Authors

Helen N. Lyon, Boston Children's Hospital
Valur Emilsson, deCODE genetics
Anke Hinney, Universität Duisburg-Essen
Iris M. Heid, Helmholtz Center Munich German Research Center for Environmental Health
Jessica Lasky-Su, Brigham and Women's Hospital
Xiaofeng Zhu, Case Western Reserve University
Gudmar Thorleifsson, deCODE genetics
Steinunn Gunnarsdottir, deCODE genetics
G. Bragi Walters, deCODE genetics
Unnur Thorsteinsdottir, deCODE genetics
Augustine Kong, deCODE genetics
Jeffrey Gulcher, deCODE genetics
Thuy Trang Nguyen, Philipps-Universität Marburg
André Scherag, Philipps-Universität Marburg
Arne Pfeufer, Technische Universität München
Thomas Meitinger, Technische Universität München
Günter Brönner, Universität Duisburg-Essen
Winfried Rief, Philipps-Universität Marburg
Manuel E. Soto-Quiros, Hospital Nacional de Niños Dr. Carlos Sáenz Herrera
Lydiana Avila, Hospital Nacional de Niños Dr. Carlos Sáenz Herrera
Barbara Klanderman, Brigham and Women's Hospital
Benjamin A. Raby, Brigham and Women's Hospital
Edwin K. Silverman, Brigham and Women's Hospital
Scott T. Weiss, Brigham and Women's Hospital
Nan Laird, Brigham and Women's Hospital
Xiao Ding, Brigham and Women's Hospital
Leif Groop, Skånes Universitetssjukhus
Tiinamaija Tuomi, Helsinki University Hospital
Bo Isomaa, Folkhälsan
Kristina Bengtsson, Helsinki University Hospital
Johannah L. Butler, Boston Children's Hospital
Richard S. Cooper, Loyola University Medical Center
Caroline S. Fox, Framingham Heart Study

Document Type

Article

Publication Date

4-1-2007

Abstract

A SNP upstream of the INSIG2 gene, rs7566605, was recently found to be associated with obesity as measured by body mass index (BMI) by Herbert and colleagues. The association between increased BMI and homozygosity for the minor allele was first observed in data from a genome-wide association scan of 86,604 SNPs in 923 related individuals from the Framingham Heart Study offspring cohort. The association was reproduced in four additional cohorts, but was not seen in a fifth cohort. To further assess the general reproducibility of this association, we genotyped rs7566605 in nine large cohorts from eight populations across multiple ethnicities (total n=16,969). We tested this variant for association with BMI in each sample under a recessive model using family-based, population-based, and case-control designs. We observed a significant (p < 0.05) association in five cohorts but saw no association in three other cohorts. There was variability in the strength of association evidence across examination cycles in longitudinal data from unrelated individuals in the Framingham Heart Study Offspring cohort. A combined analysis revealed significant independent validation of this association in both unrelated (p=0.046) and family-based (p=0.004) samples. The estimated risk conferred by this allele is small, and could easily be masked by small sample size, population stratification, or other confounders. These validation studies suggest that the original association is less likely to be spurious, but the failure to observe an association in every data set suggests that the effect of SNP rs7566605 on BMI may be heterogeneous across population samples.

Publication Source (Journal or Book title)

PLoS Genetics

First Page

0627

Last Page

0633

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