Ruyi Zhang1, Jiao Wang2, Rui Yang3, Jia Sun4, Rongping Chen5, Haizhao Luo6, Duan Liu7, Dehong Cai8. 1. Department of Endocrinology, Southern Medical University, Zhujiang Hospital, 253# Industry Road, 510282 Guangzhou, Guangdong, China. Electronic address: zhangruyi133@126.com. 2. Department of Endocrinology, Southern Medical University, Zhujiang Hospital, 253# Industry Road, 510282 Guangzhou, Guangdong, China. Electronic address: wangjiao150303@163.com. 3. Department of Endocrinology, Southern Medical University, Zhujiang Hospital, 253# Industry Road, 510282 Guangzhou, Guangdong, China. Electronic address: yangrui91@163.com. 4. Department of Endocrinology, Southern Medical University, Zhujiang Hospital, 253# Industry Road, 510282 Guangzhou, Guangdong, China. Electronic address: 13751822925@163.com. 5. Department of Endocrinology, Southern Medical University, Zhujiang Hospital, 253# Industry Road, 510282 Guangzhou, Guangdong, China. Electronic address: 62782333@163.com. 6. Department of Endocrinology, Southern Medical University, Zhujiang Hospital, 253# Industry Road, 510282 Guangzhou, Guangdong, China. Electronic address: luohaizhao@126.com. 7. Department of Endocrinology, Southern Medical University, Zhujiang Hospital, 253# Industry Road, 510282 Guangzhou, Guangdong, China. Electronic address: ludenjl@yahoo.com.cn. 8. Department of Endocrinology, Southern Medical University, Zhujiang Hospital, 253# Industry Road, 510282 Guangzhou, Guangdong, China. Electronic address: dehongcaizj@163.com.
Abstract
BACKGROUND: Associations between peroxisome proliferator-activated receptor γ2 (PPARγ2) gene polymorphism and metabolic syndrome risk remained controversial and ambiguous. Thus, we performed a meta-analysis to assess the association between Pro12Ala polymorphism in PPARγ2 gene and metabolic syndrome susceptibility. METHODS: An electronic literature search was conducted on Medline, OVID, Cochrane Library database, and the China National Knowledge Internet up to March 2013. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to calculate the strength of association in the fixed or random effects model. RESULTS: Ten studies involving a total of 4456 cases and 10343 controls were included in this meta-analysis. No statistical evidence of association was found between Pro12Ala polymorphism and metabolic syndrome risk in all genetic models (homozygote model: OR=0.83, 95% CI=0.62-1.12; heterozygote model: OR=1.04, 95% CI=0.94-1.14; dominant model: OR=1.02, 95% CI=0.93-1.12; recessive model: OR=0.83, 95% CI=0.62-1.11). No statistical evidence of significant association was observed when stratified by ethnicity, definition of metabolic syndrome, source of control groups and quality score of the selected articles. All in all, the results did not support a major role of the Pro12Ala variant of the PPARγ2 gene in metabolic syndrome risk. CONCLUSIONS: This meta-analysis suggested that the effect of Pro12Ala polymorphism in PPARγ2 gene may not be related to metabolic syndrome as an entity. However, Pro12Ala may affect the single component of metabolic syndrome. A large, well designed study is required to more adequately assess the role for Pro12Ala polymorphism on metabolic syndrome.
BACKGROUND: Associations between peroxisome proliferator-activated receptor γ2 (PPARγ2) gene polymorphism and metabolic syndrome risk remained controversial and ambiguous. Thus, we performed a meta-analysis to assess the association between Pro12Ala polymorphism in PPARγ2 gene and metabolic syndrome susceptibility. METHODS: An electronic literature search was conducted on Medline, OVID, Cochrane Library database, and the China National Knowledge Internet up to March 2013. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to calculate the strength of association in the fixed or random effects model. RESULTS: Ten studies involving a total of 4456 cases and 10343 controls were included in this meta-analysis. No statistical evidence of association was found between Pro12Ala polymorphism and metabolic syndrome risk in all genetic models (homozygote model: OR=0.83, 95% CI=0.62-1.12; heterozygote model: OR=1.04, 95% CI=0.94-1.14; dominant model: OR=1.02, 95% CI=0.93-1.12; recessive model: OR=0.83, 95% CI=0.62-1.11). No statistical evidence of significant association was observed when stratified by ethnicity, definition of metabolic syndrome, source of control groups and quality score of the selected articles. All in all, the results did not support a major role of the Pro12Ala variant of the PPARγ2 gene in metabolic syndrome risk. CONCLUSIONS: This meta-analysis suggested that the effect of Pro12Ala polymorphism in PPARγ2 gene may not be related to metabolic syndrome as an entity. However, Pro12Ala may affect the single component of metabolic syndrome. A large, well designed study is required to more adequately assess the role for Pro12Ala polymorphism on metabolic syndrome.
Keywords:
Ala; BMI; CI; EGIR; European Group for the study of Insulin Resistance; HB; HDL-C; HOMA; HWE; Hardy–Weinberg equilibrium; Homeostasis Model Assessment; IDF; International Diabetes Federation; LDL-C; MOOSE; Meta-analysis; Meta-analysis of Observational Studies in Epidemiology; Metabolic syndrome; NCEP ATP III; NOS; National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adult; Newcastle–Ottawa Scale; OR; PB; PPARγ; PPARγ2 (gamma2); PRISMA; Polymorphism; Preferred Reporting Items for Systematic Reviews and Meta-analysis; Pro12Ala; SNP; TC; TG; WHO; World Health Organization; alanine; body mass index; confidence interval; high density lipoprotein cholesterol; hospital-based; low density lipoprotein cholesterol; odds ratio; peroxisome proliferator-activated receptor γ2 (gamma2); population-based; single nucleotide polymorphism; substitution of proline to alanine; total cholesterol; triglyceride
Authors: Pilar García-Broncano; Juan Berenguer; Amanda Fernández-Rodríguez; Daniel Pineda-Tenor; María Ángeles Jiménez-Sousa; Mónica García-Alvarez; Pilar Miralles; Teresa Aldámiz-Echevarria; Juan Carlos López; Dariela Micheloud; Salvador Resino Journal: J Transl Med Date: 2014-08-27 Impact factor: 5.531