Meta-analyses of the association of G6PC2 allele variants with elevated fasting glucose and type 2 diabetes.
Meta-analyses of the association of G6PC2 allele variants with elevated fasting glucose and type 2 diabetes.
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G6PC2 等位基因变异与空腹血糖升高和 2 型糖尿病关联的荟萃分析
DOI：
10.1371/journal.pone.0181232
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发表时间：
2017
期刊：
影响因子：
3.7
通讯作者：
Li L
中科院分区：
文献类型：
--
作者：
Shi Y;Li Y;Wang J;Wang C;Fan J;Zhao J;Yin L;Liu X;Zhang D;Li L
共同评价葡萄糖-6-磷酸酶催化单元2（G6 PC 2）等位基因变异与空腹血糖（FG）升高和2型糖尿病（T2 D）的相关性。荟萃分析PubMed、Web of Knowledge和Embase数据库。确定G6 PC 2与T2 D和FG升高相关的研究文章全文。FG与G6 PC 2相关性分析中无T2 D患者参与，T2 D患者和非糖尿病患者参与T2 D与G6 PC 2相关性分析。使用随机效应荟萃分析计算合并效应量。采用I2度量和H2检验计算异质性。用Begg漏斗图和Egger线性回归检验评估发表偏倚。在确定的423项研究中，有21项合格并纳入。三个位点（rs 560887，rs 16856187和rs 573225）的数据是可用的。3个民族rs 560887的G等位基因、rs 16856187的C等位基因和rs 573225的A等位基因均与FG升高呈正相关。rs 560887处G等位基因和rs 573225处A等位基因的每次增量导致FG升高0.070 mmol/l和0.075 mmol/l（分别为P（95% CI）= 0.070（0.060，0.079），p = 4.635e-50和0.075（0.065，0.085），p = 5.856e-48）。rs 16856187与FG的相关性增加了0.152（95% CI：0.034-0.270; p = 0.011）和0.317（95%置信区间：0.193-0.442，p = 6.046e-07）分别见于AC和CC基因型FG的标准化平均差（SMD），与AA参考基因型相比。然而，在加性模型下高加索人rs 560887的G等位基因和在等位基因和显性模型下rs 16856187的C等位基因与T2 D风险降低相关（OR（95% CI）= 0.964（0.947，0.981），p = 0.570 e-4; OR（95% CI）= 0.892（0.832，0.956），p = 0.001; OR（95% CI）= 0.923（0.892，0.955），p = 5.301 e-6）。我们的荟萃分析表明，G6 PC 2的所有三种等位基因变体（rs 560887、rs 16856187和rs 573225）均与FG升高相关，其中两种变体（白人亚组中的rs 560887和等位基因和显性模型下的rs 16856187）也与T2 D相关。需要利用更大样本量和不同种族人群进行进一步研究，以扩展和证实这些发现。
To collectively evaluate the association of glucose-6-phosphatase catalytic unit 2 (G6PC2) allele variants with elevated fasting glucose (FG) and type 2 diabetes (T2D). Meta-analysis PubMed, Web of Knowledge and Embase databases. Full text articles of studies that identified an association of G6PC2 with T2D and elevated FG. There was no T2D patient involvement in the analyses on the association of FG with G6PC2, there were T2D patients and non-diabetes patient involvement in the analyses on the association of T2D with G6PC2. Random-effects meta-analyses were used to calculate the pool effect sizes. I2 metric and H2 tests were used to calculate the heterogeneity. Begg's funnel plot and Egger’s linear regression test were done to assess publication bias. Of the 423 studies identified, 21 were eligible and included. Data on three loci (rs560887, rs16856187 and rs573225) were available. The G allele at rs560887 in three ethnicities, the C allele at rs16856187 and the A allele at rs573225 all had a positive association with elevated FG. Per increment of G allele at rs560887 and A allele at rs573225 resulted in a FG 0.070 mmol/l and 0.075 mmol/l higher (ß (95% CI) = 0.070 (0.060, 0.079), p = 4.635e-50 and 0.075 (0.065, 0.085), p = 5.856e-48, respectively). With regard to the relationship of rs16856187 and FG, an increase of 0.152 (95% CI: 0.034–0.270; p = 0.011) and 0.317 (95% CI: 0.193–0.442, p = 6.046e-07) was found in the standardized mean difference (SMD) of FG for the AC and CC genotypes, respectively, when compared with the AA reference genotype. However, the G-allele of rs560887 in Caucasians under the additive model and the C-allele of rs16856187 under the allele and dominant models were associated with a decreased risk of T2D (OR (95% CI) = 0.964 (0.947, 0.981), p = 0.570e-4; OR (95% CI) = 0.892 (0.832, 0.956), p = 0.001; and OR (95% CI) = 0.923(0.892, 0.955), p = 5.301e-6, respectively). Our meta-analyses demonstrate that all three allele variants of G6PC2 (rs560887, rs16856187 and rs573225) are associated with elevated FG, with two variants (rs560887 in the Caucasians subgroup and rs16856187 under the allele and dominant model) being associated with T2D as well. Further studies utilizing larger sample sizes and different ethnic populations are needed to extend and confirm these findings.
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影响因子：
7.7
作者：
Dos Santos C;Bougnères P;Fradin D
通讯作者：
Fradin D
影响因子：
7.7
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Barker A;Sharp SJ;Timpson NJ;Bouatia-Naji N;Warrington NM;Kanoni S;Beilin LJ;Brage S;Deloukas P;Evans DM;Grontved A;Hassanali N;Lawlor DA;Lecoeur C;Loos RJ;Lye SJ;McCarthy MI;Mori TA;Ndiaye NC;Newnham JP;Ntalla I;Pennell CE;St Pourcain B;Prokopenko I;Ring SM;Sattar N;Visvikis-Siest S;Dedoussis GV;Palmer LJ;Froguel P;Smith GD;Ekelund U;Wareham NJ;Langenberg C
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作者：
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通讯作者：
Fritsche, Andreas
影响因子：
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作者：
Hruby, Adela;Ngwa, Julius S.;Nettleton, Jennifer A.
通讯作者：
Nettleton, Jennifer A.