تاثیر دوازده هفته تمرین تداومی و تناوبی روی برخی آدیپوکاین و هپاتوکاین ها و مقاومت به انسولین در موش های دیابتی نوع یک

فصلنامه زیست شناسی جانوری

دوره 16، شماره 1، آذر 1402، صفحه 83-101   

نوع مقاله: مقالات پژوهشی

شناسه دیجیتال (DOI): 10.22034/ascij.2023.1979751.1466

نویسندگان

محمد سلماسی؛ محمد رضا ذولفقاری دیدنی^* ؛ اکبر نوری حبشی

گروه فیزیولوژی ورزشی و حرکات اصلاحی، دانشکده علوم ورزشی، دانشگاه ارومیه، ارومیه، ایران

چکیده

دیابت به عنوان یکی از بیماری­های بسیار توسعه یافته در جهان و از دلایل اصلی مرگ و میر در نظر گرفته می­شود. از راه­های پیشگیری از دیابت و جلوگیری از عوارض ناشی از آن، انجام فعالیت به روش­های مختلف است. هدف از پژوهش حاضر بررسی مقایسه تاثیر دوازده هفته تمرین تداومی و تناوبی روی فتوئین b، فتوئین a و گلیپیکان 4 پلاسما و مقاومت به انسولین در موش های دیابتی نوع 1 بود. برای این منظور 40 موش دیابتی نوع یک به 4 گروه کنترل-سالم، کنترل دیابت، دیابت تمرین تداومی و دیابت تمرین تناوبی تقسیم شدند.گروه تناوبی با دویدن روی در وهله­های 3 دقیقه‌ای با سرعت 20 متر در دقیقه و ریکاوری فعال با سرعت 10 متر در دقیقه با شیب صفر درصد به مدت 3 دقیقه روی تردمیل، شش تکرار در هر جلسه انجام شد (مدت زمان کل 36 دقیقه). گروه‌ تمرین تداومی نیز دویدن را با سرعت 15 متر در دقیقه به مدت 36 دقیقه با شیب 0% درصد انجام دادند. کشتار موشها 48 ساعت بعد از آخرین جلسه تمرینی انجام و خونگیری انجام شد. جهت مقایسه بین گروه‌ها از آزمون آنالیز واریانس یک طرفه و آزمون تعقیبی بونفرونی استفاده شد. بررسی تغییرات بین گروهی نشان داد که تفاوت معنی دار بین گروه­ها برای مقاومت به انسولین، فتوئین b، فتوئین a و گلیپیکان 4 پلاسما وجود دارد (001/0p <). بررسی تغییرات بین کروهی نشان داد که مقاومت به انسولین، فتوئین b، فتوئین a و گلیپیکان 4 پلاسما کاهش معنی دار در گروه سالم نسبت به گروه دیابتی داشتند  (001/0p <). همچنین بین گروه کنترل دیابت با گروه های تمرین تداومی و تمرین تناوبی تفاوت معنی دار بین همه شاخص­ها وجود داشت (001/0p <). نتایج پژوهش حاضر نشان داد که تمرین هوازی و تمرین تناوبی میتوانند باعث کاهش فتوئین b، فتوئین a و گلیپیکان 4 پلاسما در موشهای دیابتی نوع 1 شوند. این بهبودها در گروه تمرین تناوبی نسبت به تمرین تداومی بهتر بود.

