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اثر تمرین هوازی روی تردمیل بر سطوح آدیپولین، گلوکز و انسولین در رت‌‌های نر دیابتی نوع 2 | ||
| مطالعات کاربردی تندرستی در فیزیولوژی ورزش | ||
| مقاله 12، دوره 5، شماره 1، بهار 1397، صفحه 93-105 اصل مقاله (1.07 MB) | ||
| نوع مقاله: مقاله پژوهشی | ||
| شناسه دیجیتال (DOI): 10.22049/jassp.2019.26571.1238 | ||
| نویسندگان | ||
رحیم رحیم پور1؛ جواد مهربانی   2
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| 1کارشناس ارشد فیزیولوژی ورزشی، دانشکده تربیت بدنی و علوم ورزشی دانشگاه گیلان، رشت، ایران | ||
| 2استادیار گروه فیزیولوژی ورزش، دانشکده تربیت بدنی و علوم ورزشی دانشگاه گیلان، رشت، ایران. | ||
| چکیده | ||
| Secretion of pro-inflammatory and anti-inflammatory cytokines play a critical role in the regulation of metabolic conditions. This study examines the effect of eight weeks aerobic training on Adipolin cytokine and insulin resistance index in type 2 diabetic male rats. Eighteen 8-10 weeks Wister rats with 200-220 gr are selected and they divided equaly into two diabetes [DBT] and control [CON] groups randomly. The training program includes 8 weeks of endurance training on a treadmill at a constant dip of 5%. The speed started from 10 meters per minute and it rised to the 25 meters per minute and its time started from 15 minutes to 45 minutes. In end of 8 weeks training, blood samples were taken after 12 hours of fasting in order to determination of insulin, glucose and Adipulin levels. The homeostatic model assessment [HOMA] was calculated as insulin resistance index. The data were analyzed using the an independent t test with the SPSS software ver. 16. A meaningful increase was observed in adipolin (1.36±0.054 vs. 1.11±0.065 ng/ml; p=0.002), and decrease in glucose (276.88±27.59 vs. 324.55±16.04 mg/dl; p=0.001), insulin (0.206±0.02 vs. 0.235±0.02 mU/l; p=0.033) and insulin resistance (2.55±0.495 vs. 3.40±0.468 mg/dl; p=0.002). According to the findings, it seems that aerobic training with moderate intensity will lead to decreasing in insulin resistance and increase in serum levels of Adipulin in type 2 diabetic rats. | ||
| کلیدواژه‌ها | ||
| تمرین هوازی؛ آدیپولین؛ مقاومت به انسولین؛ دیابت نوع 2 | ||
| مراجع | ||
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1. Tan, B.K., et al. (2014). Circulatory changes of the novel adipokine adipolin/CTRP12 in response to metformin treatment and an oral glucose challenge in humans. Clinical endocrinology, 81(6): 841-846. 2. Enomoto, T., et al., (2011). Adipolin/C1qdc2/CTRP12 protein functions as an adipokine that improves glucose metabol ism. Journal of Biological Chemistry, 286(40): 34552-34558. 3. Yang, Q., et al. (2005). Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes. Nature, 436(7049): p. 356-362. 4. Peterson, J.M., Z. Wei, and G.W. Wong. (2010). C1q/TNF-related protein-3 (CTRP3), a novel adipokine that regulates hepatic glucose output. Journal of Biological Chemistry, 285(51): 39691-39701. 5. Frydelund-Larsen, L., et al. (2007). Visfatin mRNA expression in human subcutaneous adipose tissue is regulated by exercise. American Journal of Physiology-Endocrinology and Metabolism, 292(1): p. E24-E31. 6. Tan, B.K., et al. (2013). Metformin increases the novel adipokine adipolin/CTRP12: role of the AMPK pathway. Journal of Endocrinology, 219(2): p. 101-108. 7. Wei, Z., et al. (2012). C1q/TNF-related protein-12 (CTRP12), a novel adipokine that improves insulin sensitivity and glycemic control in mouse models of obesity and diabetes. Journal of Biological Chemistry, 287(13): p. 10301-10315. 8. Shehzad, A., et al. (2012). Adiponectin: regulation of its production and its role in human diseases. Hormones (Athens), 11(1): p. 8-20. 9. Choi, K., et al. (2007). Effect of exercise training on plasma visfatin and eotaxin levels. European Journal of Endocrinology, 157(4): p. 437-442. 10. Arner, P. (2006). Visfatin-a true or false trail to type 2 diabetes mellitus. The Journal of clinical endocrinology and metabolism, 91(1): p. 28. 11. Balducci S, Zanuso S, Nicolucci A, et al. (2010). Anti-inflammatoryeffect of exercise training in subjects with type 2 diabetes and the metabolic syndrome isdependenton exercise modalities and independent of weightloss. Nutr Metab Cardiovasc Dis, 20(8): 608-17. 12. Kawamata Y, Imamura T, Babendure JL, et al. (2007). Tumor necrosis factor receptor-1 can function through a G alphaq/11-betaarrestin- 1 signaling complex. J Biol Chem, 282(39): 28549-56. 13. Ouchi N, Higuchi A, Ohashi K, et al. (2010). Sfrp5 is an anti-inflammatory adipokine that modulates metabolic dysfunction in obesity. Science, 329:454-457. 14. CnopM, FoufelleF, VellosoLA. (2012). Endoplasmicreticulum stress, obesity and diabetes. Trends Mol Med, 18(1): 59-68. 15. Hotamisligil GS, Shargill NS, Spiegelman BM. (1993). Adipose expression of tumor necrosisfactor-alpha: direct role in obesity-linked insulin resistance. Science, 259: 87-91. 16. Henriksen EJ. (2002). Effects of acuteexercise and exercise training on insulin resistance. J Appl Physiol, 93(2): 788-96. 17. Brooks N, Layne JE, Gordon PL, et al. (2007). Strength trainingimproves muscle quality and insulin sensitivity inHispanic older adults with type 2 diabetes. Int JMed Sci, 4(1): 19-27. 18. Rodrigues B, Figueroa D, Mostarda C, et al. (2007). Maxima exercise test is a useful method for physical capacity and oxygen consumption determination in streptozotocin-diabetic rats. Cardiovascular Dialectology, 6(38):125-131. | ||
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