Common polymorphisms in MTNR1B, G6PC2 and GCK are associated with increased fasting plasma glucose and impaired beta-cell function in Chinese subjects
Previous studies identified melatonin receptor 1B (MTNR1B), islet-specific glucose 6 phosphatase catalytic subunit-related protein (G6PC2), glucokinase (GCK) and glucokinase regulatory protein (GCKR) as candidate genes for type 2 diabetes (T2D) acting through elevated fasting plasma glucose (FPG). W...
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| Veröffentlicht in: | PloS one 2010-07, Vol.5 (7), p.e11428-e11428 |
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| creator | Tam, Claudia Ha Ting Ho, Janice Sin Ka Wang, Ying Lee, Heung Man Lam, Vincent Kwok Lim Germer, Soren Martin, Mitchell So, Wing Yee Ma, Ronald Ching Wan Chan, Juliana Chung Ngor Ng, Maggie Chor Yin |
| description | Previous studies identified melatonin receptor 1B (MTNR1B), islet-specific glucose 6 phosphatase catalytic subunit-related protein (G6PC2), glucokinase (GCK) and glucokinase regulatory protein (GCKR) as candidate genes for type 2 diabetes (T2D) acting through elevated fasting plasma glucose (FPG). We examined the associations of the reported common variants of these genes with T2D and glucose homeostasis in three independent Chinese cohorts.
Five single nucleotide polymorphisms (SNPs), MTNR1B rs10830963, G6PC2 rs16856187 and rs478333, GCK rs1799884 and GCKR rs780094, were genotyped in 1644 controls (583 adults and 1061 adolescents) and 1342 T2D patients. The G-allele of MTNR1B rs10830963 and the C-alleles of both G6PC2 rs16856187 and rs478333 were associated with higher FPG (0.0034 |
| doi_str_mv | 10.1371/journal.pone.0011428 |
| format | Article |
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Five single nucleotide polymorphisms (SNPs), MTNR1B rs10830963, G6PC2 rs16856187 and rs478333, GCK rs1799884 and GCKR rs780094, were genotyped in 1644 controls (583 adults and 1061 adolescents) and 1342 T2D patients. The G-allele of MTNR1B rs10830963 and the C-alleles of both G6PC2 rs16856187 and rs478333 were associated with higher FPG (0.0034<P<6.6x10(-5)) in healthy controls. In addition to our previous report for association with FPG, the A-allele of GCK rs1799884 was also associated with reduced homeostasis model assessment of beta-cell function (HOMA-B) (P=0.0015). Together with GCKR rs780094, the risk alleles of these SNPs exhibited dosage effect in their associations with increased FPG (P=2.9x10(-9)) and reduced HOMA-B (P=1.1x10(-3)). Meta-analyses strongly supported additive effects of MTNR1B rs10830963 and G6PC2 rs16856187 on FPG.
Common variants of MTNR1B, G6PC2 and GCK are associated with elevated FPG and impaired insulin secretion, both individually and jointly, suggesting that these risk alleles may precipitate or perpetuate hyperglycemia in predisposed individuals.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0011428</identifier><identifier>PMID: 20628598</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adaptor Proteins, Signal Transducing - genetics ; Adenosine ; Adolescents ; Adult ; Adults ; Alleles ; Analysis ; Asian Continental Ancestry Group - genetics ; Beta cells ; Binding sites ; Blood Glucose - metabolism ; Blood proteins ; Catalysis ; Chromosomes ; Circadian rhythm ; Diabetes ; Diabetes and Endocrinology/Type 2 Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - genetics ; Fasting ; Fasting - blood ; Female ; Gene expression ; Gene loci ; Genes ; Genetic aspects ; Genetics