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Angiotensin converting enzyme D allele is associated with an increased risk of type 2 diabetes: evidence from a meta-analysis

机译:血管紧张素转换酶D等位基因与2型糖尿病的风险增加相关:一项荟萃分析的证据

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References(34) Cited-By(12) Associations of angiotensin converting enzyme gene (ACE) insertion/deletion (I/D) polymorphism with type 2 diabetes (T2D) have been inconsistent with both positive, null and negative results. We thereby performed a meta-analysis from all English-published reports to examine ACE I/D polymorphism in association with T2D risk. Case-control studies were identified from MEDLINE, EMBASE and Web of Science as of Dec 10, 2009. A total of 14 studies with 1985 patients with T2D and 4602 controls were finally identified. Random-effects model was applied irrespective of between-study heterogeneity. Study quality was assessed in duplicate. Compared with ACE I allele, presence of D allele conferred a significant increased risk for T2D (OR=1.33; 95% CI, 1.10-1.61; p=0.003). This trend was potentiated after comparing homozygotes of D allele with I allele with a 90% increased risk (p=0.0008). Carriers of D allele had a moderate increased risk for T2D compared with the II genotype carriers (OR=1.34; 95% CI, 1.04-1.72; p=0.02), whereas under recessive model this effect was significantly enhanced (OR=1.73; 95% CI, 1.26-2.38; p=0.0008). Subgroup analyses indicated significant association for population-based study design only, as well as among populations from Africa and Europe ancestries rather than from Asia ancestry. No publication bias was observed using the fail-safe number at the level of 0.05. Our results demonstrated that ACE D allele was significantly associated with an increased risk of T2D, and this effect appeared to be additive. Moreover, this association was more prominent for population-based studies and among Africans and Caucasians.
机译:参考文献(34)被引用(12)血管紧张素转换酶基因(ACE)插入/缺失(I / D)多态性与2型糖尿病(T2D)的关联一直与阳性,无效和阴性结果不一致。因此,我们对所有英文发表的报告进行了荟萃分析,以检查与T2D风险相关的ACE I / D多态性。截至2009年12月10日,已从MEDLINE,EMBASE和Web of Science中确定了病例对照研究。最终确定了1985年T2D患者和4602对照的14项研究。无论研究之间的异质性如何,均采用随机效应模型。研究质量一式两份进行评估。与ACE I等位基因相比,D等位基因的存在显着增加了T2D的风险(OR = 1.33; 95%CI,1.10-1.61; p = 0.003)。在比较D等位基因与I等位基因的纯合子后,这种趋势得到了加强,风险增加了90%(p = 0.0008)。与II基因型携带者相比,D等位基因携带者患T2D的风险有所增加(OR = 1.34; 95%CI,1.04-1.72; p = 0.02),而在隐性模型中,这种效应显着增强(OR = 1.73; 95) %CI,1.26-2.38; p = 0.0008)。亚组分析表明,仅基于人群的研究设计以及来自非洲和欧洲祖先而不是亚洲祖先的人群之间存在显着关联。使用故障安全数0.05时,未观察到任何发布偏差。我们的结果表明,ACE D等位基因与T2D风险增加显着相关,并且这种作用似乎是累加的。此外,在基于人群的研究以及非洲人和高加索人中,这种联系更为突出。

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