Genetic polymorphism of glucokinase on the risk of type 2 diabetes and impaired glucose regulation: evidence based on 298,468 subjects
Glucokinase (GCK) is the key glucose phosphorylation enzyme which has attracted considerable attention as a candidate gene for type 2 diabetes (T2D) based on its enzyme function as the first rate-limiting step in the glycolysis pathway and regulates glucose-stimulated insulin secretion. In the past...
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| description | Glucokinase (GCK) is the key glucose phosphorylation enzyme which has attracted considerable attention as a candidate gene for type 2 diabetes (T2D) based on its enzyme function as the first rate-limiting step in the glycolysis pathway and regulates glucose-stimulated insulin secretion. In the past decade, the relationship between GCK and T2D has been reported in various ethnic groups. To derive a more precise estimation of the relationship and the effect of factors that might modify the risk, we performed this meta-analysis.
Databases including Pubmed, EMBASE, Web of Science and China National Knowledge Infrastructure (CNKI) were searched to find relevant studies. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association.
A total of 24 articles involving 88,229 cases and 210,239 controls were included. An overall random-effects per-allele OR of 1.06 (95% CI: 1.03-1.09; PA polymorphism. Significant results were also observed using dominant or recessive genetic models. In the subgroup analyses by ethnicity, significant results were found in Caucasians; whereas no significant associations were found among Asians. In addition, we found that the -30G>A polymorphism is a risk factor associated with increased impaired glucose regulation susceptibility. Besides, -30G>A homozygous was found to be significantly associated with increased fasting plasma glucose level with weighted mean difference (WMD) of 0.15 (95%: 0.05-0.24, P = 0.001) compared with G/G genotype.
This meta-analysis demonstrated that the -30G>A polymorphism of GCK is a risk factor associated with increased T2D susceptibility, but these associations vary in different ethnic populations. |
| doi_str_mv | 10.1371/journal.pone.0055727 |
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Databases including Pubmed, EMBASE, Web of Science and China National Knowledge Infrastructure (CNKI) were searched to find relevant studies. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association.
A total of 24 articles involving 88,229 cases and 210,239 controls were included. An overall random-effects per-allele OR of 1.06 (95% CI: 1.03-1.09; P<10(-4)) was found for the GCK -30G>A polymorphism. Significant results were also observed using dominant or recessive genetic models. In the subgroup analyses by ethnicity, significant results were found in Caucasians; whereas no significant associations were found among Asians. In addition, we found that the -30G>A polymorphism is a risk factor associated with increased impaired glucose regulation susceptibility. Besides, -30G>A homozygous was found to be significantly associated with increased fasting plasma glucose level with weighted mean difference (WMD) of 0.15 (95%: 0.05-0.24, P = 0.001) compared with G/G genotype.
This meta-analysis demonstrated that the -30G>A polymorphism of GCK is a risk factor associated with increased T2D susceptibility, but these associations vary in different ethnic populations.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0055727</identifier><identifier>PMID: 23441155</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Asians - genetics ; Biology ; Blood Glucose ; Confidence intervals ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - metabolism ; Fasting ; Gene polymorphism ; Genes ; Genetic aspects ; Genetic polymorphisms ; Genetic Predisposition to Disease ; Glucokinase ; Glucokinase - genetics ; Glucokinase - metabolism ; Glucose ; Glucose - metabolism ; Glycolysis ; Health risks ; Humans ; Hypothesis testing ; Insulin ; Insulin resistance ; Insulin secretion ; Isoenzymes ; Medicine ; Meta-analysis ; Minority & ethnic groups ; Mutation ; Nuclear medicine ; Phosphorylation ; Polymorphism ; Polymorphism, Genetic ; Population ; Publication Bias ; Risk ; Risk factors ; Secretion ; Studies ; Type 2 diabetes ; Whites - genetics</subject><ispartof>PloS one, 2013-02, Vol.8 (2), p.e55727-e55727</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Fu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Fu et al 2013 