Relationship between TCF7L2 Relative Expression in Pancreas Tissue with Changes in Insulin by High Intensity Interval Training (HIIT) in Type 2 Diabetes Rats

Eizadi, Mojtaba; Soory, Rahman; Ravasi, Aliasghar; Baesy, Kazem; Choobineh, Sirous

Volume 24, Issue 12 (Feb-Mar 2017) JSSU 2017, 24(12): 981-993 | Back to browse issues page

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Eizadi M, Soory R, Ravasi A, Baesy K, Choobineh S. Relationship between TCF7L2 Relative Expression in Pancreas Tissue with Changes in Insulin by High Intensity Interval Training (HIIT) in Type 2 Diabetes Rats . JSSU 2017; 24 (12) :981-993
URL: http://jssu.ssu.ac.ir/article-1-3750-en.html

Relationship between TCF7L2 Relative Expression in Pancreas Tissue with Changes in Insulin by High Intensity Interval Training (HIIT) in Type 2 Diabetes Rats

Mojtaba Eizadi ^*

Abstract: (6678 Views)

Introduction: Both environmental and genetic factors have been implicated in the development of type 2 diabetes (T2D). The objectives of the present study were: 1) to investigate the effect of high intensity interval training (HIIT) on fasting glucose, insulin and TCF7L2 expression in pancreas tissue of T2D rats, 2) to determine the relation between TCF7L2 expression with insulin changes in the HIIT and control groups.

Methods: In the present applied-experimental study, T2D male Wistar rats induced by intraperitoneal streptozotocin-nicotinamide were assigned to control (no-training) and HIIT (5 times/week/12-week) groups. Fasting glucose, serum insulin and TCF7L2 expression in pancreas tissues of both groups were measured after lasted exercise and compared between 2 groups by independent T test. Also, the relation between TCF7L2 expression and insulin of HIIT to the control group was assessed by Pearson correlations.

Results: The HIIT training in the training group was associated with improved fasting glucose compared with the control group (P<0.001). A significant increase was observed in serum insulin levels (P< 0.001). Also, there was seen a significant decrease in TCF7L2 expression in pancreas tissues in HIIT group compared with the control group (P= 0.038). Significant negative correlation was found between TCF7L2 expression and insulin changes of the HIIT to control groups (r=0.84, P=0.034).

conclusion: HIIT training is associated with improvements in glycemic control and insulin secretion in T2D rats. Based on these data, this improvement can be attributed to decrease in TCF7L2 expression at pancreas tissues by HIIT training.

Keywords: Interval training, Type 2 diabetes, Pancreas, Gene expression, Transcription factor 7-like 2

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Type of Study: Original article | Subject: Exercise Physiology
Received: 2016/05/31 | Accepted: 2017/01/7 | Published: 2017/05/2

References

1. Adeghate E, Schattner P, Dunn E. An update on the etiology and epidemiology of diabetes mellitus. Ann N Y Acad Sci 2006; 1084:1-29.

2. Bergman RN, Finegood DT, Kahn SE. The evaluation of β-cell dysfunction and insulin resistance in type 2 diabetes. Eur J Clin Invest 2002; 32: 35-45.

3. Da Silva Xavier GQ, Cullen PJ, Rutter GA. Distinct roles for insulin and insulin-like growth factor-1 receptors in pancreatic beta-cell glucose sensing revealed by RNA silencing. Biochem J 2004; 377(1): 149-58.

4. Amra C. The T-Allele of TCF7L2 rs7903146 Associates with a Reduced Compensation of Insulin Secretion for Insulin Resistance Induced by 9 Days of Bed Rest. DIABETES 2010; 59: 836-43.

5. 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 PPARG Pro12Ala variant: results from the HERITAGE Family Study. Diabetologia 2010; 53(4): 679-89.

6. Anders R, Ola H. Mechanisms whereby genetic variation in the TCF7L2 gene causes diabetes: novel targets for anti-diabetic therapy? New grants from Hjelt foundation 2013.

7. Parton LE, McMillen PJ, Shen Y. Limited role for SREBP-1c in defective glucose-induced insulin secretion from Zucker diabetic fatty rat islets: a functional and gene proﬁling analysis. Am J Physiol Endocrinol Metab 2006; 291: 982–94.

8. Florez JC. The new type 2 diabetes gene TCF7L2. Curr Opin Clin Nutr Metab Care 2007; 10: 391–6.

9. Savic D, Ye H, Aneas I, Park SY, Bell GI, Nobrega A. Alterations in TCF7L2 expression deﬁne its role as a key regulator of glucose metabolism. Genome Res 2011; 21: 1417–1425.

10. Saxena R, Voight BF, Lyssenko V, Burtt NP, de Bakker PI, Chen H, et al. Genome-wide association analysis identiﬁes loci for type 2 diabetes and triglyceride levels. Science 2007; 316: 1331–1336.

11. Villareal DT, Robertson H, Bell GI. TCF7L2 variant rs7903146 affects the risk of type 2 diabetes by modulating incretin action. Diabetes 2010; 59: 479–485.

