The Role of Chemerin and Myostatin after Physical Activity
Authors: M. J. Pourvaghar, M. E. Bahram
Abstract:
Obesity and overweight is one of the most common metabolic disorders in industrialized countries and in developing countries. One consequence of pathological obesity is cardiovascular disease and metabolic syndrome. Chemerin is an adipocyne that plays a role in the regulation of the adipocyte function and the metabolism of glucose in the liver and musculoskeletal system. Most likely, chemerin is involved in obesity-related disorders such as type 2 diabetes and cardiovascular disease. Aerobic exercises reduce the level of chemerin and cause macrophage penetration into fat cells and inflammatory factors. Several efforts have been made to clarify the cellular and molecular mechanisms of hypertrophy and muscular atrophy. Myostatin, a new member of the TGF-β family, is a transforming growth factor β that its expression negatively regulates the growth of the skeletal muscle; and the increase of this hormone has been observed in conditions of muscular atrophy. While in response to muscle overload, its levels decrease after the atrophy period, TGF-β is the most important cytokine in the development of skeletal muscle. Myostatin plays an important role in muscle control, and animal and human studies show a negative role of myostatin in the growth of skeletal muscle. Separation of myostatin from Golgi begins on the ninth day of the onset period and continues until birth at all times of muscle growth. Higher levels of myostatin are found in obese people. Resistance training for 10 weeks could reduce levels of plasma myostatin.
Keywords: Chemerin, myostatin, obesity, physical activity.
Digital Object Identifier (DOI): doi.org/10.5281/zenodo.1474618
Procedia APA BibTeX Chicago EndNote Harvard JSON MLA RIS XML ISO 690 PDF Downloads 777References:
[1] C. Martins, MD. Robertson, LM. Morgan, “Effects of exercise and restrained eating behaviour on appetite control,” Proc Nutr Soc., 67 (1): 28-41. 2008.
[2] YJ. Hah, NK. Kim, MK. Kim, HS. Kim, SH. Hur, HJ. Yoon, et al. “Relationship between chemerin levels and cardiometaolic parameters and degree of coronary stenosis in korean patients with coronary artery disease,” Diabetes and Meta J., 35(3): 248-54. 2011.
[3] E. Maury, SM. Brichard, “Adipokine dysregulation, adipose tissue inflammation and metabolic syndrome,” Mol Cell Endocrinol., 314:1-16. 2010.
[4] M. Saghebjoo, R. Fathi, E. Talebi-Ghorghani, A. Hosseini-Kakhak, A. Ghanbari-Niaki, M. Hedayati, “Obestatin and the regulation of energy balance in physical activity,” Iranian Journal of Endocrinology and Metabolism., 12 (6): 647-55. 2010.
[5] A. Saremi, M. Moslehabadi, M. Parastesh, “Effects of twelve-week strength training on serum chemerin,” TNF-Α And CRP Level in Subjects with the Metabolic Syndrome. Iranian Journal of Endocrinology and Metabolism., 12 (5): 536-43. 2011.
[6] D. Stejskal, M. Karpisek, Z. Hanulova, “Chemerin is an independent marker of the metabolic syndrome in a Caucasian population--a pilot study,” Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub., 152: 217-21. 2008.
[7] B. Dong, W. Ji, Y. Zhang, “Elevated serum chemerin levels are associated with the presence of coronary artery disease in patients with metabolic syndrome,” Inter Med., 50 (10): 1093-97. 2011.
[8] C. Matthew, J. Ernst Christopher, “Chemerin: at the crossroads of inflammation and obesity,” Trends In Endo And Meta., 21(11): 660-67. 2010.
[9] MC. Ernst, CJ. Sinal, “Chemerin: at the crossroad of inflammation and obesity,” Trends Endo Meta., 21: 660-7. 2010.
[10] OA. Mac Dougald, CF. Burant, “The rapidly expanding family of adipokines,” Cell Metab., 6: 159-61. 2007.
[11] S. Mora, IM. Lee, JE. Buring, PM. Ridker, “Association of physical activity and body mass index with novel and traditional cardiovascular biomarkers in women,” JAMA., 295(12):1412-1419. 2006.
[12] M. Sherafati-Moghadam, F. Daryanoosh, M. Mohammadi, M. Kooshki Jahromi, H. Alizadeh-Palavani, “The effect of eight-week intense sprint exercise on plasma levels of vaspin and chemerin in female Sprague-Dawley rats,” Scientific-Research Journal of Shahed University., 21(107):1-9. 2013.
[13] S. Fadaei Raehanabadi, R. Fathi, B. Nokhostin Rohi, “Effects of aerobic training on resting levels of chemerin and plasma lipids in overweight women,” Exercise physiology., 18, 121-136. 2011.
[14] A. Saremi, N. Shavandi, M. Parastesh, H. Daneshmand “Twelve-week aerobic training decreases chemerin level and improves cardiometabolic risk facrors in overweight and obese men,” Asian Journal of Sports Medicine., 1(3): 151-158. 2010.
