An RBP4 promoter polymorphism increases risk of type 2 diabetes
| Autor: | J. C. M. Witteman, M. van Hoek, Albert Hofman, M. C. Zillikens, Eric J.G. Sijbrands, Abbas Dehghan |
|---|---|
| Přispěvatelé: | Internal Medicine, Epidemiology |
| Rok vydání: | 2008 |
| Předmět: |
Male
Vitamin medicine.medical_specialty Genotype Endocrinology Diabetes and Metabolism Retinol transport Population Blood Pressure Type 2 diabetes Biology Article Body Mass Index Rotterdam Study chemistry.chemical_compound Insulin resistance SDG 3 - Good Health and Well-being Risk Factors Internal medicine Internal Medicine medicine Body Size Humans Hepatocyte Nuclear Factor 1-alpha Polymorphism Vitamin A Promoter Regions Genetic education Aged Netherlands education.field_of_study Polymorphism Genetic Retinol RBP4 medicine.disease Endocrinology Diabetes Mellitus Type 2 Liver chemistry Hypertension Female Insulin Resistance Retinol-Binding Proteins Plasma |
| Zdroj: | Diabetologia, 51(8), 1423-1428. Springer-Verlag Diabetologia |
| ISSN: | 0012-186X |
| DOI: | 10.1007/s00125-008-1042-8 |
| Popis: | Aims/hypothesis Retinol-binding protein 4 (RBP4), originally known for retinol transport, was recently identified as an adipokine affecting insulin resistance. The RBP4 −803GA promoter polymorphism influences binding of hepatic nuclear factor 1α and is associated with type 2 diabetes in case–control studies. We hypothesised that the RBP4 −803GA polymorphism increases type 2 diabetes risk at a population-based level. In addition, information on retinol intake and plasma vitamin A levels enabled us to explore the possible underlying mechanism. Methods In the Rotterdam Study, a prospective, population-based, follow-up study, the −803GA polymorphism was genotyped. In Cox proportional hazards models, associations of the −803GA polymorphism and retinol intake with type 2 diabetes risk were examined. Moreover, the interaction of the polymorphism with retinol intake on type 2 diabetes risk was assessed. In a subgroup of participants the association of the polymorphism and vitamin A plasma levels was investigated. Results Homozygous carriers of the −803A allele had increased risk of type 2 diabetes (HR 1.83; 95% CI 1.26–2.66). Retinol intake was not associated with type 2 diabetes risk and showed no interaction with the RBP4 −803GA polymorphism. Furthermore, there was no significant association of the polymorphism with plasma vitamin A levels. Conclusions/interpretation Our results provide evidence that homozygosity for the RBP4 −803A allele is associated with increased risk of type 2 diabetes in the Rotterdam population. This relationship was not clearly explained by retinol intake and vitamin A plasma levels. Therefore, we cannot differentiate between a retinol-dependent or -independent mechanism of this RBP4 variant. |
| Databáze: | OpenAIRE |
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