تأثیر 12 هفته تمرینات تناوبی شدید (HIIT) بر بیان ژن MTNR1B و سطوح انسولین و گلوکز در رتهای دیابتی نوع 2
DOI::
https://doi.org/10.22100/jkh.v14i1.2151کلمات کلیدی:
بیان ژن MTNR1B، رتهای دیابتی نوع 2، تمرینات تناوبی شدید، سطوح گلوکز، سطوح انسولینچکیده
مقدمه: ژن MTNR1B با میزان ابتلا به دیابت نوع 2 مرتبط است و افزایش بیان آن خطر دیابت نوع 2 را افزایش میدهد. هدف از این مطالعه بررسی تأثیر 12 هفته تمرینات تناوبی شدید بر بیان ژن MTNR1B و گلوکز و انسولین ناشنا در رتهای نر ویستار مبتلابه دیابت نوع 2 است.
مواد و روشها: دراین مطالعه از 30 سر رت نر نژاد ویستار با محدوده وزنی 20±220گرم، استفاده شد. در طول دوره در شرایط استاندارد یعنی دمای 3±22 سانتیگراد و رطوبت 45 درصد و دورههای 12 ساعته متوالی نور و تاریکی نگهداری شدند. رتها به سه گروه تقسیم شدند. القای دیابت از طریق محلول نیکوتین آمید و STZ انجام شد و برنامه تمرینی برای یک دوره تمرینات تناوبی شدید به مدت 12 هفته به تعداد 5 جلسه 30 دقیقهای در هفته بود. غلظت گلوکز به روش آنزیمی رنگسنجی گلوکز اکسیداز، انسولین به روش الیزا و بیان ژن به روش RT-Real time PCR اندازهگیری شد.
نتایج: برنامه تمرینی به کاهش سطوح گلوکز ناشتا و افزایش سطوح انسولین سرم نسبتبه گروه دیابتی کنترل منجر شد (001/0=P). از طرفی، اجرای تمرینات تناوبی شدید بیان ژن MTNR1B در بافت پانکراس را به میزان 39 درصد نسبتبه گروه کنترل دیابتی کاهش داد (023/0=P). ارتباط معکوس و معنیداری بین سطوح نسبی بیان MTNR1B و سطوح نسبی انسولین سرم در گروه اینتروال نسبتبه کنترل مشاهده شد (039/0=P، 84/0=r).
نتیجهگیری: نتایج این مطالعه نشان داد که دوازده هفته ورزش تناوبی شدید باعث کاهش گلوکز خون و افزایش سرم انسولین و کاهش بیان ژن MTNR1B در بافت پانکراس ميشود.
مراجع
Hogan P, Dall T, Nikolov P. Economic costs of diabetes in the US in 2002. ADA. Diabetes Care 2003;26:917-32. doi:10.2337/diacare.26.3.917
Risch N. Linkage strategies for genetically complex traits. I. Multilocus models. Am J Hum Genet 1990;46:222-8.
Ng SW, Popkin BM. Time use and physical activity: a shift away from movement across the globe. Obes Rev 2012;13:659–80. doi:10.1111/j.1467-789X.2011.00982.x
McCarthy MI. Genomics, type 2 diabetes, and obesity. N Engl J Med 2010; 363: 2339-2350. doi: 10.1056/NEJMra0906948
Almgren P, Lehtovirta M, Isomaa B, Sarelin L, Taskinen MR, Lyssenko V, et al. Heritability and familiality of type 2 diabetes and related quantitative traits in the Botnia Study. Diabetologia 2011;54:2811-9. doi: 10.1007/s00125-011-2267-5
Groop L, Forsblom C, Lehtovirta M, Tuomi T, Karanko S, Nissén M, et al. Metabolic consequences of a family history of NIDDM (the Botnia study): evidence for sex-specific parental effects. Diabetes. 1996;45:1585-93. doi: 10.2337/diab.45.11.1585
Isomaa B, Forsen B, Lahti K, Holmstrom N, Waden J, et al. A family history of diabetes is associated with reduced physical fitness in the Prevalence, Prediction and Prevention of Diabetes (PPP)-Botnia study. Diabetologia 2010; 53: 1709–1713. doi: 10.1007/s00125-010-1776-y
Lyssenko V, Nagorny CL, Erdos MR, Wierup N, Jonsson A, Spégel P, et al. Common variant in MTNR1B associated with increased risk of type 2 diabetes and impaired earlyinsulin secretion. Nat Genet 2009; 41:82-88. doi: 10.1038/ng.288
Ciaran J, McMullan, et al. Melatonin Secretion and the Incidence of Type 2 Diabetes. JAMA 2013;13:309. doi: 10.1001/jama.2013.2710
Lisa Nainggolan. Low levels of melatonin up risk for type 2 diabetes. Medscape Medical News 2013.
