Li Jiaying, Zhao Yuening, Zhang Hongxiang, Hua Wenxi, Jiao Wenzhi, Du Xuan, Rui Jingwen, Li Si, Teng Haiying, Shi Bimin, Yang Xiaoqin, Zhu Liyan
Center for Systems Biology, Department of Bioinformatics, School of Biology and Basic Medical Sciences, Soochow University, Suzhou 215123, China.
Medical College, Soochow University, Suzhou 215123, China.
Endocr Metab Immune Disord Drug Targets. 2021;21(9):1696-1708. doi: 10.2174/1871530320999201126202706.
Many published studies attempted to elucidate the implication of glucokinase regulator gene (GCKR) polymorphisms in the susceptibility to non-alcoholic fatty liver disease (NAFLD), but the results among them were still controversial.
This meta-analysis aims to precisely assess the relationship between the GCKR polymorphisms and the risk of NAFLD.
Systematic computerized searches in six databases were performed and updated on April 6, 2020. Meta-analyses were conducted by calling the R programs based on accumulated epidemiological data. Odds ratio (OR) and 95% confidential interval (CI) were calculated to summarize the effect estimates.
In total, 25 studies including 6,598 cases and 19,954 controls were included. The pooled estimates indicated that the T allele carrier of the GCKR rs780094 polymorphism has predisposition to NAFLD (allele model: OR: 1.20, 95% CI: 1.111.29; homozygote model: OR: 1.38, 95% CI: 1.151.67; heterozygote model: OR: 1.25, 95% CI: 1.121.39; dominant model: OR: 1.29, 95% CI: 1.131.47; recessive model: OR: 1.18, 95% CI: 1.061.31), and the same as the rs1260326 polymorphism (allele model: OR: 1.32, 95% CI: 1.221.42; homozygote model: OR: 1.65, 95% CI: 1.401.94; heterozygote model: OR: 1.24, 95% CI: 1.071.43; dominant model: OR: 1.39, 95% CI: 1.211.59; recessive model: OR: 1.44, 95% CI: 1.281.62). Further stratified analyses according to age and ethnicity confirmed the statistical existence in most subgroups.
This meta-analysis suggested that both of the GCKR rs780094 and rs1260326 polymorphisms are significantly associated with the increased risk of NAFLD.
许多已发表的研究试图阐明葡萄糖激酶调节基因(GCKR)多态性在非酒精性脂肪性肝病(NAFLD)易感性中的作用,但这些研究结果仍存在争议。
本荟萃分析旨在精确评估GCKR多态性与NAFLD风险之间的关系。
于2020年4月6日对六个数据库进行了系统的计算机检索并更新。基于累积的流行病学数据,通过调用R程序进行荟萃分析。计算比值比(OR)和95%置信区间(CI)以汇总效应估计值。
共纳入25项研究,包括6598例病例和19954例对照。汇总估计表明,GCKR rs780094多态性的T等位基因携带者易患NAFLD(等位基因模型:OR:1.20,95%CI:1.111.29;纯合子模型:OR:1.38,95%CI:1.151.67;杂合子模型:OR:1.25,95%CI:1.121.39;显性模型:OR:1.29,95%CI:1.131.47;隐性模型:OR:1.18,95%CI:1.061.31),rs1260326多态性情况相同(等位基因模型:OR:1.32,95%CI:1.221.42;纯合子模型:OR:1.65,95%CI:1.401.94;杂合子模型:OR:1.24,95%CI:1.071.43;显性模型:OR:1.39,95%CI:1.211.59;隐性模型:OR:1.44,95%CI:1.281.62)。根据年龄和种族进行的进一步分层分析证实了大多数亚组中的统计学显著性。
本荟萃分析表明,GCKR rs780094和rs1260326多态性均与NAFLD风险增加显著相关。