An autosomal genomic scan for loci linked to type II diabetes mellitus and body-mass index in Pima Indians

被引:392
作者
Hanson, RL
Ehm, MG
Pettitt, DJ
Prochazka, M
Thompson, DB
Timberlake, D
Foroud, T
Kobes, S
Baler, L
Burns, DK
Almasy, L
Blangero, J
Garvey, WT
Bennett, PH
Knowler, WC
机构
[1] NIDDKD, Diabet & Arthritis Epidemiol Sect, NIH, Phoenix Epidemiol & Clin Res Branch, Phoenix, AZ 85014 USA
[2] Glaxo Wellcome Inc, Res Triangle Pk, NC 27709 USA
[3] Sequana Therapeut Inc, Dept Stat Genet, La Jolla, CA USA
[4] Indiana Univ, Sch Med, Dept Med Genet, Indianapolis, IN USA
[5] SW Fdn Biomed Res, Dept Genet, San Antonio, TX USA
[6] Med Univ S Carolina, Dept Med, Charleston, SC 29425 USA
[7] Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA
关键词
D O I
10.1086/302061
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Genetic factors influence the development of type II diabetes mellitus, but genetic loci for the most common forms of diabetes have not been identified. A genomic scan was conducted to identify loci linked to diabetes and body-mass index (BMI) in Pima Indians, a Native American population with a high prevalence of type II diabetes. Among 264 nuclear families containing 966 siblings, 516 autosomal markers with a median distance between adjacent markers of 6.4 cM were genotyped. Variance-components methods were used to test for linkage with an age-adjusted diabetes score and with BMI. In multipoint analyses, the strongest evidence for linkage with age-adjusted diabetes (LOD = 1.7) was on chromosome 11q, in the region that was also linked most strongly with BMI (LOD = 3.6). Bivariate linkage analyses strongly rejected both the null hypothesis of no linkage with either trait and the null hypothesis of no contribution of the locus to the covariation among the two traits. Sib-pair analyses suggest additional potential diabetes-susceptibility loci on chromosomes Iq and 7q.
引用
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页码:1130 / 1138
页数:9
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