P: 0.001) and insulin (P: 0.031) and decreases in glucose concentration (P: 0.001) compared with the control group. No change was observed in the GLP-1R gene expression response to HIIT (P: 0.093).
Conclusion: HIIT is associated with increased serum insulin levels in T2D obese rats. Despite no change in GLP-1R, this improvement is probably rooted in increased expression PKBα in pancreas in response to this type of exercise training.

Keywords: GLP-1R, PKBα, High fat diet, High intensity interval training, Diabetes

Full-Text [PDF 468 kb] (143 Downloads)

Type of Study: Research | Subject: Special
Received: 2023/07/8 | Accepted: 2023/10/10 | Published: 2023/12/19

References

1. Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes care. 2004;27(5):1047-53. [DOI:10.2337/diacare.27.5.1047]

2. Lazar MA. How obesity causes diabetes: not a tall tale. Science. 2005;307(5708):373-5. [DOI:10.1126/science.1104342]

3. Wang J, Chen C, Wang RY. Influence of short-and long-term treadmill exercises on levels of ghrelin, obestatin and NPY in plasma and brain extraction of obese rats. Endocrine. 2008;33:77-83. [DOI:10.1007/s12020-008-9056-z]

4. Zeng Q, Fu L, Takekoshi K, Kawakami Y, Isobe K. Effects of short-term exercise on adiponectin and adiponectin receptor levels in rats. Journal of atherosclerosis and thrombosis. 2007;14(5):261-5. [DOI:10.5551/jat.E498]

5. Imbeault P. Environmental influences on adiponectin levels in humans. Applied Physiology, Nutrition, and Metabolism. 2007;32(3):505-11. [DOI:10.1139/H07-017]

6. Ruchat SM, Rankinen T, Weisnagel SJ, Rice T, Rao DC, Bergman RN, et al. Improvements in glucose homeostasis in response to regular exercise are influenced by the PPARG Pro12Ala variant: results from the HERITAGE Family Study. Diabetologia. 2010;53:679-89. [DOI:10.1007/s00125-009-1630-2]

7. Seino Y, Fukushima M, Yabe D. GIP and GLP‐1, the two incretin hormones: similarities and differences. Journal of diabetes investigation. 2010;1(1‐2):8-23. [DOI:10.1111/j.2040-1124.2010.00022.x]

8. MacDonald PE, El-Kholy W, Riedel MJ, Salapatek AM, Light PE, Wheeler MB. The multiple actions of GLP-1 on the process of glucose-stimulated insulin secretion. Diabetes. 2002;51(suppl_3):S434-42. [DOI:10.2337/diabetes.51.2007.S434]

9. Leech CA, Dzhura I, Chepurny OG, Kang G, Schwede F, Genieser HG, et al. Molecular physiology of glucagon-like peptide-1 insulin secretagogue action in pancreatic β cells. Progress in biophysics and molecular biology. 2011;107(2):236-47. [DOI:10.1016/j.pbiomolbio.2011.07.005]

10. Drucker DJ, Philippe J, Mojsov S, Chick WL, Habener JF. Glucagon-like peptide I stimulates insulin gene expression and increases cyclic AMP levels in a rat islet cell line. Proceedings of the National Academy of Sciences. 1987;84(10):3434-8. [DOI:10.1073/pnas.84.10.3434]

11. Wang Q, Brubaker P. Glucagon-like peptide-1 treatment delays the onset of diabetes in 8 week-old db/db mice. Diabetologia. 2002;45:1263-73. [DOI:10.1007/s00125-002-0828-3]

12. Wang Q, Li L, Xu E, Wong V, Rhodes C, Brubaker PL. Glucagon-like peptide-1 regulates proliferation and apoptosis via activation of protein kinase B in pancreatic INS-1 beta cells. Diabetologia. 2004;47:478-87. [DOI:10.1007/s00125-004-1327-5]

13. Trümper K, Trümper A, Trusheim H, Arnold R, Göke B, Hörsch D. Integrative mitogenic role of protein kinase B/Akt in β‐cells. Annals of the New York academy of sciences. 2000;921(1):242-50. [DOI:10.1111/j.1749-6632.2000.tb06972.x]

14. Holst LS, Mulder H, Manganiello V, Sundler F, Ahrén B, Holm C, et al. Protein kinase B is expressed in pancreatic β cells and activated upon stimulation with insulin-like growth factor I. Biochemical and biophysical research communications. 1998;250(1):181-6. [DOI:10.1006/bbrc.1998.9166]

