Published in

Nature Research, Nature Genetics, 5(40), p. 638-645, 2008

DOI: 10.1038/ng.120

Elsevier, Year Book of Endocrinology, (2008), p. 38-39

DOI: 10.1016/s0084-3741(08)79224-2

Links

Tools

Export citation

Search in Google Scholar

Meta-analysis of genome-wide association data and large-scale replication identifies additional susceptibility loci for type 2 diabetes

Journal article published in 2008 by Paul Iw W. de Bakker, Laura J. Scott, de Bakker Piw, Bonnycastle Ll, Burtt Np, Chines Ps, Eleftheria Zeggini ORCID, Daly Mj, Duren Wl, Erdos Mr, Frayling Tm, Freathy Rm, Hughes Te, Morken Ma, Rayner Nw and other authors.
This paper is available in a repository.
This paper is available in a repository.

Full text: Download

Green circle
Preprint: archiving allowed
Upload
Orange circle
Postprint: archiving restricted
Upload
Red circle
Published version: archiving forbidden
Policy details
Data provided by SHERPA/RoMEO

Abstract

Genome-wide association (GWA) studies have identified multiple new genomic loci at which common variants modestly but reproducibly influence risk of type 2 diabetes (T2D)1-11. Established associations to common and rare variants explain only a small proportion of the heritability of T2D. As previously published analyses had limited power to discover loci at which common alleles have modest effects, we performed meta-analysis of three T2D GWA scans encompassing 10,128 individuals of European-descent and ~2.2 million SNPs (directly genotyped and imputed). Replication testing was performed in an independent sample with an effective sample size of up to 53,975. At least six new loci with robust evidence for association were detected, including the JAZF1 (p=5.0×10−14), CDC123/CAMK1D (p=1.2×10−10), TSPAN8/LGR5 (p=1.1×10−9), THADA (p=1.1×10−9), ADAMTS9 (p=1.2×10−8), and NOTCH2 (p=4.1×10−8) gene regions. The large number of loci with relatively small effects indicates the value of large discovery and follow-up samples in identifying additional clues about the inherited basis of T2D.