ABSTRACT Objective: Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease and a growing global epidemic. In NAFLD, liver fat surpasses 5% of hepatocytes without the secondary causes of lipid accumulation or excessive alcohol consumption. Given the link between NAFLD and insulin resistance, the possible association between the rs2854744 (−202 G>T) promoter polymorphism of insulin-like growth factor binding protein 3 (IGFBP3) gene and NAFLD was investigated in this study. Materials and methods: In this genetic case-control association study, the IGFBP3 rs2854744 genotypes of 315 unrelated individuals, including 156 patients with biopsy-proven NAFLD and 159 controls, were determined using polymerase chain reaction/restriction fragment length polymorphism analyses. Results: The “GT+TT” genotype of the IGFBP3 rs2854744 polymorphism, compared with the “GG” genotype, was associated with a 2.7-fold increased risk of NAFLD after adjustment for confounding factors (P = 0.009; odds ratio [OR] = 2.71; 95% confidence interval [CI] = 1.19-3.18). Additionally, the IGFBP3 rs2854744 “T” allele, in comparison with the “G” allele, was significantly overrepresented in NAFLD patients than the controls (P = 0.008; OR = 1.85; 95%CI = 1.23-2.94). Conclusion: Our findings first indicated that the IGFBP3 rs2854744 “GT+TT” genotype is a marker of increased NAFLD susceptibility; however, it needs to be supported by further investigations in other populations. Objective (NAFLD epidemic 5 consumption resistance rs rs285474 −202 202 (−20 G>T GT G T insulinlike like IGFBP (IGFBP3 study methods casecontrol case control 31 individuals 15 biopsyproven biopsy proven reactionrestriction reaction restriction analyses Results GT+TT GTTT TT “GT+TT GG “GG 2.7fold 27fold fold 2.7 2 7 P 0.009 0009 0 009 [OR 2.71 271 71 95 CI [CI 1.193.18. 119318 1.19 3.18 . 1 19 18 1.19-3.18) Additionally “T allele “G 0.008 0008 008 1.85 185 85 95CI 1.232.94. 123294 1.23 2.94 23 94 1.23-2.94) Conclusion susceptibility however populations rs28547 −20 20 (−2 (IGFBP 7fold 27 2. 0.00 000 00 9 193 1.193.18 11931 119 1.1 318 3.1 1.19-3.18 1.8 8 232 1.232.94 12329 123 1.2 294 2.9 1.23-2.94 rs2854 −2 (− 0.0 1.193.1 1193 11 1. 3. 1.19-3.1 1.232.9 1232 12 29 1.23-2.9 rs285 − ( 0. 1.193. 1.19-3. 1.232. 1.23-2. rs28 1.193 1.19-3 1.232 1.23-2 rs2 1.19- 1.23-

SUMMARY OBJECTIVES: Nonalcoholic fatty liver disease is the term used for a range of conditions in which fat builds up in the liver and exceeds 5% of hepatocytes without inordinate alcohol intake or other causes of lipid accumulation. Regarding the fact that insulin resistance and obesity play key roles in the pathogenesis of nonalcoholic fatty liver disease, as well as the connection between resistin and these metabolic diseases, the association between nonalcoholic fatty liver disease and a resistin gene (RETN) polymorphism was examined. METHODS: In this genetic case–control association study, 150 biopsy-proven nonalcoholic fatty liver disease patients and 154 controls were enrolled and genotyped for the RETN rs1862513 (-420C>G) gene polymorphism using PCR–RFLP method. RESULTS: The −420C>G genotype frequency distributions in both groups were consistent with Hardy-Weinberg equilibrium (HWE; p>0.05). The carriers of the RETN −420C>G "CC" genotype compared with the "GG" genotype occurred less frequently in the cases with nonalcoholic fatty liver disease than in the controls, and the difference remained significant even after adjustment for confounding factors (p=0.030; OR=0.47, 95%CI=0.36–0.93). Interestingly, the RETN −420C>G "C" allele was also associated with a decreased risk for nonalcoholic fatty liver disease too (p=0.042; OR=0.72, 95%CI=0.53–0.95). CONCLUSION: We found for the first time an association between biopsy-proven nonalcoholic fatty liver disease and RETN −420C>G promoter polymorphism. The carriers of the RETN −420C>G "CC" genotype had a 53% decreased risk for nonalcoholic fatty liver disease. Our findings, however, need to be corroborated by further studies. OBJECTIVES 5 accumulation diseases (RETN examined METHODS casecontrol case control study 15 biopsyproven biopsy proven rs rs186251 420C>G 420CG CG 420C G C (-420C>G PCRRFLP PCR RFLP method RESULTS HardyWeinberg Hardy Weinberg HWE (HWE p>0.05. p005 p p>0.05 . 