and Genomics/Complex Traits ; Genetics and Genomics/Genetics of Disease ; Genetics and Genomics/Medical Genetics ; Genetics and Genomics/Population Genetics ; Genomics ; Genotype ; Glucokinase ; Glucokinase - genetics ; Glucose ; Glucose-6-Phosphatase - genetics ; Homeostasis ; Hospitals ; Humans ; Hyperglycemia ; Insulin ; Insulin secretion ; Insulin-Secreting Cells - pathology ; Insulin-Secreting Cells - physiology ; Isoenzymes ; Laboratory testing ; Male ; Medicine ; Melatonin ; Meta-analysis ; Middle Aged ; Pancreatic beta cells ; Phosphatases ; Plasma ; Polymorphism, Single Nucleotide - genetics ; Receptors, Melatonin - genetics ; Rodents ; Secretion ; Single nucleotide polymorphisms ; Single-nucleotide polymorphism ; Studies ; Type 2 diabetes</subject><ispartof>PloS one, 2010-07, Vol.5 (7), p.e11428-e11428</ispartof><rights>COPYRIGHT 2010 Public Library of Science</rights><rights>2010 Tam 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>Tam et al. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c691t-18cc3226a50f61a39a65c4a4f4ddf193dc3662416966e9bd8538e2ac89d7c21b3</citedby><cites>FETCH-LOGICAL-c691t-18cc3226a50f61a39a65c4a4f4ddf193dc3662416966e9bd8538e2ac89d7c21b3</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/PMC2900202/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2900202/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20628598$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Maedler, Kathrin</contributor><creatorcontrib>Tam, Claudia Ha Ting</creatorcontrib><creatorcontrib>Ho, Janice Sin Ka</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Lee, Heung Man</creatorcontrib><creatorcontrib>Lam, Vincent Kwok Lim</creatorcontrib><creatorcontrib>Germer, Soren</creatorcontrib><creatorcontrib>Martin, Mitchell</creatorcontrib><creatorcontrib>So, Wing Yee</creatorcontrib><creatorcontrib>Ma, Ronald Ching Wan</creatorcontrib><creatorcontrib>Chan, Juliana Chung Ngor</creatorcontrib><creatorcontrib>Ng, Maggie Chor Yin</creatorcontrib><title>Common polymorphisms in MTNR1B, G6PC2 and GCK are associated with increased fasting plasma glucose and impaired beta-cell function in Chinese subjects</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Previous studies identified melatonin receptor 1B (MTNR1B), islet-specific glucose 6 phosphatase catalytic subunit-related protein (G6PC2), glucokinase (GCK) and glucokinase regulatory protein (GCKR) as candidate genes for type 2 diabetes (T2D) acting through elevated fasting plasma glucose (FPG). We examined the associations of the reported common variants of these genes with T2D and glucose homeostasis in three independent Chinese cohorts.
Five single nucleotide polymorphisms (SNPs), MTNR1B rs10830963, G6PC2 rs16856187 and rs478333, GCK rs1799884 and GCKR rs780094, were genotyped in 1644 controls (583 adults and 1061 adolescents) and 1342 T2D patients. The G-allele of MTNR1B rs10830963 and the C-alleles of both G6PC2 rs16856187 and rs478333 were associated with higher FPG (0.0034<P<6.6x10(-5)) in healthy controls. In addition to our previous report for association with FPG, the A-allele of GCK rs1799884 was also associated with reduced homeostasis model assessment of beta-cell function (HOMA-B) (P=0.0015). Together with GCKR rs780094, the risk alleles of these SNPs exhibited dosage effect in their associations with increased FPG (P=2.9x10(-9)) and reduced HOMA-B (P=1.1x10(-3)). Meta-analyses strongly supported additive effects of MTNR1B rs10830963 and G6PC2 rs16856187 on FPG.