کلیدواژه‌ها

تمرین تناوبی؛ تمرین هوازی؛ دیابت نوع 1؛ مقاومت به انسولین

مراجع

1. Gesta, S., et al., Evidence for a role of developmental genes in the origin of obesity and body fat distribution. Proceedings of the National Academy of Sciences, 2006. 103(17): p. 6676-6681.
2. Kyu, H.H., et al., Physical activity and risk of breast cancer, colon cancer, diabetes, ischemic heart disease, and ischemic stroke events: systematic review and dose-response meta-analysis for the Global Burden of Disease Study 2013. bmj, 2016. 354: p. i3857.
3. Maury, E. and S. Brichard, Adipokine dysregulation, adipose tissue inflammation and metabolic syndrome. Molecular and cellular endocrinology, 2010. 314(1): p. 1-16.
4. Grundy, S.M., et al., Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute scientific statement. Circulation, 2005. 112(17): p. 2735-2752.
5. Ussar, S., et al., Glypican-4 enhances insulin signaling via interaction with the insulin receptor and serves as a novel adipokine. Diabetes, 2012. 61(9): p. 2289-2298.
6. Zhu, K., et al., Increased serum levels of fetuin B in patients with coronary artery disease. Endocrine, 2017. 58(1): p. 97-105.
7. Pérez-Sotelo, D., et al., Visceral and subcutaneous adipose tissue express and secrete functional alpha2hsglycoprotein (fetuin a) especially in obesity. 2017. 55(2): p. 435-446.
8. Reinehr, T., C.L.J.T.J.o.C.E. Roth, and Metabolism, Fetuin-A and its relation to metabolic syndrome and fatty liver disease in obese children before and after weight loss. 2008. 93(11): p. 4479-4485.
9. Srinivas, P., et al., Serum alpha 2-HS-glycoprotein is an inhibitor of the human insulin receptor at the tyrosine kinase level. Molecular Endocrinology, 1993. 7(11): p. 1445-1455.
10. Mathews, S.T., et al., Improved insulin sensitivity and resistance to weight gain in mice null for the Ahsg gene. 2002. 51(8): p. 2450-2458.
11. Pal, D., et al., Fetuin-A acts as an endogenous ligand of TLR4 to promote lipid-induced insulin resistance. Nature medicine, 2012. 18(8): p. nm. 2851.
12. Stefan, N., et al., Plasma fetuin-A levels and the risk of type 2 diabetes. 2008.
13. Jensen, M.K., et al., Fetuin-A, type 2 diabetes, and risk of cardiovascular disease in older adults: the cardiovascular health study. Diabetes care, 2013. 36(5): p. 1222-1228.
14. Hennige, A.M., et al., Fetuin-A induces cytokine expression and suppresses adiponectin production. 2008. 3(3): p. e1765.
15. Ismail, N.A., et al., Fetuin-A levels in obesity: differences in relation to metabolic syndrome and correlation with clinical and laboratory variables. 2012. 8(5): p. 826.
16. Singh, M., et al., Role of fetuin‐A in atherosclerosis associated with diabetic patients. 2012. 64(12): p. 1703-1708.
17. Xu, Y., et al., Serum fetuin-A is correlated with metabolic syndrome in middle-aged and elderly Chinese. 2011. 216(1): p. 180-186.
18. Kralisch, S., et al., The novel adipokine/hepatokine fetuin B in severe human and murine diabetic kidney disease. 2017. 43(5): p. 465-468.
19. Fenske, W., et al., Obesity-related cardiorenal disease: the benefits of bariatric surgery. 2013. 9(9): p. 539.
20. Meex, R.C., et al., Fetuin B is a secreted hepatocyte factor linking steatosis to impaired glucose metabolism. 2015. 22(6): p. 1078-1089.
21. Zhu, J., et al., Serum fetuin B level increased in subjects of nonalcoholic fatty liver disease: a case-control study. Endocrine, 2017. 56(1): p. 208-211.
22. Choi, J.W., et al., Plasma proteome analysis in diet‐induced obesity‐prone and obesity‐resistant rats. Proteomics, 2010. 10(24): p. 4386-4400.
23. Jung, S.H., et al., The serum protein fetuin-B is involved in the development of acute myocardial infarction. Clinical Science, 2015. 129(1): p. 27-38.
24. Watts, G. and D. Playford, Dyslipoproteinaemia and hyperoxidative stress in the pathogenesis of endothelial dysfunction in non-insulin dependent diabetes mellitus: an hypothesis. Atherosclerosis, 1998. 141(1): p. 17-30.
