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Cho, Y.S.* ; Chen, C.H.* ; Hu, C.* ; Long, J.* ; Ong, R.T.* ; Sim, X.* ; Takeuchi, F.* ; Wu, Y.* ; Go, M.J.* ; Yamauchi, T.* ; Chang, Y.C.* ; Kwak, S.H.* ; Ma, R.C.* ; Yamamoto, K.* ; Adair, L.S.* ; Aung, T.* ; Cai, Q.* ; Chang, L.C.* ; Chen, Y.T.* ; Gao, Y.* ; Hu, F.B.* ; Kim, H.L.* ; Kim, S.* ; Kim, Y.J.* ; Lee, J.J.* ; Lee, N.R.* ; Li, Y.* ; Liu, J.J.* ; Lu, W.* ; Nakamura, J.* ; Nakashima, E.* ; Ng, D.P.* ; Tay, W.T.* ; Tsai, F.J.* ; Wong, T.Y.* ; Yokota, M.* ; Zheng, W.* ; Zhang, R.* ; Wang, C.* ; So, W.Y.* ; Ohnaka, K.* ; Ikegami, H.* ; Hara, K.* ; Cho, Y.M.* ; Cho, N.H.* ; Chang, T.J.* ; Bao, Y.* ; Hedman, A.K.* ; Morris, A.P.* ; McCarthy, M.I.* ; DIAGRAM Consortium (Huth, C. ; Grallert, H. ; Gieger, C. ; Meitinger, T. ; Petersen, A.-K. ; Thorand, B. ; Illig, T. ; Wichmann, H.-E.) ; MuTHER Consortium (*) ; Takayanagi, R.* ; Park, K.S.* ; Jia, W.* ; Chuang, L.M.* ; Chan, J.C.* ; Maeda, S.* ; Kadowaki, T.* ; Lee, J.Y.* ; Wu, J.Y.* ; Teo, Y.Y.* ; Tai, E.S.* ; Shu, X.O.* ; Mohlke, K.L.* ; Kato, N.* ; Han, B.G.* ; Seielstad, M.*

Meta-analysis of genome-wide association studies identifies eight new loci for type 2 diabetes in east Asians.

Nat. Genet. 44, 67-72 (2012)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
We 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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Susceptibility loci; Japanese population; Genetic-loci; Variants; Risk; Childhood; Mellitus; Complex; KCNQ1
ISSN (print) / ISBN 1061-4036
e-ISSN 1546-1718
Zeitschrift Nature Genetics
Quellenangaben Band: 44, Heft: 1, Seiten: 67-72 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Verlagsort New York, NY
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Epidemiology II (EPI2)
Research Unit Molecular Epidemiology (AME)
Institute of Genetic Epidemiology (IGE)
Institute of Epidemiology (EPI)
Institute of Human Genetics (IHG)