Polymorphisms in the SLC2A2 (GLUT2) Gene Are Associated With the Conversion From Impaired Glucose Tolerance to Type 2 Diabetes

Author:

Laukkanen Olli1,Lindström Jaana2,Eriksson Johan2,Valle Timo T.2,Hämäläinen Helena3,Ilanne-Parikka Pirjo4,Keinänen-Kiukaanniemi Sirkka56,Tuomilehto Jaakko27,Uusitupa Matti8,Laakso Markku1

Affiliation:

1. Department of Medicine, University of Kuopio, Kuopio, Finland

2. Department of Epidemiology and Health Promotion, Diabetes and Genetic Epidemiology Unit, National Public Health Institute, Helsinki, Finland

3. Research Department, Social Insurance Institution, Turku, Finland

4. Finnish Diabetes Association and Department of Internal Medicine, Tampere University Hospital, Tampere, Finland

5. Department of Public Health Science and General Practice, University of Oulu, Oulu University Hospital, Oulu, Finland

6. Department of Sport Medicine, Oulu Deaconess Institute, Oulu, Finland

7. Department of Public Health, University of Helsinki, Helsinki, Finland

8. Department of Clinical Nutrition, University of Kuopio, Kuopio, Finland

Abstract

Impaired insulin secretion is a fundamental defect in type 2 diabetes. The aim of this study was to investigate whether single nucleotide polymorphisms (SNPs) in the genes regulating insulin secretion (SLC2A2 [encoding GLUT2], GCK, TCF1 [encoding HNF-1α], HNF4A, GIP, and GLP1R) are associated with the conversion from impaired glucose tolerance (IGT) to type 2 diabetes in participants of the Finnish Diabetes Prevention Study. With the exception of SLC2A2, other genes were not associated with the risk of type 2 diabetes. All four SNPs of SLC2A2 predicted the conversion to diabetes, and rs5393 (AA genotype) increased the risk of type 2 diabetes in the entire study population by threefold (odds ratio 3.04, 95% CI 1.34–6.88, P = 0.008). The risk for type 2 diabetes in the AA genotype carriers was increased in the control group (5.56 [1.78–17.39], P = 0.003) but not in the intervention group. We conclude that the SNPs of SLC2A2 predict the conversion to diabetes in obese subjects with IGT.

Publisher

American Diabetes Association

Subject

Endocrinology, Diabetes and Metabolism,Internal Medicine

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