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Loci Contributing to Adult Height and Body Mass Index in African American Families Ascertained for Type 2 Diabetes
Author(s) -
Sale M.M.,
Freedman B. I.,
Hicks P. J.,
Williams A. H.,
Langefeld C. D.,
Gallagher C. J.,
Bowden D. W.,
Rich S. S.
Publication year - 2005
Publication title -
annals of human genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.537
H-Index - 77
eISSN - 1469-1809
pISSN - 0003-4800
DOI - 10.1046/j.1529-8817.2005.00176.x
Subject(s) - heritability , quantitative trait locus , body mass index , genetics , linkage (software) , biology , type 2 diabetes , genetic linkage , obesity , trait , demography , diabetes mellitus , endocrinology , gene , sociology , computer science , programming language
Summary Height and body mass index (BMI) have high heritability in most studies. High BMI and reduced height are well‐recognized as important risk factors for a number of cardiovascular diseases. We investigated these phenotypes in African American families originally ascertained for studies of linkage with type 2 diabetes using self‐reported height and weight. We conducted a genome wide scan in 221 families containing 580 individuals and 672 relative pairs of African American descent. Estimates of heritability and support for linkage were assessed by genetic variance component analyses using SOLAR software. The estimated heritabilities for height and BMI were 0.43 and 0.64, respectively. We have identified major loci contributing to variation in height on chromosomes 15 (LOD = 2.61 at 35 cM, p = 0.0004), 3 (LOD = 1.82 at 84 cM, p = 0.0029), 8 (LOD = 1.92 at 135 cM, p = 0.0024) and 17 (LOD = 1.70 at 110 cM, p = 0.0044). A broad region on chromosome 4 supported evidence of linkage to variation in BMI, with the highest LOD = 2.66 at 168 cM (p = 0.0005). Two height loci and two BMI loci appear to confirm the existence of quantitative trait loci previously identified by other studies, providing important replicative data to allow further resolution of linkage regions suitable for positional cloning of these cardiovascular disease risk loci.

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