Yaghootkar H ,Timothy M Frayling. Recent progress in the use of genetics to understand links between type 2 diabetes and related metabolic traits. Genome Biology 2013;14:203. doi:10.1186/gb-2013-14-3-203
Prokopenko I, Langenberg C, Florez JC, Saxena R, Soranzo N, Thorleifsson G, et al. Variants in MTNR1B influence fasting glucose levels. Nat Genet 2009;41:77-81. doi: 10.1038/ng.290
Been LF, Hatfield JL, Shankar A, Aston CE, Ralhan S, Wander GS, et al. A low frequency variant within the GWAS locus of MTNR1B affects fasting glucose concentrations: genetic risk is modulated by obesity, Nutr Metab Cardiovasc Dis 2012;22:944-51. doi: 10.1016/j.numecd.2011.01.006
Bonnefond A, Clément N, Fawcett K, Yengo L, Vaillant E, Guillaume JL, et al. Rare MTNR1B variants impairing melatonin receptor 1B function contribute to type 2 diabetes. Nat Genet 2012; 44:297-301. doi: 10.1038/ng.1053
Larsen S, Skaaby S, Helge JW, Dela F. Effects of exercise training on mitochondrial function in patients with type 2 diabetes.World J Diabetes 2014;5:482-92. doi: 10.4239/wjd.v5.i4.482
Marwick TH, Hordern MD, Miller T, Chyun DA, Bertoni AG, Blumenthal RS, et al. Exercise training for type 2 diabetes mellitus: impact on cardiovascular risk: a scientific statement from the American Heart Association. Circulation 2009;119:3244-62. doi: 10.1161/CIRCULATIONAHA
Kjaer M, Hollenbeck CB, Frey-Hewitt B, Galbo H, HaskellW, Reaven GM. Glucoregulation and hormonal responses to maximal exercise in non-insulin-dependent diabetes. J Appl Physiol 1990; 68:2067–2074. doi: 10.1152/jappl.1990.68.5.2067
Gillen JB, Little JP, Punthakee Z, Tarnopolsky MA, Riddell MC, Gibala MJ. Acute high-intensity interval exercise reduces the postprandial glucose response and prevalence of hyperglycaemia in patients with type 2 diabetes. Diabetes Obes Metab 2012;14:575-7. doi: 10.1111/j.1463-1326.2012.01564.x
Eriksen L, Dahl-Petersen I, Haugaard SB, Dela F. Comparison of the effect of multiple short-duration with single long-duration exercise sessions on glucose homeostasis in type 2 diabetes mellitus. Diabetologia 2007;50:2245-2253. doi:10.1007/s00125-007-0783-0
Goedecke JH, Dave JA, Faulenbach MV, Utzschneider KM, Lambert EV,West S, et al. Insulin response in relation to insulin sensitivity: an appropriate beta-cell response in black South African women. Diabetes Care 2009;32:860-5. doi: 10.2337/dc08-2048
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;10:0133286. doi: 10.1371/journal.pone.0133286
Taylor JD, Fletcher JP, Mathis RA, Cade WT. Effects of moderate- versus high-intensity exercise training on physical fitness and physical function in people with type 2 diabetes: a randomized clinical trial. Phys Ther 2014;94:1720-30. doi: 10.2522/ptj.20140097
McCarthy MI, Zeggini E: Genome-wide association studies in type 2 diabetes. Curr Diab Rep 2009;9:164-171.