Fu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-fc0d22797b2d6e106bb28ccdfabd76d25cdf9a6b8ccce6ae08b7b9385ddb03d63</citedby><cites>FETCH-LOGICAL-c758t-fc0d22797b2d6e106bb28ccdfabd76d25cdf9a6b8ccce6ae08b7b9385ddb03d63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3575415/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3575415/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,2096,2915,23847,27905,27906,53772,53774,79349,79350</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23441155$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Baroni, Marco Giorgio</contributor><creatorcontrib>Fu, Da</creatorcontrib><creatorcontrib>Cong, Xianling</creatorcontrib><creatorcontrib>Ma, Yushui</creatorcontrib><creatorcontrib>Cai, Haidong</creatorcontrib><creatorcontrib>Cai, Mingxiang</creatorcontrib><creatorcontrib>Li, Dan</creatorcontrib><creatorcontrib>Lv, Mingli</creatorcontrib><creatorcontrib>Yuan, Xueyu</creatorcontrib><creatorcontrib>Huang, Yinghui</creatorcontrib><creatorcontrib>Lv, Zhongwei</creatorcontrib><title>Genetic polymorphism of glucokinase on the risk of type 2 diabetes and impaired glucose regulation: evidence based on 298,468 subjects</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Glucokinase (GCK) is the key glucose phosphorylation enzyme which has attracted considerable attention as a candidate gene for type 2 diabetes (T2D) based on its enzyme function as the first rate-limiting step in the glycolysis pathway and regulates glucose-stimulated insulin secretion. In the past decade, the relationship between GCK and T2D has been reported in various ethnic groups. To derive a more precise estimation of the relationship and the effect of factors that might modify the risk, we performed this meta-analysis.
Databases including Pubmed, EMBASE, Web of Science and China National Knowledge Infrastructure (CNKI) were searched to find relevant studies. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association.
A total of 24 articles involving 88,229 cases and 210,239 controls were included. An overall random-effects per-allele OR of 1.06 (95% CI: 1.03-1.09; P<10(-4)) was found for the GCK -30G>A polymorphism. Significant results were also observed using dominant or recessive genetic models. In the subgroup analyses by ethnicity, significant results were found in Caucasians; whereas no significant associations were found among Asians. In addition, we found that the -30G>A polymorphism is a risk factor associated with increased impaired glucose regulation susceptibility. Besides, -30G>A homozygous was found to be significantly associated with increased fasting plasma glucose level with weighted mean difference (WMD) of 0.15 (95%: 0.05-0.24, P = 0.001) compared with G/G genotype.
This meta-analysis demonstrated that the -30G>A polymorphism of GCK is a risk factor associated with increased T2D susceptibility, but these associations vary in different ethnic populations.</description><subject>Asians - genetics</subject><subject>Biology</subject><subject>Blood Glucose</subject><subject>Confidence intervals</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Fasting</subject><subject>Gene polymorphism</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic polymorphisms</subject><subject>Genetic Predisposition to Disease</subject><subject>Glucokinase</subject><subject>Glucokinase - genetics</subject><subject>Glucokinase - metabolism</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Glycolysis</subject><subject>Health risks</subject><subject>Humans</subject><subject>Hypothesis testing</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Insulin secretion</subject><subject>Isoenzymes</subject><subject>Medicine</subject><subject>Meta-analysis</subject><subject>Minority & ethnic groups</subject><subject>Mutation</subject><subject>Nuclear medicine</subject><subject>Phosphorylation</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Population</subject><subject>Publication Bias</subject><subject>Risk</subject><subject>Risk factors</subject><subject>Secretion</subject><subject>Studies</subject><subject>Type 2 diabetes</subject><subject>Whites - 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genetics</topic><topic>Biology</topic><topic>Blood Glucose</topic><topic>Confidence intervals</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Fasting</topic><topic>Gene polymorphism</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic polymorphisms</topic><topic>Genetic Predisposition to Disease</topic><topic>Glucokinase</topic><topic>Glucokinase - genetics</topic><topic>Glucokinase - metabolism</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Glycolysis</topic><topic>Health risks</topic><topic>Humans</topic><topic>Hypothesis testing</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Insulin