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Diabetes 51:2313-2316, 2002
© 2002 by the American Diabetes Association, Inc.

Brief Genetics Report

A Putative Functional Polymorphism in the IGF-I Gene

Association Studies With Type 2 Diabetes, Adult Height, Glucose Tolerance, and Fetal Growth in U.K. Populations

Timothy M. Frayling1, Andrew T. Hattersley1, Anne McCarthy2, Jeff Holly3, Simon M.S. Mitchell1, Anna L. Gloyn1, Katharine Owen1, David Davies4, George Davey Smith2, and Yoav Ben-Shlomo2

1 Department of Diabetes and Vascular Medicine, University of Exeter, Exeter, U.K.
2 Department of Social Medicine, University of Bristol, Bristol, U.K.
3 Bristol Royal Infirmary, Bristol, U.K.
4 University of Wales College of Medicine, Cardiff, U.K.

IGF-I has a critical role in growth and metabolism. A microsatellite polymorphism 1 kb upstream to the IGF-I gene has recently been associated with several adult phenotypes. In a large Dutch cohort, the absence of the commonest allele (Z) was associated with reduced serum IGF-I levels, reduced height, and an increased risk of type 2 diabetes and myocardial infarction. This result has not been replicated, and the role of this polymorphism in these traits in U.K. subjects is not known. We sought further evidence for the involvement of this variant in type 2 diabetes using a case-control study and IGF-I and diabetes-related traits in a population cohort of 640 U.K. individuals aged 25 years. Absence of the common allele was not associated with type 2 diabetes (odds ratio 0.70, 95% CI 0.47–1.04 for X/X versus Z/Z genotype, {chi}2 test for trend across genotypes, P = 0.018). In the population cohort, the common allele (Z) was associated with decreased IGF-I levels (P = 0.01), contrary to the Dutch study, but not with adult height (P = 0.23), glucose tolerance (P = 0.84), oral glucose tolerance test-derived values of ß-cell function (P = 0.90), or insulin resistance (P = 0.66). There was no association with measures of fetal growth, including birth weight (P = 0.17). Our results do not support the previous associations and suggest that the promoter microsatellite is unlikely to be functionally important.


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Copyright © 2002 by the American Diabetes Association.