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Diabetes 53:870-873, 2004
© 2004 by the American Diabetes Association, Inc.

Brief Genetics Report

Analysis of the Type 2 Diabetes-Associated Single Nucleotide Polymorphisms in the Genes IRS1, KCNJ11, and PPARG2 in Type 1 Diabetes

Christina Eftychi1, Joanna M.M. Howson1, Bryan J. Barratt1, Adrian Vella1, Felicity Payne1, Deborah J. Smyth1, Rebecca C.J. Twells1, Neil M. Walker1, Helen E. Rance1, Eva Tuomilehto-Wolf2, Jaakko Tuomilehto2,3, Dag E. Undlien4, Kjersti S. Rønningen5, Cristian Guja6, Constantin Ionescu-Tîirgoviste6, David A. Savage7, and John A. Todd1

1 Juvenile Diabetes Research Foundation/Wellcome Trust Diabetes and Inflammation Laboratory, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, U.K
2 Diabetes and Genetic Epidemiology Unit, National Public Health Institute, University of Helsinki, Helsinki, Finland
3 Department of Public Health, University of Helsinki, Helsinki, Finland
4 Institute of Medical Genetics, Ulleval University Hospital, University of Oslo, Oslo, Norway
5 Laboratory of Molecular Epidemiology, Division of Epidemiology, Norwegian Institute of Public Health, Oslo, Norway
6 Clinic of Diabetes, Institute of Diabetes, Nutrition and Metabolic Diseases, Bucharest, Romania
7 Department of Medical Genetics, Queen’s University Belfast, Belfast City Hospital, Belfast, Northern Ireland

It has been proposed that type 1 and 2 diabetes might share common pathophysiological pathways and, to some extent, genetic background. However, to date there has been no convincing data to establish a molecular genetic link between them. We have genotyped three single nucleotide polymorphisms associated with type 2 diabetes in a large type 1 diabetic family collection of European descent: Gly972Arg in the insulin receptor substrate 1 (IRS1) gene, Glu23Lys in the potassium inwardly-rectifying channel gene (KCNJ11), and Pro12Ala in the peroxisome proliferative-activated receptor {gamma}2 gene (PPARG2). We were unable to confirm a recently published association of the IRS1 Gly972Arg variant with type 1 diabetes. Moreover, KCNJ11 Glu23Lys showed no association with type 1 diabetes (P > 0.05). However, the PPARG2 Pro12Ala variant showed evidence of association (RR 1.15, 95% CI 1.04–1.28, P = 0.008). Additional studies need to be conducted to confirm this result.

Address correspondence and reprint requests to John A. Todd, JDRF/WT Diabetes and Inflammation Laboratory, Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Hills Rd., Cambridge CB2 2XY, U.K. E-mail: john.todd{at}cimr.cam.ac.uk


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