The Effect of an Acute Maximal Exercise on Serum Uncoupling Protein 1 (UCP1) Level and the Role of UCP1-3826 A/G Polymorphism
Project no. 20485 · Status: Kapanmış (Yayın bekleniyor) · 2019
Summary
Chronic diseases are mainly caused by obesity. Exercise induced irisin is thought to turn white adipose tissue (WAT) into brown adipose tissue by increasing the amount of uncoupling protein 1 (UCP-1) in WAT. UCP-1 causes heat generation instead of ATP synthesis during oxidative phosphorylation, resulting in reduction of adipose tissue through thermogenesis. Therefore, exercise is used as a means of preventing obesity. However, the effect of exercise on serum UCP-1 levels and the role of UCP- 1 A-3826G polymorphism (UCP1P) in this effect are uncertain. Therefore, this study investigated the effect of an acute maximal exercise on serum UCP-1, irisin, nitric oxide (NO) and interleukin 6 (IL-6) levels and the mediating role of UCP1P in sedentary individuals and athletes doing regular anaerobic training. For this purpose, Yo-Yo IR-1 test was applied to male basketball, volleyball and handball players (SG, n = 43, age: 20.65 ± 2.46 years) and healthy sedentary men (CG, n = 43, age: 22.49 ± 3.51 years). From pre-and post-test postprandial venous blood samples, serum UCP- 1, irisin, IL-6 and NO levels was determined by ELISA method; hemogram, serum urea, glucose levels, as well as serum total, high and low density lipoprotein cholesterol (TC, HDL-C and LDL-C), non-HDL cholesterol and triglyceride (TG) levels as blood lipid and lipoproteins, total oxidant/antioxidant status (TOS/TAS) ratio as oxidative stress (OS) index (OSI) and thiobarbituric acid reactive substances (TBARS) as another indicator of OS, creatine kinase (CK), alanine and aspartate amino transferase (ALT and AST) enzyme activities as indicators of muscle damage, C reactive protein (CRP) and leukocyte (WBC) levels as indicators of inflammation was measured by standard biochemical methods; and UCP1P was determined from genomic DNA samples by restriction fragment length polymorphism analysis (PCRRFLP) method. Acute exercise increased serum UCP-1, irisin, IL-6, NO, urea, creatinine, glucose, blood lipoprotein levels, inflammation, OS and muscle damage indicators, while decreasing serum TG levels p<0.05). CG's serum UCP-1, TAS, LDLC and non-HDL cholesterol levels were higher, while serum OSI, TBARS and IL-6 levels were lower compared to SG (p<0.05). While TBARS levels of CG decreased after exercise, SG's increased (p<0.05). OSI levels were higher in all G-carriers individuals and in GG homozygous athletes compared to other genotype groups VI (p<0.05). Serum NO levels were higher in G-carriers sedentary individuals compared to other genotype groups (p<0.05). Compared to other genotype groups, urea increase after exercise was higher in all AA homozygous individuals, while increases in CK and urea after exercise were higher in AA homozygous sedentary individuals (p<0.05). In conclusion, acute exercise significantly increased serum UCP-1, NO, irisin and IL- 6 levels in all participants. Moreover, while chronic anaerobic training significantly decreased serum UCP-1 and increased serum IL-6, it did not affect serum irisin and NO levels. However, UCP1P only modified the effects of acute and/or chronic exercises on serum NO, OSİ, CK and urea levels. GG homozygous athletes, G-carriers sedentary individuals, and AA homozygous sedentary individuals may have respectively higher OS, higher serum NO level, and a greater risk of muscle damage after acute exercise.