2.50
Hdl Handle:
http://hdl.handle.net/2336/12499
Title:
A variant in CDKAL1 influences insulin response and risk of type 2 diabetes.
Authors:
Steinthorsdottir, Valgerdur; Thorleifsson, Gudmar; Reynisdottir, Inga; Benediktsson, Rafn; Jonsdottir, Thorbjorg; Walters, G Bragi; Styrkarsdottir, Unnur; Gretarsdottir, Solveig; Emilsson, Valur; Ghosh, Shyamali; Baker, Adam; Snorradottir, Steinunn; Bjarnason, Hjordis; Ng, Maggie C Y; Hansen, Torben; Bagger, Yu; Wilensky, Robert L; Reilly, Muredach P; Adeyemo, Adebowale; Chen, Yuanxiu; Zhou, Jie; Gudnason, Vilmundur; Chen, Guanjie; Huang, Hanxia; Lashley, Kerrie; Doumatey, Ayo; So, Wing-Yee; Ma, Ronald C Y; Andersen, Gitte; Borch-Johnsen, Knut; Jorgensen, Torben; van Vliet-Ostaptchouk, Jana V; Hofker, Marten H; Wijmenga, Cisca; Christiansen, Claus; Rader, Daniel J; Rotimi, Charles; Gurney, Mark; Chan, Juliana C N; Pedersen, Oluf; Sigurdsson, Gunnar; Gulcher, Jeffrey R; Thorsteinsdottir, Unnur; Kong, Augustine; Stefansson, Kari
Citation:
Nat. Genet. 2007, 39(6):770-5
Issue Date:
1-Jun-2007
Abstract:
We conducted a genome-wide association study for type 2 diabetes (T2D) in Icelandic cases and controls, and we found that a previously described variant in the transcription factor 7-like 2 gene (TCF7L2) gene conferred the most significant risk. In addition to confirming two recently identified risk variants, we identified a variant in the CDKAL1 gene that was associated with T2D in individuals of European ancestry (allele-specific odds ratio (OR) = 1.20 (95% confidence interval, 1.13-1.27), P = 7.7 x 10(-9)) and individuals from Hong Kong of Han Chinese ancestry (OR = 1.25 (1.11-1.40), P = 0.00018). The genotype OR of this variant suggested that the effect was substantially stronger in homozygous carriers than in heterozygous carriers. The ORs for homozygotes were 1.50 (1.31-1.72) and 1.55 (1.23-1.95) in the European and Hong Kong groups, respectively. The insulin response for homozygotes was approximately 20% lower than for heterozygotes or noncarriers, suggesting that this variant confers risk of T2D through reduced insulin secretion.
Description:
To access publisher full text version of this article. Please click on the hyperlink in Additional Link
Additional Links:
http://www.nature.com/ng/journal/v39/n6/full/ng2043.html

Full metadata record

DC FieldValue Language
dc.contributor.authorSteinthorsdottir, Valgerdur-
dc.contributor.authorThorleifsson, Gudmar-
dc.contributor.authorReynisdottir, Inga-
dc.contributor.authorBenediktsson, Rafn-
dc.contributor.authorJonsdottir, Thorbjorg-
dc.contributor.authorWalters, G Bragi-
dc.contributor.authorStyrkarsdottir, Unnur-
dc.contributor.authorGretarsdottir, Solveig-
dc.contributor.authorEmilsson, Valur-
dc.contributor.authorGhosh, Shyamali-
dc.contributor.authorBaker, Adam-
dc.contributor.authorSnorradottir, Steinunn-
dc.contributor.authorBjarnason, Hjordis-
dc.contributor.authorNg, Maggie C Y-
dc.contributor.authorHansen, Torben-
dc.contributor.authorBagger, Yu-
dc.contributor.authorWilensky, Robert L-
dc.contributor.authorReilly, Muredach P-
dc.contributor.authorAdeyemo, Adebowale-
dc.contributor.authorChen, Yuanxiu-
dc.contributor.authorZhou, Jie-
dc.contributor.authorGudnason, Vilmundur-
dc.contributor.authorChen, Guanjie-
dc.contributor.authorHuang, Hanxia-
dc.contributor.authorLashley, Kerrie-
dc.contributor.authorDoumatey, Ayo-
dc.contributor.authorSo, Wing-Yee-
dc.contributor.authorMa, Ronald C Y-
dc.contributor.authorAndersen, Gitte-
dc.contributor.authorBorch-Johnsen, Knut-
dc.contributor.authorJorgensen, Torben-
dc.contributor.authorvan Vliet-Ostaptchouk, Jana V-
dc.contributor.authorHofker, Marten H-
dc.contributor.authorWijmenga, Cisca-
dc.contributor.authorChristiansen, Claus-
dc.contributor.authorRader, Daniel J-
dc.contributor.authorRotimi, Charles-
dc.contributor.authorGurney, Mark-
dc.contributor.authorChan, Juliana C N-
dc.contributor.authorPedersen, Oluf-
dc.contributor.authorSigurdsson, Gunnar-
dc.contributor.authorGulcher, Jeffrey R-
dc.contributor.authorThorsteinsdottir, Unnur-
dc.contributor.authorKong, Augustine-
dc.contributor.authorStefansson, Kari-
dc.date.accessioned2007-07-02T11:10:27Z-
dc.date.available2007-07-02T11:10:27Z-
dc.date.issued2007-06-01-
dc.date.submitted2007-07-02-
dc.identifier.citationNat. Genet. 2007, 39(6):770-5en
dc.identifier.issn1061-4036-
dc.identifier.pmid17460697-
dc.identifier.doi10.1038/ng2043-
dc.identifier.urihttp://hdl.handle.net/2336/12499-
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Linken
dc.description.abstractWe conducted a genome-wide association study for type 2 diabetes (T2D) in Icelandic cases and controls, and we found that a previously described variant in the transcription factor 7-like 2 gene (TCF7L2) gene conferred the most significant risk. In addition to confirming two recently identified risk variants, we identified a variant in the CDKAL1 gene that was associated with T2D in individuals of European ancestry (allele-specific odds ratio (OR) = 1.20 (95% confidence interval, 1.13-1.27), P = 7.7 x 10(-9)) and individuals from Hong Kong of Han Chinese ancestry (OR = 1.25 (1.11-1.40), P = 0.00018). The genotype OR of this variant suggested that the effect was substantially stronger in homozygous carriers than in heterozygous carriers. The ORs for homozygotes were 1.50 (1.31-1.72) and 1.55 (1.23-1.95) in the European and Hong Kong groups, respectively. The insulin response for homozygotes was approximately 20% lower than for heterozygotes or noncarriers, suggesting that this variant confers risk of T2D through reduced insulin secretion.en
dc.language.isoenen
dc.publisherNature Pub. Co.,en
dc.relation.urlhttp://www.nature.com/ng/journal/v39/n6/full/ng2043.htmlen
dc.subject.meshPubMed - in processen
dc.titleA variant in CDKAL1 influences insulin response and risk of type 2 diabetes.en
dc.typeArticleen
dc.format.digYES-

Related articles on PubMed

All Items in Hirsla are protected by copyright, with all rights reserved, unless otherwise indicated.