0 05 p>0.05) CC "CC GG "GG p=0.030 p0030 030 (p=0.030 OR047 OR 47 OR=0.47 95%CI=0.36–0.93. 95CI036093 CI 95%CI=0.36–0.93 95 36 93 95%CI=0.36–0.93) Interestingly "C p=0.042 p0042 042 (p=0.042 OR072 72 OR=0.72 95%CI=0.53–0.95. 95CI053095 95%CI=0.53–0.95 53 95%CI=0.53–0.95) CONCLUSION findings however studies 1 rs18625 p00 p>0.0 p=0.03 p003 03 (p=0.03 OR04 4 OR=0.4 95CI03609 95%CI=0.36–0.9 9 3 p=0.04 p004 04 (p=0.04 OR07 7 OR=0.7 95CI05309 95%CI=0.53–0.9 rs1862 p0 p>0. p=0.0 (p=0.0 OR0 OR=0. 95CI0360 95%CI=0.36–0. 95CI0530 95%CI=0.53–0. rs186 p>0 p=0. (p=0. OR=0 95CI036 95%CI=0.36–0 95CI053 95%CI=0.53–0 rs18 p> p=0 (p=0 OR= 95CI03 95%CI=0.36– 95CI05 95%CI=0.53– rs1 p= (p= 95CI0 95%CI=0.36 95%CI=0.53 (p 95CI 95%CI=0.3 95%CI=0.5 95%CI=0. 95%CI=0 95%CI= 95%CI

SUMMARY OBJECTIVE: Nonalcoholic fatty liver disease is a chronic liver disease and a growing global epidemic. The aim of this study was to investigate the association between a visfatin gene (NAMPT) variant and nonalcoholic fatty liver disease, owing to the connection between this disease and insulin resistance, obesity, inflammation, and oxidative stress, and the role of visfatin in these metabolic disorders. METHODS: In the present case-control study, we enrolled 312 genetically unrelated individuals, including 154 patients with biopsy-proven nonalcoholic fatty liver disease and 158 controls. The rs2058539 polymorphism of NAMPT gene was genotyped using the PCR-RFLP method. RESULTS: Genotype and allele distributions of NAMPT gene rs2058539 polymorphism conformed to the Hardy-Weinberg equilibrium both in the case and control groups (p>0.05). The distribution of NAMPT rs2058539 genotypes and alleles differed significantly between the cases with nonalcoholic fatty liver disease and controls. The "CC" genotype of the NAMPT rs2058539 compared with "AA" genotype was associated with a 2.5-fold increased risk of nonalcoholic fatty liver disease after adjustment for confounding factors [p=0.034; odds ratio (OR)=2.52, 95% confidence interval (CI)=1.36–4.37]. Moreover, the NAMPT rs2058539 "C" allele was significantly overrepresented in the nonalcoholic fatty liver disease patients than controls (p=0.022; OR=1.77, 95%CI=1.14–2.31). CONCLUSION: Our findings indicated for the first time that the NAMPT rs2058539 "CC" genotype is a marker of increased nonalcoholic fatty liver disease susceptibility; however, it needs to be supported by further investigations in other populations. OBJECTIVE epidemic (NAMPT resistance obesity inflammation stress disorders METHODS casecontrol 31 individuals 15 biopsyproven biopsy proven rs rs205853 PCRRFLP PCR RFLP method RESULTS HardyWeinberg Hardy Weinberg p>0.05. p005 p p>0.05 . 0 05 (p>0.05) CC "CC AA "AA 2.5fold 25fold fold 2.5 2 5 p=0.034 p0034 034 [p=0.034 OR=2.52, OR252 OR =2.52, 52 (OR)=2.52 95 CI=1.36–4.37. CI136437 CI =1.36–4.37 1 36 4 37 (CI)=1.36–4.37] Moreover C "C p=0.022 p0022 022 (p=0.022 OR177 77 OR=1.77 95%CI=1.14–2.31. 95CI114231 95%CI=1.14–2.31 14 95%CI=1.14–2.31) CONCLUSION susceptibility however populations 3 rs20585 p00 p>0.0 (p>0.05 5fold 25 2. p=0.03 p003 03 [p=0.03 OR=2.52 OR25 252 =2.52 (OR)=2.5 9 CI=1.36–4.37 CI13643 136437 =1.36–4.3 (CI)=1.36–4.37 p=0.02 p002 02 (p=0.02 OR17 7 OR=1.7 95CI11423 95%CI=1.14–2.3 rs2058 p0 p>0. (p>0.0 p=0.0 [p=0.0 OR=2.5 OR2 =2.5 (OR)=2. CI=1.36–4.3 CI1364 13643 =1.36–4. (CI)=1.36–4.3 (p=0.0 OR1 OR=1. 95CI1142 95%CI=1.14–2. rs205 p>0 (p>0. p=0. [p=0. OR=2. =2. (OR)=2 CI=1.36–4. CI136 1364 =1.36–4 (CI)=1.36–4. (p=0. OR=1 95CI114 95%CI=1.14–2 rs20 p> (p>0 p=0 [p=0 OR=2 =2 (OR)= CI=1.36–4 CI13 136 =1.36– (CI)=1.36–4 (p=0 OR= 95CI11 95%CI=1.14– rs2 (p> p= [p= = (OR) CI=1.36– CI1 13 =1.36 (CI)=1.36– (p= 95CI1 95%CI=1.14 (p [p (OR CI=1.36 =1.3 (CI)=1.36 95CI 95%CI=1.1 CI=1.3 =1. (CI)=1.3 95%CI=1. CI=1. =1 (CI)=1. 95%CI=1 CI=1 (CI)=1 95%CI= CI= (CI)= 95%CI (CI) (CI