12. Lyssenko V, Lupi R, Marchetti P, Del-Guerra S, Orho-Melander M, Almgren P, et al. Mechanisms by which common variants in the TCF7L2 gene increase risk of type 2 diabetes. J Clin Invest 2004; 117: 2155-2163.

13. Samson S. Role of Wnt signaling and TCF7L2 for beta cell function and regeneration in mouse models of diabetes. Baylor College of Medicine, Houston, Texas. 2011.

14. Cornelis MC, Qi L, Kraft P, Hu FB. TCF7L2, dietary carbohydrate, and risk of type 2 diabetes in US women. Am J Clin Nutr 2009; 89: 1256–62.

15. Eizadi M, Behboudi L, Zahedmanesh F, Afsharmand Z. Effect of Acute and Chronic Exercise on Beta-Cell Function in Diabetic Patients. Knowledge & Health 2012; 6(4): 15-19.

16. Gibala MJ. High intensity interval training: new insights. Sports Science Exchange 2007; 20(2): 1-8.

17. Little JP, Gillen JB, Percival ME, Safdar A, Tarnopolsky MA, Punthakee Z, et al. Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes. J Appl Physiol 2011; 111(6): 1554–1560.

18. Slentz CA, Tanner CJ, Bateman LA, Durheim MT, Huffman KM, Houmard JA, et al. Effects of exercise training intensity on pancreatic beta-cell function. Diabetes Care 2009; 32(10): 1807–1811.

19. William C, Knowler MD, Elizabeth BC, Sarah E, Richard F, Hamman MD et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002; 346:393-403.

21. Garrow JS. Obesity: definition, Aetiology and Assessment. Encyclopedia of human nutrition. Academic press. 1999; 1430-34.

22. Mogharnasi M, Gaeini A, Kordi M, Ravasi A, Javadi E, Sheykholeslami D. The Effect of Four Weeks of Detraining after a Period of Intense Sprint Training on Risk Factors of Atherogenic Inflammatory Damages. J Sport Biosciences 2011; 3(9): 5-20.

23. Coughlin CC, Finck BN, Eagon JC, Halpin VJ, Magkos F, Mohammed BS, et al. Effect of marked weight loss on adiponectin gene expression and plasma concentrations. Obesity (Silver Spring) 2007; 15(3): 640-5.

24. De Fronzo RA, Sherwin RS, Kraemer N. Effect of physical training on insulin action in obesity. Diabetes 1987; 36: 1379–1385.

25. Donges CE, Duffield R, Guelfi KJ, Smith GC, Adams DR, Edge JA. Comparative effects of single-mode vs. duration-matched concurrent exercise training on body composition, low-grade inflammation, and glucose regulation in sedentary, overweight, middle-aged men. Appl Physiol Nutr Metab 2013; 38(7): 779-88.

26. Madsen SM, Thorup AC, Overgaard K, Jeppesen PB. High Intensity Interval Training Improves Glycaemic Control and Pancreatic β Cell Function of Type 2 Diabetes Patients. PLoS One 2015;10(8): e0133286.

27. Marquis-Gravel G, Hayami D, Juneau M, Nigam A, Guilbeault V, Latour É, Gayda M. Intensive lifestyle intervention including high-intensity interval training program improves insulin resistance and fasting plasma glucose in obese patients. Prev Med Rep 2015; 2: 314-8.

28. Westermark P, Wilander E. The influence of amyloid deposits on the islet volume in maturity onset diabetes mellitus. Diabetologia 1978; 15: 417–421.

29. Levy J. 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. Diabet Med 1998; 15: 290–296.

30. Fujino T, Asaba H, Kang MJ. Low-density lipoprotein receptor-related protein 5 (LRP5) is essential for normal choles- terol metabolism and glucose-induced insulin secretion. Proc Natl Acad Sci USA 2003; 100: 229–234.

31. Murtaugh LC, Law AC, Dor Y. Beta-catenin is essential for pancreatic acinar but not islet development. Development 2005; 132: 4663– 4674.

32. Liu Z, Haben er JF. Stromal cell-derived factor-1 promotes survival of pancreatic beta cells by the stabilisation of beta catenin and activation of transcription factor 7-like 2 (TCF7L2). Diabetologia 2009; 52: 1589–1598.

33. Shu L, Sauter NS, Schulthess FT. Transcription factor 7-like 2 regulates beta-cell survival and function in human pancreatic islets. Diabetes 2008; 57: 645–653.

34. Shu L, Matveyenko AV, Kerr-Conte J. Decreased TCF7L2 protein levels in type 2 diabetes mellitu s correlate with down- regulation of GIP- and GLP-1 receptors and impaired beta-cell function. Hum Mol Genet 2009; 18: 2388– 2399.

35. Ross A, Leveritt M. Long-term metabolic and skeletal muscle adaptations to short-sprint training:implications for sprint training and tapering. Sports Med 2001; 31: 1063-1082.

36. Delghingaro-Augusto V, Décary S, Peyot ML, Latour MG, Lamontagne J, Paradis-Isler N, et al. Voluntary running exercise prevents-cell failure in susceptible islets of the Zucker diabetic fatty rat. Am J Physiol Endocrinol Metab 2012; 302: 254 –264.