PDF(Pubmed)
Abstract：
UNASSIGNED: The CDK5 regulatory subunit-associated protein 1-like 1 (CDKAL1) contributes to islet β-cell function and insulin secretion by inhibiting the activation of CDK5. The current studies on the relationship between CDKAL1 polymorphisms rs7756992 A>G and rs7754840 C>G and the risk of gestational diabetes mellitus (GDM) have drawn contradictory conclusions.
UNASSIGNED: A meta-analysis with a fixed- or random-effects model was conducted to estimate the correlation between studied CDKAL1 polymorphisms and GDM risk with the summary odds ratio (OR) and 95% confidence interval (CI). In addition, trial sequential analysis (TSA) and false-positive report probability (FPRP) analysis were performed to confirm the study findings.
UNASSIGNED: A total of 13,306 subjects were included in the present study. Meta-analysis results showed that the variant heterozygous and homozygous genotypes of the two polymorphisms were associated with increased GDM risk in comparison with the wild-type AA genotype (AG vs. AA: OR = 1.23, 95% CI = 1.08, 1.41, p = 0.002; GG vs. AA: OR = 1.47, 95% CI = 1.05, 2.05, p = 0.024 for rs7756992; and CG vs. GG: OR = 1.36, 95% CI = 1.13, 1.65, p = 0.002; CC vs. GG: OR = 1.76, 95% CI = 1.37, 2.26, p < 0.001 for rs7754840). The TSA confirmed a significant association between rs7754840 and the susceptibility to GDM because the cumulative Z-curve crossed both the conventional cutoff value and the TSA boundaries under the heterozygote and homozygote models.
UNASSIGNED: This study supported the finding that rs7756992 and rs7754840 are associated with susceptibility to GDM. However, further functional studies are warranted to clarify the mechanism.
UNASSIGNED: A meta-analysis with a fixed- or random-effects model was conducted to estimate the correlation between studied CDKAL1 polymorphisms and GDM risk with the summary odds ratio (OR) and 95% confidence interval (CI). In addition, trial sequential analysis (TSA) and false-positive report probability (FPRP) analysis were performed to confirm the study findings.
UNASSIGNED: A total of 13,306 subjects were included in the present study. Meta-analysis results showed that the variant heterozygous and homozygous genotypes of the two polymorphisms were associated with increased GDM risk in comparison with the wild-type AA genotype (AG vs. AA: OR = 1.23, 95% CI = 1.08, 1.41, p = 0.002; GG vs. AA: OR = 1.47, 95% CI = 1.05, 2.05, p = 0.024 for rs7756992; and CG vs. GG: OR = 1.36, 95% CI = 1.13, 1.65, p = 0.002; CC vs. GG: OR = 1.76, 95% CI = 1.37, 2.26, p < 0.001 for rs7754840). The TSA confirmed a significant association between rs7754840 and the susceptibility to GDM because the cumulative Z-curve crossed both the conventional cutoff value and the TSA boundaries under the heterozygote and homozygote models.
UNASSIGNED: This study supported the finding that rs7756992 and rs7754840 are associated with susceptibility to GDM. However, further functional studies are warranted to clarify the mechanism.
摘要：
■CDK5调节亚基相关蛋白1-like1（CDKAL1）通过抑制CDK5的激活而促进胰岛β细胞功能和胰岛素分泌。目前关于CDKAL1多态性rs7756992A>G和rs7754840C>G与妊娠期糖尿病(GDM)风险关系的研究得出了矛盾的结论。
■使用固定或随机效应模型进行荟萃分析，以汇总比值比（OR）和95％置信区间（CI）评估所研究的CDKAL1多态性与GDM风险之间的相关性。此外,试验序贯分析(TSA)和假阳性报告概率(FPRP)分析证实了研究结果.
■本研究共纳入13,306名受试者。Meta分析结果表明，与野生型AA基因型相比，两种多态性的变异杂合和纯合基因型与GDM风险增加相关（AGvs.AA：OR=1.23，95%CI=1.08，1.41，p=0.002；GGvs.对于rs7756992，AA：OR=1.47，95%CI=1.05，2.05，p=0.024；CG与GG：OR=1.36，95%CI=1.13，1.65，p=0.002；CCvs.GG：OR=1.76，95%CI=1.37，2.26，rs7754840p<0.001）。TSA证实了rs7754840与GDM易感性之间的显着关联，因为累积Z曲线在杂合子和纯合子模型下跨越了常规截止值和TSA边界。
■本研究支持rs7756992和rs7754840与GDM易感性相关的发现。然而,需要进一步的功能研究来阐明机制.
■使用固定或随机效应模型进行荟萃分析，以汇总比值比（OR）和95％置信区间（CI）评估所研究的CDKAL1多态性与GDM风险之间的相关性。此外,试验序贯分析(TSA)和假阳性报告概率(FPRP)分析证实了研究结果.
■本研究共纳入13,306名受试者。Meta分析结果表明，与野生型AA基因型相比，两种多态性的变异杂合和纯合基因型与GDM风险增加相关（AGvs.AA：OR=1.23，95%CI=1.08，1.41，p=0.002；GGvs.对于rs7756992，AA：OR=1.47，95%CI=1.05，2.05，p=0.024；CG与GG：OR=1.36，95%CI=1.13，1.65，p=0.002；CCvs.GG：OR=1.76，95%CI=1.37，2.26，rs7754840p<0.001）。TSA证实了rs7754840与GDM易感性之间的显着关联，因为累积Z曲线在杂合子和纯合子模型下跨越了常规截止值和TSA边界。
■本研究支持rs7756992和rs7754840与GDM易感性相关的发现。然而,需要进一步的功能研究来阐明机制.
