Haiyan Chu1, Meilin Wang, Dongyan Zhong, Danni Shi, Lan Ma, Na Tong, Zhengdong Zhang. 1. State Key Laboratory of Reproductive Medicine, Institute of Toxicology, Nanjing Medical University, Nanjing, China; Department of Environmental Genomics, Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing Medical University, Nanjing, China; Department of Genetic Toxicology, the Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, China.
Abstract
OBJECTIVE: Adiponectin (AdipoQ) plays an important role in the pathogenesis of diabetes mellitus and is considered as an important candidate gene for type 2 diabetes mellitus (T2DM). So far, there have been many studies to investigate the association between the adiponectin polymorphisms and T2DM risk. However, the results are conflicting. To derive a more precise estimation, we performed a meta-analysis to assess the association between five AdipoQ polymorphisms [-11426A > G (rs16861194), -11391G > A (rs17300539), -11377C > G (rs266729), +45T > G (rs2241766) and +276G > T (rs1501299)], and T2DM risk. METHODS: The fixed and random-effects model should be used to assess the summary odds ratios (ORs) of each study. ORs with 95% confidence intervals (CIs) were used to evaluate the strength of association. On the basis of the included criteria, we selected 39 papers, among which eight for -11426A > G, 14 for -11391G > A, 21 for -11377C > G, 28 for +45 T > G and 24 for +276G > T. Sensitivity analyses were conducted to assess the stability of the results. Both Begg's funnel plots and Egger's test are commonly used to evaluate publication bias. RESULTS: Overall, we found that individuals with the -11426G allele had a 0.15-fold significantly increased T2DM risk (additive model: 1.15, 1.04-1.27, 0.222). In the stratified analyses, we found that the -11426A > G, -11391G > A and -11377C > G polymorphisms could increase T2DM risk in European populations in the additive model. For Asian populations, we found that the -11377C > G polymorphism also could elevate T2DM risk. CONCLUSIONS: Our results suggested that the adiponectin -11426A > G polymorphism could contribute to the T2DM risk.
OBJECTIVE:Adiponectin (AdipoQ) plays an important role in the pathogenesis of diabetes mellitus and is considered as an important candidate gene for type 2 diabetes mellitus (T2DM). So far, there have been many studies to investigate the association between the adiponectin polymorphisms and T2DM risk. However, the results are conflicting. To derive a more precise estimation, we performed a meta-analysis to assess the association between five AdipoQ polymorphisms [-11426A > G (rs16861194), -11391G > A (rs17300539), -11377C > G (rs266729), +45T > G (rs2241766) and +276G > T (rs1501299)], and T2DM risk. METHODS: The fixed and random-effects model should be used to assess the summary odds ratios (ORs) of each study. ORs with 95% confidence intervals (CIs) were used to evaluate the strength of association. On the basis of the included criteria, we selected 39 papers, among which eight for -11426A > G, 14 for -11391G > A, 21 for -11377C > G, 28 for +45 T > G and 24 for +276G > T. Sensitivity analyses were conducted to assess the stability of the results. Both Begg's funnel plots and Egger's test are commonly used to evaluate publication bias. RESULTS: Overall, we found that individuals with the -11426G allele had a 0.15-fold significantly increased T2DM risk (additive model: 1.15, 1.04-1.27, 0.222). In the stratified analyses, we found that the -11426A > G, -11391G > A and -11377C > G polymorphisms could increase T2DM risk in European populations in the additive model. For Asian populations, we found that the -11377C > G polymorphism also could elevate T2DM risk. CONCLUSIONS: Our results suggested that the adiponectin -11426A > G polymorphism could contribute to the T2DM risk.
Authors: Andrey S Glotov; Evgeny S Tiys; Elena S Vashukova; Vladimir S Pakin; Pavel S Demenkov; Olga V Saik; Timofey V Ivanisenko; Olga N Arzhanova; Elena V Mozgovaya; Marina S Zainulina; Nikolay A Kolchanov; Vladislav S Baranov; Vladimir A Ivanisenko Journal: BMC Syst Biol Date: 2015-04-15