25. Renard, C.B., et al., Diabetes and diabetes-associated lipid abnormalities have distinct effects on initiation and progression of atherosclerotic lesions. The Journal of clinical investigation, 2004. 114(5): p. 659-668.
26. Ballor, D.L., et al., Contrasting effects of resistance and aerobic training on body composition and metabolism after diet-induced weight loss. Metabolism, 1996. 45(2): p. 179-183.
27. Gibala, M.J. and S.L. McGee, Metabolic adaptations to short-term high-intensity interval training: a little pain for a lot of gain? Exercise and sport sciences reviews, 2008. 36(2): p. 58-63.
28. Blumenthal, J.B., et al., Effects of exercise training and weight loss on plasma Fetuin-a levels and insulin sensitivity in overweight older men. Journal of diabetes research, 2017. 2017.
29. Schultes, B., et al., The effect of 6-weeks of aerobic exercise training on serum fetuin-A levels in non-diabetic obese women. Experimental and clinical endocrinology & diabetes, 2010. 118(10): p. 754.
30. Malin, S.K., et al., Exercise-induced lowering of fetuin-A may increase hepatic insulin sensitivity. Medicine and science in sports and exercise, 2014. 46(11): p. 2085.
31. Roberts, I., et al., Does animal experimentation inform human healthcare? Observations from a systematic review of international animal experiments on fluid resuscitation. BMJ: British Medical Journal, 2002. 324(7335): p. 474.
32. Islas-Andrade, S., et al., Streptozotocin and alloxan in experimental diabetes: comparison of the two models in rats. Acta Histochemica et Cytochemica, 2001. 33(3): p. 201-208.
33. Moreira, J.B., et al., High-versus moderate-intensity aerobic exercise training effects on skeletal muscle of infarcted rats. Journal of Applied Physiology, 2013. 114(8): p. 1029-1041.
34. Linden, M.A., et al., Treating NAFLD in OLETF rats with vigorous-intensity interval exercise training. Medicine and science in sports and exercise, 2015. 47(3): p. 556.
35. Gorbanian, B. and Y. Saberi, Changes in Fetuin-B and RBP4 During A Course of High-Intensity Interval Training in Women with Nonalcoholic Fatty Liver. Journal of Babol University of Medical Sciences, 2021. 23(1): p. 398-404.
36. Samadi, A., et al., The effect of twelve weeks of combined training with and without canagliflozin consumption on fetuin A and fetuin B in type 2 diabetic men. Journal of Basic Research in Medical Sciences, 2020. 7(4): p. 20-30.
37. Schultes, B., et al., The effect of 6-weeks of aerobic exercise training on serum fetuin-A levels in non-diabetic obese women. Experimental and clinical endocrinology & diabetes, 2010. 118(10): p. 754-756.
38. Keihanian, A., H. Arazi, and M. Kargarfard, Effects of aerobic versus resistance training on serum fetuin-A, fetuin-B, and fibroblast growth factor-21 levels in male diabetic patients. Physiology International, 2019. 106(1): p. 70-80.
39. Ramírez-Vélez, R., et al., Effects of exercise training on Fetuin-a in obese, type 2 diabetes and cardiovascular disease in adults and elderly: a systematic review and Meta-analysis. Lipids in health and disease, 2019. 18(1): p. 1-11.
40. Ix, J.H. and K. Sharma, Mechanisms linking obesity, chronic kidney disease, and fatty liver disease: the roles of fetuin-A, adiponectin, and AMPK. Journal of the American Society of Nephrology, 2010. 21(3): p. 406-412.
41. Song, A., et al., Serum fetuin-A associates with type 2 diabetes and insulin resistance in Chinese adults. PloS one, 2011. 6(4): p. e19228.
42. Stefan, N., et al., α2-Heremans-Schmid glycoprotein/fetuin-A is associated with insulin resistance and fat accumulation in the liver in humans. Diabetes care, 2006. 29(4): p. 853-857.
43. Brown, W., et al., Fetuin‐an old friend revisited. Bioessays, 1992. 14(11): p. 749-755.