Pierre W, Gildas AJ, Ulrich MC, Modeste WN, Benoit NT, Albert K. Hypoglycemic and hypolipidemic effects of Bersama engleriana leaves in nicotinamide streptozotocin-induced type 2 diabetic rats. BMC Complementary and Alternative Medicine 2012;12:264-69. doi: 10.1186/1472-6882-12-264
Staiger H, Machicao F, Schäfer SA, Kirchhoff K, Kantartzis K, Guthoff M, et al. Polymorphisms within the novel type 2 diabetes risk locus MTNR1B determine beta-cell function. PLoS One 2008;3:e3962. doi: 10.1371/journal.pone.0003962
Chambers JC, Zhang W, Zabaneh D, Sehmi J, Jain P, McCarthy MI, et al. Common genetic variation near melatonin receptor MTNR1B contributes to raised plasma glucose and increased risk of type 2 diabetes among Indian Asians and European Caucasians. Diabetes 2009;58:2703-8. doi: 10.2337/db08-1805
Park S, Hong SM, Lee JE, Sung SR. Exercise improves glucose homeostasis that has been impaired by a high-fat diet by potentiating pancreatic B- cell function and mass through IRS2 in diabetic rats. J Appl Physiol 2007;103:1764-71. doi:10.1152/japplphysiol.00434.2007
Sigal RJ, Armstrong MJ, Colby P, et al. Canadian diabetes association 2013 clinical practice guidelines for the prevention and management of diabetes in Canada. Can J Diabetes 2013;37:S1-3. doi: 0.1016/j.jcjd.2013.01.009
Adeghate E, Schattner P, Dunn E. An update on the etiology and epidemiology of diabetes mellitus. Ann NY Acad Sci 2006;1084,1-29. doi:10.1196/annals.1372.029
Amra C, Alibegovic, Mette P. Sonne, Lise Højbjerre, Torben Hansen, Oluf Pedersen, Gerrit van Hall, et al 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. doi: 10.2337/db09-0918
Dupuis J, Langenberg C, Prokopenko I, Saxena R, Soranzo N, Jackson AU, et al. New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk. Nat Genet 2010; 42:105-116. doi: 10.1038/ng.520
Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002;346:393-403. doi: 10.1056/NEJMoa012512
Tuomilehto J, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med 2001; 344:1343-1350. doi:10.1056/NEJM200105033441801
Teixeira-Lemos E, Nunes S, Teixeira F, Reis F. Regular physical exercise training assists in preventing type 2 diabetes development: focus on its antioxidant and anti-inflammatory properties. Cardiovasc Diabetol 2011;10:1-15. doi: 10.1186/1475-2840-10-12
Gleeson M, Bishop NC, Stensel DJ, Lindley MR, Mastana SS, Nimmo MA. The anti-inflammatory effects of exercise: mechanisms and implications for the prevention and treatment of disease. Nat Rev Immunol 2011;11:607-15. doi: 10.1038/nri3041
Stephan F, E Praet , Luc J. C, van Loon. Exercise therapy in Type 2 diabetes. Acta Diabetol 2009;46:263-278. doi: 10.1007/s00592-009-0129-0
Joy A. Dugan, CSCS, MPH, PA-C. Exercise recommendations for patients with type 2 diabetes. JAAPA 2016;29:13-8. doi: 10.1097/01.JAA.0000475460.77476.f6
Colberg SR, Sigal RJ, Fernhall B, Regensteiner JG, Blissmer BJ, Rubin RR, et al. Exercise and type 2 diabetes: the American College of Sports Medicine and the American Diabetes Association: joint position statement. Diabetes Care 2010;33:e147-67. doi: 10.2337/dc10-9990
Duncan GE, Anton SD, Sydeman SJ, Newton RL Jr, Corsica JA, Durning PE, et al. Prescribing exercise at varied levels of intensity and frequency: a randomized trial. Arch Intern Med 2005;165:2362-9. doi:10.1001/archinte.165.20.2362
Bjorntorp P, Fahlen M, Grimby G, Gustafson A, Holm J, Renstrom P, et al. Carbohydrate and lipid metabolism in middle-aged, physically well-trained men. Metabolism 1972;21:1037-44. doi: 10.1016/0026-0495(72)90034-0
Gibala MJ. High intensity interval training: new insights. Sports Science Exchange 2007;20:1-8.
Shaban N, Kenno KA, Milne KJ. The effects of a 2 weekmodified high intensity interval training program on the homeostatic model of insulin resistance (HOMA-IR) in adults with type 2 diabetes. J Sports Med Phys Fitness 2014;54:203-9.
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;111:1554-60. doi: 10.1152/japplphysiol.00921
Karstoft K,Winding K, Knudsen SH, James NG, Scheel MM, Olesen J, et al. Mechanisms behind the superior effects of interval vs continuous training on glycaemic control in individuals with type 2 diabetes: a randomised controlled trial. Diabetologia 2014;57:2081-93. doi: 10.1007/s00125-014-3334-5
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;32:1807-11. doi: 10.2337/dc09-0032
Mikus CR, Oberlin DJ, Libla J, Boyle LJ, Thyfault JP. Glycaemic control is improved by 7 days of aerobic exercise training in patients with type 2 diabetes. Diabetologia 2012;55:1417-23. doi: 10.1007/s00125-012-2490-8
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