15. Bernal-Mizrachi E, Wen W, Stahlhut S, Welling CM, Permutt MA. Islet β cell expression of constitutively active Akt1/PKBα induces striking hypertrophy, hyperplasia, and hyperinsulinemia. The Journal of clinical investigation. 2001;108(11):1631-8. [DOI:10.1172/JCI200113785]

16. Tuttle RL, Gill NS, Pugh W, Lee JP, Koeberlein B, Furth EE, et al. Regulation of pancreatic β-cell growth and survival by the serine/threonine protein kinase Akt1/PKBα. Nature medicine. 2001;7(10):1133-7. [DOI:10.1038/nm1001-1133]

17. Ramazani Rad M, Hajirasouli M, Eizadi M. The effect of 12 weeks of aerobic training on GLP-1 receptor expression in pancreatic tissue and glycemic control in type 2 diabetic rats. Qom University of Medical Sciences Journal. 2017;11(6):36-45.

18. Eizadi M, Ravasi AA, Soory R, Baesi K, Choobineh S. The effect of three months of resistance training on TCF7L2 expression in pancreas tissues of type 2 diabetic rats. Avicenna Journal of Medical Biochemistry. 2016;4(1):12-34014. [DOI:10.17795/ajmb-34014]

19. Yazdanpazhooh S, Banaeifar A, Arshadi S, Eizadi M. Six weeks resistance training effect on FTO expression in type II diabetes rats. Iranian Journal of Diabetes and Obesity. 2018;10(4):216-2.

20. EL, Diniz YS, Galhardi CM, Ebaid GM, Rodrigues HG, Mani F, et al. Anthropometrical parameters and markers of obesity in rats. Laboratory animals. 2007;41(1):111-9. [DOI:10.1258/002367707779399518]

21. Daryanoosh F, Tanideh N, Bazgir B, Alizadeh H. Effect of aerobic trainings on heart's functioned and structure in diabetic Sprague-dawely albino species male rats. Res Applied Exercise Physiology. 2010;6(12):59-72.

22. Karimi M, Eizadi M. The effect of interval training on FOXO1 expression in pancreas tissue of diabetes rats with high fat diet and STZ. Razi Journal of Medical Sciences. 2019 ;26(6):95-104. (in Persian)

23. Rawal S, Huang H, Novikova L, Hamedi T, Smirnova I, Stehno‐Bittel L. Effects of exercise on pancreatic islets in zucker diabetic fatty rats. Journal of Diabetes and Metabolism.2013;10(2):1-7. [DOI:10.4172/2155-6156.S10-007]

24. Király MA, Bates HE, Kaniuk NA, Yue JT, Brumell JH, Matthews SG, et al. Swim training prevents hyperglycemia in ZDF rats: mechanisms involved in the partial maintenance of β-cell function. American Journal of Physiology-Endocrinology and Metabolism. 2008;294(2):E271-83. [DOI:10.1152/ajpendo.00476.2007]

25. 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. [DOI:10.1016/j.metabol.2005.06.003]

26. Dela F, von Linstow ME, Mikines KJ, Galbo H. Physical training may enhance β-cell function in type 2 diabetes. American Journal of Physiology-Endocrinology and Metabolism. 2004;287(5):E1024-31. [DOI:10.1152/ajpendo.00056.2004]

27. Hayashi T, Wojtaszewski JF, Goodyear LJ. Exercise regulation of glucose transport in skeletal muscle. American Journal of Physiology-Endocrinology and Metabolism. 1997;273(6):E1039-51. [DOI:10.1152/ajpendo.1997.273.6.E1039]

28. Yakubovich N, Gerstein HC. Serious cardiovascular outcomes in diabetes: the role of hypoglycemia. Circulation. 2011;123(3):342-8. [DOI:10.1161/CIRCULATIONAHA.110.948489]

29. Dickson LM, Rhodes CJ. Pancreatic β-cell growth and survival in the onset of type 2 diabetes: a role for protein kinase B in the Akt?. American Journal of Physiology-Endocrinology and Metabolism. 2004;287(2):E192-8. [DOI:10.1152/ajpendo.00031.2004]

30. Li L, El-Kholy W, Rhodes CJ, Brubaker PL. Glucagon-like peptide-1 protects beta cells from cytokine-induced apoptosis and necrosis: role of protein kinase B. Diabetologia. 2005;48:1339-49. [DOI:10.1007/s00125-005-1787-2]