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dc.contributor.authorCho, Yoon Shin
dc.contributor.authorChen, Chien-Hsiun
dc.contributor.authorHu, Cheng
dc.contributor.authorLong, Jirong
dc.contributor.authorOng, Rick Twee Hee
dc.contributor.authorSim, Xueling
dc.contributor.authorTakeuchi, Fumihiko
dc.contributor.authorWu, Ying
dc.contributor.authorGo, Min Jin
dc.contributor.authorYamauchi, Toshimasa
dc.contributor.authorChang, Yi-Cheng
dc.contributor.authorKwak, Soo Heon
dc.contributor.authorMa, Ronald C W
dc.contributor.authorYamamoto, Ken
dc.contributor.authorAdair, Linda S
dc.contributor.authorAung, Tin
dc.contributor.authorCai, Qiuyin
dc.contributor.authorChang, Li-Ching
dc.contributor.authorChen, Yuan-Tsong
dc.contributor.authorGao, Yutang
dc.contributor.authorHu, Frank B
dc.contributor.authorKim, Hyung-Lae
dc.contributor.authorKim, Sangsoo
dc.contributor.authorKim, Young Jin
dc.contributor.authorLee, Jeannette Jen-Mai
dc.contributor.authorLee, Nanette R
dc.contributor.authorLi, Yun
dc.contributor.authorLiu, Jian Jun
dc.contributor.authorLu, Wei
dc.contributor.authorNakamura, Jiro
dc.contributor.authorNakashima, Eitaro
dc.contributor.authorNg, Daniel Peng-Keat
dc.contributor.authorTay, Wan Ting
dc.contributor.authorTsai, Fuu-Jen
dc.contributor.authorWong, Tien Yin
dc.contributor.authorYokota, Mitsuhiro
dc.contributor.authorZheng, Wei
dc.contributor.authorZhang, Rong
dc.contributor.authorWang, Congrong
dc.contributor.authorSo, Wing Yee
dc.contributor.authorOhnaka, Keizo
dc.contributor.authorIkegami, Hiroshi
dc.contributor.authorHara, Kazuo
dc.contributor.authorCho, Young Min
dc.contributor.authorCho, Nam H
dc.contributor.authorChang, Tien-Jyun
dc.contributor.authorBao, Yuqian
dc.contributor.authorHedman, Åsa K
dc.contributor.authorMorris, Andrew P
dc.contributor.authorMcCarthy, Mark I
dc.contributor.authorTakayanagi, Ryoichi
dc.contributor.authorPark, Kyong Soo
dc.contributor.authorJia, Weiping
dc.contributor.authorChuang, Lee-Ming
dc.contributor.authorChan, Juliana C N
dc.contributor.authorMaeda, Shiro
dc.contributor.authorKadowaki, Takashi
dc.contributor.authorLee, Jong-Young
dc.contributor.authorWu, Jer-Yuarn
dc.contributor.authorTeo, Yik Ying
dc.contributor.authorTai, E Shyong
dc.contributor.authorShu, Xiao Ou
dc.contributor.authorMohlke, Karen L
dc.contributor.authorKato, Norihiro
dc.contributor.authorHan, Bok-Ghee
dc.contributor.authorSeielstad, Mark
dc.date.accessioned2012-05-14T10:59:57Z
dc.date.available2012-05-14T10:59:57Z
dc.date.issued2012-01
dc.date.submitted2012-05-14
dc.identifier.citationNat. Genet. 2012, 44 (1):67-72en_GB
dc.identifier.issn1546-1718
dc.identifier.pmid22158537
dc.identifier.doi10.1038/ng.1019
dc.identifier.urihttp://hdl.handle.net/2336/223483
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links field.en_GB
dc.description.abstractWe conducted a three-stage genetic study to identify susceptibility loci for type 2 diabetes (T2D) in east Asian populations. We followed our stage 1 meta-analysis of eight T2D genome-wide association studies (6,952 cases with T2D and 11,865 controls) with a stage 2 in silico replication analysis (5,843 cases and 4,574 controls) and a stage 3 de novo replication analysis (12,284 cases and 13,172 controls). The combined analysis identified eight new T2D loci reaching genome-wide significance, which mapped in or near GLIS3, PEPD, FITM2-R3HDML-HNF4A, KCNK16, MAEA, GCC1-PAX4, PSMD6 and ZFAND3. GLIS3, which is involved in pancreatic beta cell development and insulin gene expression, is known for its association with fasting glucose levels. The evidence of an association with T2D for PEPD and HNF4A has been shown in previous studies. KCNK16 may regulate glucose-dependent insulin secretion in the pancreas. These findings, derived from an east Asian population, provide new perspectives on the etiology of T2D.
dc.language.isoenen
dc.publisherNature Pub. Groupen_GB
dc.relation.urlhttp://dx.doi.org/10.1038/ng.1019en_GB
dc.rightsArchived with thanks to Nature geneticsen_GB
dc.subject.meshAdulten_GB
dc.subject.meshAsian Continental Ancestry Groupen_GB
dc.subject.meshBlood Glucoseen_GB
dc.subject.meshCase-Control Studiesen_GB
dc.subject.meshChromosome Mappingen_GB
dc.subject.meshDiabetes Mellitus, Type 2en_GB
dc.subject.meshFar Easten_GB
dc.subject.meshGenetic Predisposition to Diseaseen_GB
dc.subject.meshGenome-Wide Association Studyen_GB
dc.subject.meshHumansen_GB
dc.subject.meshPolymorphism, Single Nucleotideen_GB
dc.titleMeta-analysis of genome-wide association studies identifies eight new loci for type 2 diabetes in east Asians.en
dc.typeArticleen
dc.contributor.departmentCenter for Genome Science, National Institute of Health, Osong Health Technology Administration Complex, Chungcheongbuk-do, Cheongwon-gun, Gangoe-myeon, Yeonje-ri, Korea. yooncho33@korea.kren_GB
dc.identifier.journalNature geneticsen_GB
html.description.abstractWe conducted a three-stage genetic study to identify susceptibility loci for type 2 diabetes (T2D) in east Asian populations. We followed our stage 1 meta-analysis of eight T2D genome-wide association studies (6,952 cases with T2D and 11,865 controls) with a stage 2 in silico replication analysis (5,843 cases and 4,574 controls) and a stage 3 de novo replication analysis (12,284 cases and 13,172 controls). The combined analysis identified eight new T2D loci reaching genome-wide significance, which mapped in or near GLIS3, PEPD, FITM2-R3HDML-HNF4A, KCNK16, MAEA, GCC1-PAX4, PSMD6 and ZFAND3. GLIS3, which is involved in pancreatic beta cell development and insulin gene expression, is known for its association with fasting glucose levels. The evidence of an association with T2D for PEPD and HNF4A has been shown in previous studies. KCNK16 may regulate glucose-dependent insulin secretion in the pancreas. These findings, derived from an east Asian population, provide new perspectives on the etiology of T2D.


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