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BMC Proc. 2009 Dec 15;3:S101. doi: 10.1186/1753-6561-3-s7-s101.

Identifying association under a previous linkage peak on chromosome 16 for body mass index using cross-sectional and longitudinal data of the Framingham Heart Study.

BMC proceedings

Xiaohui Li, Ling Mei, Kai Yang, Jerome I Rotter, Xiuqing Guo

Affiliations

  1. Medical Genetics Institute, Cedars-Sinai Medical Center, 8635 West Third Street, Suite 1150, Los Angeles, California 90048 USA. [email protected].

PMID: 20017965 PMCID: PMC2795872 DOI: 10.1186/1753-6561-3-s7-s101

Abstract

We performed association analysis under a previous linkage peak on chromosome 16 with genome-wide single-nucleotide polymorphism (SNP) data to identify genetic variants underlying body mass index (BMI). Data from all subjects with baseline measures and a subgroup who had complete data at four selected time points from the Framingham Heart Study were analyzed. The cross-sectional measures include BMI at baseline for all subjects, as well as BMI at selected time points for the subgroup. The longitudinal measure is the within-subject mean of BMI for the subgroup at the four time points.Association analysis was first performed using PLINK after dividing large pedigrees into nuclear families. We then followed up the identified regions by variance-components methods as implemented in SOLAR using the extended pedigrees.The strongest evidence for associations were observed at 52.3 Mbp (PLINK p = 0.00002, QTLD p = 0.005), on the FTO gene, and at 48.1 Mbp (PLINK p = 0.002, QTLD p = 0.0006) on chromosome 16, which are directly under the previous identified linkage peak. This association was consistently observed for all samples at baseline, and for the subgroup at time point 2, 3, 4 and MEAN, both by PLINK and SOLAR. In addition, another SNP/region at 46.7 Mbp on same chromosome was found to be associated with several BMI measures in the subgroup. Fine-mapping with more markers provided further evidence for SNP association with BMI in the same region (at 52.4 Mbp, QTLD p = 0.0003).These results suggest the existence of genes/DNA variations in these regions that contribute to BMI variation.

References

  1. PLoS One. 2008 Aug 13;3(8):e2958 - PubMed
  2. Am J Hum Genet. 1998 May;62(5):1198-211 - PubMed
  3. Genet Epidemiol. 2002 Mar;22(3):221-32 - PubMed
  4. Am J Hum Genet. 1998 Nov;63(5):1563-4 - PubMed
  5. Hum Biol. 2005 Oct;77(5):541-59 - PubMed
  6. Am J Hum Genet. 2007 Sep;81(3):559-75 - PubMed
  7. BMC Genet. 2003 Dec 31;4 Suppl 1:S35 - PubMed

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