Display Settings:

Format

Send to:

Choose Destination
We are sorry, but NCBI web applications do not support your browser and may not function properly. More information
Hum Mol Genet. 2009 Sep 15;18(18):3502-7. doi: 10.1093/hmg/ddp292. Epub 2009 Jun 24.

Common body mass index-associated variants confer risk of extreme obesity.

Author information

  • 1Center for Human Genetic Research, Massachusetts General Hospital, Boston, MA 02114, USA.

Erratum in

  • Hum Mol Genet. 2010 Sep 15;19(18):3690-1.

Abstract

To investigate the genetic architecture of severe obesity, we performed a genome-wide association study of 775 cases and 3197 unascertained controls at approximately 550,000 markers across the autosomal genome. We found convincing association to the previously described locus including the FTO gene. We also found evidence of association at a further six of 12 other loci previously reported to influence body mass index (BMI) in the general population and one of three associations to severe childhood and adult obesity and that cases have a higher proportion of risk-conferring alleles than controls. We found no evidence of homozygosity at any locus due to identity-by-descent associating with phenotype which would be indicative of rare, penetrant alleles, nor was there excess genome-wide homozygosity in cases relative to controls. Our results suggest that variants influencing BMI also contribute to severe obesity, a condition at the extreme of the phenotypic spectrum rather than a distinct condition.

PMID:
19553259
[PubMed - indexed for MEDLINE]
PMCID:
PMC2729668
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Write to the Help Desk