TCF7L2 and therapeutic response to sulfonylureas in patients with type 2 diabetes

BMC Medical Genetics

Research Article

Michael Stumvoll¹  Andreas Holstein²  Michael Hahn²  Peter Kovacs³  Antje Körner⁴ 

[1] Department of Medicine, University of Leipzig, Leipzig, Germany;First Department of Medicine, Clinic Lippe-Detmold, Detmold, Germany;Interdisciplinary Centre for Clinical Research, University of Leipzig, Leipzig, Germany;University Hospital for Children and Adolescents, University of Leipzig, Leipzig, Germany;

关键词: Metformin;    Glibenclamide;    Diabetes Risk;    Diabetes Duration;    Glimepiride;   

DOI  :  10.1186/1471-2350-12-30

 received in 2010-10-08, accepted in 2011-02-24,  发布年份 2011

来源: Springer

【 摘 要 】

BackgroundVariants in the TCF7L2 have been shown to be associated with an increased risk for type 2 diabetes (T2D). Since the association with diabetes could be explained by effects on insulin secretion, we investigated whether patients with diabetes risk alleles at rs7903146 might have an altered hypoglycaemic response to sulfonylureas (SUs).MethodsWe recruited 189 patients with T2D being treated with SUs and determined the rs7903146 diabetes risk genotype. We used a logistic regression with secondary SU failure defined as an A1C ≥7.0% after 6 months of SU treatment.ResultsIn univariate regression analyses, TCF7L2 genotype was the only predictor of SU treatment failure. The rs7903146 T allele was significantly more frequent in the group of patients who failed to respond to SU (36%) than in the control group (26%) [P = 0.046; odds ratio (OR): 1.57 (1.01-2.45) in an additive mode of inheritance].ConclusionsOur data suggest that patients with diabetes risk alleles in TCF7L2 have an altered hypoglycaemic response to SUs resulting in earlier secondary failure.

【 授权许可】

Unknown   
© Holstein et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.