Studies on the Association of GCK and GCKR Polymorphisms with Susceptibility to Gestational Diabetes Mellitus: A Meta-Analysis

Background: A prevalent condition during pregnancy, gestational diabetes mellitus (GDM) affects a significant proportion of pregnancies worldwide and poses substantial risks to maternal as well as fetal health. Polymorphisms in the glucokinase (GCK) and glucokinase regulatory prot...

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Main Authors: Hongxia Tu, Youyi Zhang, Mingyi Wang
Format: Article
Language:English
Published: IMR Press 2025-01-01
Series:Clinical and Experimental Obstetrics & Gynecology
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Online Access:https://www.imrpress.com/journal/CEOG/52/1/10.31083/CEOG26710
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author Hongxia Tu
Youyi Zhang
Mingyi Wang
author_facet Hongxia Tu
Youyi Zhang
Mingyi Wang
author_sort Hongxia Tu
collection DOAJ
description Background: A prevalent condition during pregnancy, gestational diabetes mellitus (GDM) affects a significant proportion of pregnancies worldwide and poses substantial risks to maternal as well as fetal health. Polymorphisms in the glucokinase (GCK) and glucokinase regulatory protein (GCKR) genes, which are crucial for glucose homeostasis, may modulate susceptibility to GDM. Hence, this meta-analysis aimed to assess the relationship between GDM and polymorphisms in GCK (rs1799884, rs4607517) and GCKR (rs780094, rs1260326). Methods: In this systematic review, we retrieved data from PubMed, EMBASE, Medline, EBSCO, Cochrane Library, and Chinese National Knowledge Infrastructure (CNKI) databases. Studies were critically appraised using the Newcastle-Ottawa Scale, and meta-analyses were performed using STATA 12.0. The odds ratios (ORs) were calculated with 95% confidence intervals (CIs) and heterogeneity was assessed with Cochran’s Q test as well as I2 statistical tests, respectively. Moreover, Begg’s test helped in evaluating publication bias. Results: We included 20 studies, comprising 9745 GDM women and 15,830 controls. All genetic models showed a strong correlation between the GCK rs1799884 polymorphism and GDM, with carriers of the A allele exhibiting an increased risk. Conversely, GCK rs4607517, GCKR rs780094, and rs1260326 were not significantly associated. However, heterogeneity was influenced by ethnicity and diagnostic criteria. Conclusions: The GCK rs1799884 polymorphism can be a potential predictive marker because it is significantly associated with an increased risk of GDM.
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spelling doaj-art-b8ff87ca6a244857958bcb8fb92b852d2025-01-25T07:14:26ZengIMR PressClinical and Experimental Obstetrics & Gynecology0390-66632025-01-015212671010.31083/CEOG26710S0390-6663(24)02537-5Studies on the Association of GCK and GCKR Polymorphisms with Susceptibility to Gestational Diabetes Mellitus: A Meta-AnalysisHongxia Tu0Youyi Zhang1Mingyi Wang2Department of Gynaecology and Obstetrics, The General Hospital of Western Theater Command PLA, 610083 Chengdu, Sichuan, ChinaDepartment of Gynaecology and Obstetrics, The General Hospital of Western Theater Command PLA, 610083 Chengdu, Sichuan, ChinaDepartment of Gynaecology and Obstetrics, The General Hospital of Western Theater Command PLA, 610083 Chengdu, Sichuan, ChinaBackground: A prevalent condition during pregnancy, gestational diabetes mellitus (GDM) affects a significant proportion of pregnancies worldwide and poses substantial risks to maternal as well as fetal health. Polymorphisms in the glucokinase (GCK) and glucokinase regulatory protein (GCKR) genes, which are crucial for glucose homeostasis, may modulate susceptibility to GDM. Hence, this meta-analysis aimed to assess the relationship between GDM and polymorphisms in GCK (rs1799884, rs4607517) and GCKR (rs780094, rs1260326). Methods: In this systematic review, we retrieved data from PubMed, EMBASE, Medline, EBSCO, Cochrane Library, and Chinese National Knowledge Infrastructure (CNKI) databases. Studies were critically appraised using the Newcastle-Ottawa Scale, and meta-analyses were performed using STATA 12.0. The odds ratios (ORs) were calculated with 95% confidence intervals (CIs) and heterogeneity was assessed with Cochran’s Q test as well as I2 statistical tests, respectively. Moreover, Begg’s test helped in evaluating publication bias. Results: We included 20 studies, comprising 9745 GDM women and 15,830 controls. All genetic models showed a strong correlation between the GCK rs1799884 polymorphism and GDM, with carriers of the A allele exhibiting an increased risk. Conversely, GCK rs4607517, GCKR rs780094, and rs1260326 were not significantly associated. However, heterogeneity was influenced by ethnicity and diagnostic criteria. Conclusions: The GCK rs1799884 polymorphism can be a potential predictive marker because it is significantly associated with an increased risk of GDM.https://www.imrpress.com/journal/CEOG/52/1/10.31083/CEOG26710gestational diabetes mellitusgck genegckr genepolymorphismsmeta-analysis
spellingShingle Hongxia Tu
Youyi Zhang
Mingyi Wang
Studies on the Association of GCK and GCKR Polymorphisms with Susceptibility to Gestational Diabetes Mellitus: A Meta-Analysis
Clinical and Experimental Obstetrics & Gynecology
gestational diabetes mellitus
gck gene
gckr gene
polymorphisms
meta-analysis
title Studies on the Association of GCK and GCKR Polymorphisms with Susceptibility to Gestational Diabetes Mellitus: A Meta-Analysis
title_full Studies on the Association of GCK and GCKR Polymorphisms with Susceptibility to Gestational Diabetes Mellitus: A Meta-Analysis
title_fullStr Studies on the Association of GCK and GCKR Polymorphisms with Susceptibility to Gestational Diabetes Mellitus: A Meta-Analysis
title_full_unstemmed Studies on the Association of GCK and GCKR Polymorphisms with Susceptibility to Gestational Diabetes Mellitus: A Meta-Analysis
title_short Studies on the Association of GCK and GCKR Polymorphisms with Susceptibility to Gestational Diabetes Mellitus: A Meta-Analysis
title_sort studies on the association of gck and gckr polymorphisms with susceptibility to gestational diabetes mellitus a meta analysis
topic gestational diabetes mellitus
gck gene
gckr gene
polymorphisms
meta-analysis
url https://www.imrpress.com/journal/CEOG/52/1/10.31083/CEOG26710
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