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Departments of Medicine (O.L., J.P., M.L.) and Clinical Nutrition (M.U.), University of Kuopio, Kuopio 70210, Finland; Department of Epidemiology and Health Promotion, Diabetes and Genetic Epidemiology Unit (J.L., J.E., T.T.V., J.T.), National Public Health Institute, Helsinki 00300, Finland; Research Department (H.H.), Social Insurance Institution, Turku 20720, Finland; Finnish Diabetes Association and Department of Internal Medicine (P.I.-P.), Tampere University Hospital, Tampere 33014, Finland; Department of Public Health Science and General Practice (S.K.-K.), University of Oulu, Oulu University Hospital and Department of Sport Medicine, Oulu Deaconess Institute, Oulu 90220, Finland; and Department of Public Health (J.T.), University of Helsinki, Helsinki 00300, Finland
Address all correspondence and requests for reprints to: Markku Laakso, Professor and Chair, Department of Medicine, University of Kuopio, 70210 Kuopio, Finland. E-mail: markku.laakso{at}kuh.fi.
Type 2 diabetes is caused by defective insulin secretion and impaired insulin action. We investigated whether common polymorphisms in the SUR1 and Kir6.2 genes are associated with increased risk of type 2 diabetes in 490 subjects with impaired glucose tolerance participating in the Finnish Diabetes Prevention Study. The 1273AGA allele of the SUR1 gene was associated with a 2-fold risk of type 2 diabetes [odds ratio (OR), 2.00; 95% confidence interval (CI), 1.19–3.36; P = 0.009]. This silent polymorphism was in linkage disequilibrium with three promoter polymorphisms (G-2886A, G-1561A, and A-1273G), and they formed a high-risk haplotype having a 2-fold risk of type 2 diabetes (OR, 1.89; 95% CI, 1.09–3.27; P = 0.023). Subjects with both the high-risk haplotype of the SUR1 gene and the 23K allele of the Kir6.2 gene had a 6-fold risk for the conversion to diabetes compared with those without any of these risk genotypes (OR, 5.68; 95% CI, 1.75–18.32; P = 0.004). We conclude that the polymorphisms of the SUR1 gene predicted the conversion from impaired glucose tolerance to type 2 diabetes and that the effect of these polymorphisms on diabetes risk was additive with the E23K polymorphism of the Kir6.2 gene.
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