ECE2014 Oral Communications Diabetes and Obesity 1 (5 abstracts)
The lower postprandial glucose oxidation in nondiabetic carriers of risk variants of TCF7L2 gene
Edyta Adamska 1 , Adam Kretowski 1 , Joanna Goscik 3 , Magdalena Waszczeniuk 4 , Natalia Wawrusiewicz-Kurylonek 2 , Anna Citko 1 , Michal Ciborowski 1 , Katarzyna Maliszewska 2 & Maria Gorska 2
1Centre for Clinical Research, Medical University of Bialystok, Bialystok, Poland; 2Department of Endocrinology, Diabetology and Internal Medicine, Medical University of Bialystok, Bialystok, Poland; 3Centre for Experimental Medicine, Medical University of Bialystok, Bialystok, Poland; 4Department of Dietetics and Clinical Nutrition, Medical University of Bialystok, Bialystok, Poland.
Introduction: The transcription factor 7-like 2 gene (TCF7L2) has the strongest effect on the risk of type 2 diabetes but the mechanism for this is not fully understood. Some genetic variants are associated with pancreatic B-cell function and some single nucleotide polymorphisms show a significant correlation with obesity. The aim of the study was to analyze whether TCF7L2 variants may influence body weight and body fat content, as well as postprandial glucose metabolism in non-diabetic subjects.
Description of methods/design: We genotyped previously identified TCF7L2 SNPs: rs7901695, rs7903146 and rs4506565 in 944 subjects (329 normal-weight, 337 overweight, 278 obese) who underwent anthropometric measurements, body composition analysis and OGTT. In randomly selected 59 healthy subjects standardized high-carbohydrate meal tests were performed and postprandial carbohydrate oxidation by indirect calorimetry were evaluated. Kruskal–Wallis non-parametric analysis to evaluate difference between the studied parameters was performed.
Results: In spite of the lack of differences in BMI and body fat content between studied TCF7L2 variants, subjects with CC genotype (rs7901695) presented significantly lower carbohydrate oxidation from 60 min after meal intake and significantly lower area under the curve (AUC) for glucose oxidation (P=0.005) in postprandial state in comparison to those with other genotypes. Significantly lower glucose oxidation, as well as lower AUC for glucose oxidation (P=0.04) were observed also in the carriers of TT (rs7903146) vs CC and CT genotypes.
Conclusion: Our study suggests that the TCF7L2 variants are associated with the regulation of postprandial glucose oxidation. If our results are confirmed, TCF7L2 gene-related personalized diet with lower carbohydrate content may be considered for T2DM prevention.
Volume 35
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