[15] Khademosharie T, Amiri Parsa MR. Hamedinia MS, Hosseini-Kakhk SAR. “Effects of two aerobic training protocols on Vaspin, Chemerin and lipid profile in woman with type 2 diabetes,” ISMJ., 17(4): 571-81. 2014.
[16] M. J. Pourvaghar, “Impact of a 2-month aerobic exercise on CRP of overweight female students,” Feyz., 17(4): 380-386. 2013.
[17] M. Zolfaghary, F. Taghian, M. Hedayati, “The Effects of Green Tea Extract Consumption, Aerobic Exercise and a Combination of These on Chemerin Levels and Insulin Resistance in Obese Women,” Iranian Journal of Endocrinology and Metabolism., 3(15): 253-261. 2013.
[18] K. Bozaoglu, D. Segal, KA. Shields, N. Cummings, JE. Curran, AG. Comuzzie, et al. “Chemerin is associated with metabolic syndrome phenotypes in a Mexican-American population,” J Clin Endocrinol Metab., 94: 3085-8. 2009.
[19] H. Sell, J. Laurencikiene, A. Taube, K. Eckardt, A. Cramer, A. Horrighs, “Chemerin is a novel adipocyte-derived factor inducing insulin resistance in primary Human skeletal muscle cells,” Diabetes., 58(12): 2731–40. 2009.
[20] T. J. Sledzinski, A. Korczynska, L. Hallmann, M. Kaska, T. Proczko-Markuszewska, M. Stefaniak, “The increase of serum chemerin concentration is mainly associated with the increase of body mass index in obese, non-diabetic subjects,” J. Endocrinol. Invest., 36: 428-434, 2013.
[21] P. Poirier, TD. Giles, GA. Bray, Y. Hong, JS. Stern, FX. Pi Sunyer, “Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss,” Arterioscler Thromb Vasc Biol., 26(5): 968-76. 2006.
[22] KB. Goralski, TC. McCarthy, EA. Hanniman, BA. Zabel, EC. Butcher, SD, Parlee, “Chemerin, a novel adipokine that regulates adipogenesis and adipocyte metabolism,” J Biol Chem., 282 (38): 28175-88. 2007.
[23] J. Kaur, R. Adya, BK. Tan, J. Chen, HS. Randeva, “Identification chemerin receptor (ChemR23) in human endothelial cells: Chemerin-induced endothelial angiogenesis,” Biochem Biophys Res Commun., 391(4): 1762-8. 2010.
[24] M. J. Pourvaghar, M. E. Bahram, M. Sayyah, Sh. Khoshemehry, The Effect of a Three-Month Intensive Intermittent Training on Plasma Chemerin and Factors Related to Body Composition on Overweight Males,” Armaghan Danesh., Vol. 20 , Number 5 (100); Pp. 381-392. Aug. 2015.
[25] SE. Wozniak, LL. Gee, MS. Wachtel, EE. Frezza “Adipose tissue: the new endocrine organ? A review article. Digestive Diseases and Sciences., 54 (9): 1847–56. 2009.
[26] F. Yamaner, T. Bayraktaroğlu, H. Atmaca, MA. Ziyagil, K. Tamer, “Serum leptin, lipoprotein levels, and glucose homeostasis, between national wrestlers and sedentary males,” Turk. J Med Sci., 40 (3): 471-77. 2010.
[27] JM. Bruun, JW. Helge, B. Richelsen, B. Stallknecht, “Diet and exercise reduce low-grade inflammation and macrophage infiltration in adipose tissue but not in skeletal muscle in severely obese subjects,” Am J Physiol., Vol. 290 no. 5, Apr. 2006.
[28] E. Cadore, R. Pinto, F. Lhullier, C. Correa, C. Alberton, S. Pinto, “Physiological effects of concurrent training in elderly men,” Int J Sports Med., 31 (10): 689. 2010.
[29] A. Matsakas, A. Friedel, T. Hertrampf, P. Diel, “Short‐term endurance training results in a muscle specific decrease of myostatin mRNA content in the rat,” “Acta physiologica scandinavica., 183 (3): 299-307. 2005.
[30] RS. Taipale, K. Häkkinen, “Acute hormonal and force responses to combined strength and endurance loadings in men and women: the order effect, Plos one., 8 (2): 55051. 2013.
[31] MR. Asad, J. Vakili “Effect of resistance training on plasma myostatin level in overweight untrained men,” Applied research of sport management., 1 (1): 75-80. 2012.
[32] TR. Lundberg, R. Fernandez-Gonzalo, T. Gustafsson, PA. Tesch “Aerobic exercise alters skeletal muscle molecular responses to resistance exercise,” Medicine and Science in Sports and Exercise., 44(9):1680-8. 2012.
[33] VG. Coffey, JA. Hawley “The molecular bases of training adaptation,” Sports Medicine 2007; 37(9): 737-63.
[34] A. Bonnieu, G. Carnac, B. Vernus “Myostatin in the pathophysiology of skeletal muscle. Current genomics., 8 (7): 415-22. 2007.
[35] MS. Clarke, DL. Feeback “Mechanical load induces sarcoplasmic wounding and FGF release in differentiated human skeletal muscle cultures,” FASEB J., 10(4): 502-9. 1996.