44. BROWN, W.M., et al., The nucleotide and deduced amino acid structures of sheep and pig fetuin: common structural features of the mammalian fetuin family. European journal of biochemistry, 1992. 205(1): p. 321-331.
45. Stefan, N., et al., Plasma fetuin-A levels and the risk of type 2 diabetes. Diabetes, 2008. 57(10): p. 2762-2767.
46. Wojtysiak-Duma, B., et al., Serum fetuin-A levels in patients with type 2 diabetes mellitus. Ann UMCS Sect, 2010. 1500(2).
47. Pal, D., et al., Fetuin-A acts as an endogenous ligand of TLR4 to promote lipid-induced insulin resistance. Nature medicine, 2012. 18(8): p. 1279-1285.
48. Agarwal, S., et al., Fetuin-A downregulates adiponectin through Wnt-PPARγ pathway in lipid induced inflamed adipocyte. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 2017. 1863(1): p. 174-181.
49. Hennige, A.M., et al., Fetuin-A induces cytokine expression and suppresses adiponectin production. PloS one, 2008. 3(3): p. e1765.
50. Vickers, N.J., Animal communication: when i’m calling you, will you answer too? Current biology, 2017. 27(14): p. R713-R715.
51. Gerst, F., et al., Metabolic crosstalk between fatty pancreas and fatty liver: effects on local inflammation and insulin secretion. Diabetologia, 2017. 60(11): p. 2240-2251.
52. Kim, H.-E., et al., Tumour necrosis factor-a-induced glucose-stimulated insulin secretion inhibition in INS-1 cells is ascribed to a reduction of the glucose-stimulated Ca2+ influx. Journal of Endocrinology, 2008. 198(3): p. 549-560.
53. Lanuza-Masdeu, J., et al., In vivo JNK activation in pancreatic β-cells leads to glucose intolerance caused by insulin resistance in pancreas. Diabetes, 2013. 62(7): p. 2308-2317.
54. Almarashda, O., et al., Hepatokines Fetuin-A and Fetuin-B status in obese Saudi patient with diabetes mellitus type 2. American Journal of Translational Research, 2022. 14(5): p. 3292.
55. Saeidi, A., et al., Diabetes, Insulin Resistance, Fetuin-B and Exercise Training. Annals of applied sport science, 2019. 7(2): p. 1-2.
56. Peter, A., et al., The hepatokines fetuin-A and fetuin-B are upregulated in the state of hepatic steatosis and may differently impact on glucose homeostasis in humans. American Journal of Physiology-Endocrinology and Metabolism, 2018. 314(3): p. E266-E273.
57. Andersson, A., et al., Effects of physical exercise on phospholipid fatty acid composition in skeletal muscle. American Journal of Physiology-Endocrinology and Metabolism, 1998. 274(3): p. E432-E438.
58. Dela, F., et al., GLUT 4 and insulin receptor binding and kinase activity in trained human muscle. The Journal of physiology, 1993. 469(1): p. 615-624.
59. Dela, F., et al., Physical training increases muscle GLUT4 protein and mRNA in patients with NIDDM. Diabetes, 1994. 43(7): p. 862-865.
60. Li, K., et al., Glypican-4 is increased in human subjects with impaired glucose tolerance and decreased in patients with newly diagnosed type 2 diabetes. Acta diabetologica, 2014. 51(6): p. 981-990.
61. Yoo, H., et al., Association of glypican-4 with body fat distribution, insulin resistance, and nonalcoholic fatty liver disease. The Journal of Clinical Endocrinology & Metabolism, 2013. 98(7): p. 2897-2901.
62. Dag, H., N.C. Dag, and O. Dikker, Increased glypican-4 levels are associated with obesity in adolescents. Iranian Journal of Pediatrics, 2019. 29(6).
63. Abdolmaleki, F. and A. Heidarianpour, Endurance exercise training restores diabetes-induced alteration in circulating Glycosylphosphatidylinositol-specific phospholipase D levels in rats. Diabetology & Metabolic Syndrome, 2020. 12(1): p. 1-8.
64. Zandi, B. and B. Abedi, Effects of Aerobic Training with Ginger Consumption on Plasma Levels of Adipokine Glipican-4 and Hepatokine Fetuin-A in Rats with Non-alcoholic Fatty Livers. Iranian Journal of Nutrition Sciences & Food Technology: p. 9-18.
65. Tamori, Y. and M. Kasuga, Glypican‐4 is a new comer of adipokines working as insulin sensitizer. Journal of diabetes investigation, 2013. 4(3): p. 250.