Document Type : Research Paper I Open Access I Released under CC BY-NC 4.0 license


1 Department of Sports Physiology, Faculty of Sport Sciences and Health, University of Tehran, Tehran, Iran

2 Department of Sports Physiology, Faculty of Physical Education and Sports Sciences, Ferdowsi University of Mashhad, Mashhad, Iran.

3 Department of Sports Physiology, Faculty of Sport Sciences and Health, University of Tehran, Tehran, Iran.

4 Department of Basic Sciences, Chabahar Maritime University, Chabahar, Sistan and Baluchestan, Iran


Introduction: Asprosin is a protein hormone that is mainly secreted by fat cells and enters the bloodstream. In the present study, the effect of 8-week continuous training was investigated on serum levels of asprosin, insulin, and insulin resistance index in obese rats.
Methods: For this, 32 male Wistar rats (mean weight=180/23±7 grams) were randomly divided into four groups of Healthy Control (N=8), Obese Control (N=8), Healthy Training (N=8), and Obese Training (N=8). The continuous training group performed the training protocol for 8 weeks, and 48 hours after the end of the last training session, the rats were anesthetized and euthanized. The variables of interest (serum levels of asprosin, level of glucose, insulin, and insulin resistance index) were measured in rats. Data analysis was performed using the KruskalWallis test at the significance level of α=0.05.
Results: There was a significant difference among mean serum levels of asprosin (p<0/001), insulin (p<0/001), fasting glucose (p<0/001), and insulin resistance index (p<0/001) in the Healthy Control, Obese Control, Healthy Training, and Obese Training groups.
Conclusion: Based on the results of the present study, it seems that obesity has a significant effect on increasing asprosin levels and continuous exercise has a significant effect on reducing asprosin levels. Therefore, continuous training can be used as an important strategy to reduce asprosin levels and weight.


Main Subjects

  1. Burke V, Beilin LJ, Cutt HE, Mansour J, Williams A, Mori TA. A lifestyle program for treated hypertensives improved health-related behaviors and cardiovascular risk factors, a randomized controlled trial. J Clin Epidemiol. 2007;60(2):133–41.
  2. Carrut BR, Skinner JD. The role of dietary calcium and other nutrients in moderating body fat in preschool children. Int J Obes. 2001;25(4):559–66.
  3. Varo JJ, Martínez-González MA, de Irala-Estévez J, Kearney J, Gibney M, Martínez JA. Distribution and determinants of sedentary lifestyle in the European Union. Int J Epidemiol. 2003;32(1):138–46.
  4. Watts K, Jones TW, Davis EA, Green D. Exercise training in obese children and adolescents: Current concepts. Sport Med. 2005;35(5):375–92.
  5. Kyrölinen H, Santtila M, Nindl BC, Vasankari T. Physical fitness profiles of young men: Associations between physical fitness, obesity and health. Sport Med. 2010;40(11):907–20.
  6. O’Neill B, Simha V, Kotha V, Garg A. Body fat distribution and metabolic variables in patients with neonatal progeroid syndrome. Am J Med Genet Part A. 2007;143(13):1421–30.
  7. Milewicz DM, Grossfield J, Cao SN, Kielty C, Covitz W, Jewett T. A mutation in FBN1 disrupts profibrillin processing and results in isolated skeletal features of the Marian syndrome. J Clin Invest. 1995;95(5):2373–8.
  8. Bindlish S, Presswala LS, Schwartz F. Lipodystrophy: Syndrome of severe insulin resistance. Postgrad Med. 2015;127(5):511–6.
  9. Jacquinet A, Verloes A, Callewaert B, Coremans C, Coucke P, de Paepe A, et al. Neonatal progeroid variant of Marfan syndrome with congenital lipodystrophy results from mutations at the 3’ end of FBN1 gene. Eur J Med Genet. 2014;57(5):230–4.
  10. Goldblatt J, Hyatt J, Edwards C, Walpole I. Further evidence for a marfanoid syndrome with neonatal progeroid features and severe generalized lipodystrophy due to frameshift mutations near the 3’ end of the FBN1 gene. Am J Med Genet Part A. 2011;155(4):717–20.
  11. Romere C, Duerrschmid C, Bournat J, Constable P, Jain M, Xia F, et al. Asprosin, a Fasting-Induced Glucogenic Protein Hormone. Cell. 2016;165(3):566–79.
  12. Zhang L, Chen C, Zhou N, Fu Y, Cheng X. Circulating asprosin concentrations are increased in type 2 diabetes mellitus and independently associated with fasting glucose and triglyceride. Clin Chim Acta. 2019;489:183–8.
  13. Wang Y, Qu H, Xiong X, Qiu Y, Liao Y, Chen Y, et al. Plasma asprosin concentrations are increased in individuals with glucose dysregulation and correlated with insulin resistance and first-phase insulin secretion. Mediators Inflamm. 2018;2018.
  14. Duerrschmid C, He Y, Wang C, Li C, Bournat JC, Romere C, et al. Asprosin is a centrally acting orexigenic hormone. Nat Med. 2017;23(12):1444–53.
  15. Fathi M, Gharakanlou R, Rezaei R. The effect of endurance training on left ventricle serum response factor gene expression in Wistar male rats. J Shahrekord Uuniversity Med Sci. 2015;17:(in persian).
  16. Chang YH, Chang DM, Lin KC, Shin SJ, Lee YJ. Visfatin in overweight/obesity, type 2 diabetes mellitus, insulin resistance, metabolic syndrome and cardiovascular diseases: A meta-analysis and systemic review. Diabetes Metab Res Rev. 2011;27(6):515–27.
  17. Ghanbarzadeh M, Omidi M. The Effects of Physical Activity on Serum Visfatin Level: A Literature Review. Int J Basic Sci Med. 2017;2(2):83–9.
  18. Mir P, Mir Z. Effect of 8 weeks pilates exercise on plasma visfatin and insulin resistance index in obese women. Nurs J Vulnerable. 2016;3(8):1-12 (in persian).
  19. SEIFI L, DARYANOOSH F, SAMADI M. The effect of 12 weeks aerobic exercise training on visfatin, chemerin serum changes in 45-60 year old obese women with type2 diabetes. 2016;(in persian).
  20. Taghian F, Zolfaghary M, Hedayati M. Effect of 12 weeks aerobic exercise on visfatin level and insulin resistance in obese women. Razi J Med Sci. 2014;20(116):35-44 (in persian).