secretion</topic><topic>Isoenzymes</topic><topic>Medicine</topic><topic>Meta-analysis</topic><topic>Minority & ethnic groups</topic><topic>Mutation</topic><topic>Nuclear medicine</topic><topic>Phosphorylation</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Population</topic><topic>Publication Bias</topic><topic>Risk</topic><topic>Risk factors</topic><topic>Secretion</topic><topic>Studies</topic><topic>Type 2 diabetes</topic><topic>Whites - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fu, Da</au><au>Cong, Xianling</au><au>Ma, Yushui</au><au>Cai, Haidong</au><au>Cai, Mingxiang</au><au>Li, Dan</au><au>Lv, Mingli</au><au>Yuan, Xueyu</au><au>Huang, Yinghui</au><au>Lv, Zhongwei</au><au>Baroni, Marco Giorgio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic polymorphism of glucokinase on the risk of type 2 diabetes and impaired glucose regulation: evidence based on 298,468 subjects</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-02-18</date><risdate>2013</risdate><volume>8</volume><issue>2</issue><spage>e55727</spage><epage>e55727</epage><pages>e55727-e55727</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Glucokinase (GCK) is the key glucose phosphorylation enzyme which has attracted considerable attention as a candidate gene for type 2 diabetes (T2D) based on its enzyme function as the first rate-limiting step in the glycolysis pathway and regulates glucose-stimulated insulin secretion. In the past decade, the relationship between GCK and T2D has been reported in various ethnic groups. To derive a more precise estimation of the relationship and the effect of factors that might modify the risk, we performed this meta-analysis.
Databases including Pubmed, EMBASE, Web of Science and China National Knowledge Infrastructure (CNKI) were searched to find relevant studies. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association.
A total of 24 articles involving 88,229 cases and 210,239 controls were included. An overall random-effects per-allele OR of 1.06 (95% CI: 1.03-1.09; P<10(-4)) was found for the GCK -30G>A polymorphism. Significant results were also observed using dominant or recessive genetic models. In the subgroup analyses by ethnicity, significant results were found in Caucasians; whereas no significant associations were found among Asians. In addition, we found that the -30G>A polymorphism is a risk factor associated with increased impaired glucose regulation susceptibility. Besides, -30G>A homozygous was found to be significantly associated with increased fasting plasma glucose level with weighted mean difference (WMD) of 0.15 (95%: 0.05-0.24, P = 0.001) compared with G/G genotype.
This meta-analysis demonstrated that the -30G>A polymorphism of GCK is a risk factor associated with increased T2D susceptibility, but these associations vary in different ethnic populations.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23441155</pmid><doi>10.1371/journal.pone.0055727</doi><tpages>e55727</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | PloS one, 2013-02, Vol.8 (2), p.e55727-e55727 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1330880869 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Asians - genetics Biology Blood Glucose Confidence intervals Diabetes Diabetes mellitus Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - metabolism Fasting Gene polymorphism Genes Genetic aspects Genetic polymorphisms Genetic Predisposition to Disease Glucokinase Glucokinase - genetics Glucokinase - metabolism Glucose Glucose - metabolism Glycolysis Health risks Humans Hypothesis testing Insulin Insulin resistance Insulin secretion Isoenzymes Medicine Meta-analysis Minority & ethnic groups Mutation Nuclear medicine Phosphorylation Polymorphism Polymorphism, Genetic Population Publication Bias Risk Risk factors Secretion Studies Type 2 diabetes Whites - genetics |
| title | Genetic polymorphism of glucokinase on the risk of type 2 diabetes and impaired glucose regulation: evidence based on 298,468 subjects |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-18T17%3A38%3A36IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Genetic%20polymorphism%20of%20glucokinase%20on%20the%20risk%20of%20type%202%20diabetes%20and%20impaired%20glucose%20regulation:%20evidence%20based%20on%20298,468%20subjects&rft.jtitle=PloS%20one&rft.au=Fu,%20Da&rft.date=2013-02-18&rft.volume=8&rft.issue=2&rft.spage=e55727&rft.epage=e55727&rft.pages=e55727-e55727&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0055727&rft_dat=%3Cgale_plos_%3EA478229551%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1330880869&rft_id=info:pmid/23441155&rft_galeid=A478229551&rft_doaj_id=oai_doaj_org_article_4aefc8118c88411e90b97f9c888459aa&rfr_iscdi=true |