AbstractObjectiveThe purpose of this meta analysis was to assess the correlation between CDKAL1 rs10946398C>A single nucleotide polymorphism (SNP) and type 2 diabetes mellitus (T2DM) susceptibility by pooling the open published studies.MethodElectronic searching of PubMed, EMBASE, Medline, Cochrane, China Biology Medicine disc (CBM) and China National Knowledge Infrastructure (CNKI) databases were performed by two reviewers independently to collect the open published studies related to CDKAL1 rs10946398C>A single nucleotide polymorphism and T2DM susceptibility. The association between CDKAL1 rs10946398C>A single nucleotide polymorphism and T2DM susceptibility was expressed by odds ratio (OR) and the corresponding 95% confidence interval (95%CI).ResultsThirteen studies with a total of 13,966 T2DM and 14,274 controls were finally included for analysis in this meta-analysis. Of the included 13 publications, 2 studies were carried out in Europe, 8 in Asia, 2 in Africa and 1 in Latin America. Being significant statistical heterogeneity, the data was pooled through random effect model. In a dominant genetic model, there was significant correlation between CDKAL1 rs10946398C>A SNP and T2DM risk (OR=1.22, P<0.05). In a dominant genetic model people with CC or CA genotype had increased risk of developing T2DM; Because of statistical heterogeneity for the included studies in a recessive genetic model (AA+CA vs CC), the data was calculated by random effect method. The combined data showed people with AA or CA genotype had decreased risk of developing T2DM compared to CC genotype (OR=0.83, P<0.05); For a homozygous genetic model (CC vs AA), the OR was calculated through random effect model for statistical heterogeneity among the included 13 studies. The combined OR was 1.33 which indicated people with CC genotype had increased risk of developing T2DM.ConclusionAccording to the present results, CDKAL1 rs10946398C>A single nucleotide polymorphism had correlation with the susceptibility of type 2 diabetes mellitus.
Open Life Sciences – de Gruyter
Published: Dec 29, 2017
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