Common variants of MTNR1B, G6PC2 and GCK are associated with elevated FPG and impaired insulin secretion, both individually and jointly, suggesting that these risk alleles may precipitate or perpetuate hyperglycemia in predisposed individuals.</description><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adenosine</subject><subject>Adolescents</subject><subject>Adult</subject><subject>Adults</subject><subject>Alleles</subject><subject>Analysis</subject><subject>Asian Continental Ancestry Group - genetics</subject><subject>Beta cells</subject><subject>Binding sites</subject><subject>Blood Glucose - metabolism</subject><subject>Blood proteins</subject><subject>Catalysis</subject><subject>Chromosomes</subject><subject>Circadian rhythm</subject><subject>Diabetes</subject><subject>Diabetes and Endocrinology/Type 2 Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Fasting</subject><subject>Fasting - blood</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene loci</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetics and Genomics/Complex Traits</subject><subject>Genetics and Genomics/Genetics of Disease</subject><subject>Genetics and Genomics/Medical Genetics</subject><subject>Genetics and Genomics/Population Genetics</subject><subject>Genomics</subject><subject>Genotype</subject><subject>Glucokinase</subject><subject>Glucokinase - genetics</subject><subject>Glucose</subject><subject>Glucose-6-Phosphatase - genetics</subject><subject>Homeostasis</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Hyperglycemia</subject><subject>Insulin</subject><subject>Insulin secretion</subject><subject>Insulin-Secreting Cells - pathology</subject><subject>Insulin-Secreting Cells - physiology</subject><subject>Isoenzymes</subject><subject>Laboratory testing</subject><subject>Male</subject><subject>Medicine</subject><subject>Melatonin</subject><subject>Meta-analysis</subject><subject>Middle Aged</subject><subject>Pancreatic beta cells</subject><subject>Phosphatases</subject><subject>Plasma</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Receptors, Melatonin - genetics</subject><subject>Rodents</subject><subject>Secretion</subject><subject>Single nucleotide polymorphisms</subject><subject>Single-nucleotide polymorphism</subject><subject>Studies</subject><subject>Type 2 diabetes</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk81u1DAUhSMEoqXwBggiIYGQmME_GSfeIJUIhhGFolLYWjeOk3iUxMF2gL4Iz4unk1YN6gJlkcT-zrn2sW8UPcZoiWmKX2_NaHtol4Pp1RIhjBOS3YkOMadkwQiid298H0QPnNsitKIZY_ejA4IYyVY8O4z-5KbrTB8Ppr3ojB0a7ToX6z7-dP75DL99Fa_Zl5zE0JfxOv8Yg1UxOGekBq_K-Jf2TYClVeDCbwXO676OhxZcB3HdjtI4dSnW3QDaBqZQHhZStW1cjb30OtQO1fJG9yqgbiy2Snr3MLpXQevUo-l9FH17_-48_7A4OV1v8uOThWQc-wXOpKSEMFihimGgHNhKJpBUSVlWYfelpIyRBDPOmOJFmYUAFAGZ8TKVBBf0KHq69x1a48QUqROYcJxxRlMeiM2eKA1sxWB1B_ZCGNDicsDYWoD1WrZKFLwCtcoYxQgSVSCOkrCEJK0SQLiAKni9maqNRadKqXpvoZ2Zzmd63Yja_BSEI0QQCQYvJgNrfozKedFptwsTemVGJ1JKecp5igL57B_y9s1NVA1h_bqvTCgrd57iOElplqUpTwO1vIUKT6k6LcP1q3QYnwlezgSB8eq3r2F0Tmy-nv0_e_p9zj6_wTYKWt840467W-TmYLIHpTXOWVVdZ4yR2HXPVRpi1z1i6p4ge3LzfK5FV-1C_wIlwBV9</recordid><startdate>20100708</startdate><enddate>20100708</enddate><creator>Tam, Claudia Ha Ting</creator><creator>Ho, Janice Sin Ka</creator><creator>Wang, Ying</creator><creator>Lee, Heung Man</creator><creator>Lam, Vincent Kwok Lim</creator><creator>Germer, Soren</creator><creator>Martin, Mitchell</creator><creator>So, Wing Yee</creator><creator>Ma, Ronald Ching Wan</creator><creator>Chan, Juliana Chung Ngor</creator><creator>Ng, Maggie Chor Yin</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20100708</creationdate><title>Common polymorphisms in MTNR1B, G6PC2 and GCK are associated with increased fasting plasma glucose and impaired beta-cell function in Chinese subjects</title><author>Tam, Claudia Ha Ting ; Ho, Janice Sin Ka ; Wang, Ying ; Lee, Heung Man ; Lam, Vincent Kwok Lim ; Germer, Soren ; Martin, Mitchell ; So, Wing Yee ; Ma, Ronald Ching Wan ; Chan, Juliana Chung Ngor ; Ng, Maggie Chor Yin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c691t-18cc3226a50f61a39a65c4a4f4ddf193dc3662416966e9bd8538e2ac89d7c21b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adaptor Proteins, Signal Transducing - 