Mutations in the third gene shown to alter fasting glucose levels in the population (<i>G6PC2</i>) are not a common cause of monogenic forms of pancreatic B‐cell dysfunction

Edghill, Emma L.; McCulloch, Laura; Fulton, Piers; Beer, Nicola L.; Hattersley, Andrew T.; Gloyn, Anna L.

doi:10.1111/j.1464-5491.2008.02618.x

Cited by 2 publications

(1 citation statement)

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“…Carriage of the G allele at polymorphic site rs560887 in G6PC2 was implicated both in elevated fasting plasma glucose and higher HbA 1c levels, resulting in elevated risk of developing impaired fasting glucose [4]. Although Edghill and co‐workers found no clearly pathogenic mutations in G6PC2 in patients with diabetes of monogenic origin [5], we hypothesized that the rs560887 polymorphism in G6PC2 may result in a more pronounced clinical picture of GCK ‐ MODY, attributable to higher HbA 1c levels and more frequent diagnosis of diabetes in such individuals.…”

Section: Introductionmentioning

confidence: 99%

HbA1c‐based diabetes diagnosis among patients with glucokinase mutation (GCK‐MODY) is affected by a genetic variant of glucose‐6‐phosphatase (G6PC2)

Borowiec¹,

Fendler²,

Dušátková³

et al. 2012

Diabetic Medicine

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Section: Introductionmentioning

confidence: 99%

HbA1c‐based diabetes diagnosis among patients with glucokinase mutation (GCK‐MODY) is affected by a genetic variant of glucose‐6‐phosphatase (G6PC2)

Borowiec¹,

Fendler²,

Dušátková³

et al. 2012

Diabetic Medicine

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Meta-analyses of the association of G6PC2 allele variants with elevated fasting glucose and type 2 diabetes

Shi

Wang

et al. 2017

PLoS ONE

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ObjectiveTo collectively evaluate the association of glucose-6-phosphatase catalytic unit 2 (G6PC2) allele variants with elevated fasting glucose (FG) and type 2 diabetes (T2D).DesignMeta-analysisData sourcesPubMed, Web of Knowledge and Embase databases.Study selectionFull text articles of studies that identified an association of G6PC2 with T2D and elevated FG.Patient involvementThere 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.Statistical analysisRandom-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.ResultsOf 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).ConclusionsOur 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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Mutations in the third gene shown to alter fasting glucose levels in the population (G6PC2) are not a common cause of monogenic forms of pancreatic B‐cell dysfunction

Cited by 2 publications

References 9 publications

HbA1c‐based diabetes diagnosis among patients with glucokinase mutation (GCK‐MODY) is affected by a genetic variant of glucose‐6‐phosphatase (G6PC2)

HbA1c‐based diabetes diagnosis among patients with glucokinase mutation (GCK‐MODY) is affected by a genetic variant of glucose‐6‐phosphatase (G6PC2)

Meta-analyses of the association of G6PC2 allele variants with elevated fasting glucose and type 2 diabetes

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