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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>Tam, Claudia Ha Ting</au><au>Ho, Janice Sin Ka</au><au>Wang, Ying</au><au>Lee, Heung Man</au><au>Lam, Vincent Kwok Lim</au><au>Germer, Soren</au><au>Martin, Mitchell</au><au>So, Wing Yee</au><au>Ma, Ronald Ching Wan</au><au>Chan, Juliana Chung Ngor</au><au>Ng, Maggie Chor Yin</au><au>Maedler, Kathrin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Common polymorphisms in MTNR1B, G6PC2 and GCK are associated with increased fasting plasma glucose and impaired beta-cell function in Chinese subjects</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2010-07-08</date><risdate>2010</risdate><volume>5</volume><issue>7</issue><spage>e11428</spage><epage>e11428</epage><pages>e11428-e11428</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Previous studies identified melatonin receptor 1B (MTNR1B), islet-specific glucose 6 phosphatase catalytic subunit-related protein (G6PC2), glucokinase (GCK) and glucokinase regulatory protein (GCKR) as candidate genes for type 2 diabetes (T2D) acting through elevated fasting plasma glucose (FPG). We examined the associations of the reported common variants of these genes with T2D and glucose homeostasis in three independent Chinese cohorts.
Five single nucleotide polymorphisms (SNPs), MTNR1B rs10830963, G6PC2 rs16856187 and rs478333, GCK rs1799884 and GCKR rs780094, were genotyped in 1644 controls (583 adults and 1061 adolescents) and 1342 T2D patients. The G-allele of MTNR1B rs10830963 and the C-alleles of both G6PC2 rs16856187 and rs478333 were associated with higher FPG (0.0034<P<6.6x10(-5)) in healthy controls. In addition to our previous report for association with FPG, the A-allele of GCK rs1799884 was also associated with reduced homeostasis model assessment of beta-cell function (HOMA-B) (P=0.0015). Together with GCKR rs780094, the risk alleles of these SNPs exhibited dosage effect in their associations with increased FPG (P=2.9x10(-9)) and reduced HOMA-B (P=1.1x10(-3)). Meta-analyses strongly supported additive effects of MTNR1B rs10830963 and G6PC2 rs16856187 on FPG.
Common variants of MTNR1B, G6PC2 and GCK are associated with elevated FPG and impaired insulin secretion, both individually and jointly, suggesting that these risk alleles may precipitate or perpetuate hyperglycemia in predisposed individuals.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>20628598</pmid><doi>10.1371/journal.pone.0011428</doi><tpages>e11428</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2010-07, Vol.5 (7), p.e11428-e11428 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1291896379 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; PubMed Central(OpenAccess); DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; Free Full-Text Journals in Chemistry |
| subjects | Adaptor Proteins, Signal Transducing - genetics Adenosine Adolescents Adult Adults Alleles Analysis Asian Continental Ancestry Group - genetics Beta cells Binding sites Blood Glucose - metabolism Blood proteins Catalysis Chromosomes Circadian rhythm Diabetes Diabetes and Endocrinology/Type 2 Diabetes Diabetes mellitus Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - genetics Fasting Fasting - blood Female Gene expression Gene loci Genes Genetic aspects Genetics and Genomics/Complex Traits Genetics and Genomics/Genetics of Disease Genetics and Genomics/Medical Genetics Genetics and Genomics/Population Genetics Genomics Genotype Glucokinase Glucokinase - genetics Glucose Glucose-6-Phosphatase - genetics Homeostasis Hospitals Humans Hyperglycemia Insulin Insulin secretion Insulin-Secreting Cells - pathology Insulin-Secreting Cells - physiology Isoenzymes Laboratory testing Male Medicine Melatonin Meta-analysis Middle Aged Pancreatic beta cells Phosphatases Plasma Polymorphism, Single Nucleotide - genetics Receptors, Melatonin - genetics Rodents Secretion Single nucleotide polymorphisms Single-nucleotide polymorphism Studies Type 2 diabetes |
| title | Common polymorphisms in MTNR1B, G6PC2 and GCK are associated with increased fasting plasma glucose and impaired beta-cell function in Chinese subjects |
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