TCF7L2 gene polymorphisms may influence insulin sensitivity and leptin levels independently from BMI and body fat content

Adam Kretowski; Edyta Adamska; Natalia Wawrusiewicz-Kurylonek; Anna Citko; Joanna Goscik; Katarzyna Maliszewska; Juliusz Wilk; Magdalena Waszczeniuk; Danuta Lipinska; Justyna Pliszka; Michal Ciborowski; Maria Gorska

doi:10.1530/endoabs.32.P360

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Endocrine Abstracts (2013) 32 P360 | DOI: 10.1530/endoabs.32.P360

ECE2013 Poster Presentations Diabetes (151 abstracts)

TCF7L2 gene polymorphisms may influence insulin sensitivity and leptin levels independently from BMI and body fat content

Adam Kretowski ¹ , Edyta Adamska ² , Natalia Wawrusiewicz-Kurylonek ¹ , Anna Citko ¹ , Joanna Goscik ^3, , Katarzyna Maliszewska ¹ , Juliusz Wilk ¹ , Magdalena Waszczeniuk ⁵ , Danuta Lipinska ¹ , Justyna Pliszka ¹ , Michal Ciborowski ² & Maria Gorska ¹

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¹Department of Endocrinology, Diabetology and Internal Medicine, Medical University of Bialystok, Bialystok, Poland; ²Centre for Clinical Research, Medical University of Bialystok, Bialystok, Poland; ³Centre for Experimental Medicine, Medical University of Bialystok, Bialystok, Poland; ⁴Department of Software Engineering, Bialystok Technical University, Bialystok, Poland; ⁵Department of Dietetics and Clinical Nutrition, Medical University of Bialystok, Bialystok, Poland.

Introduction: The genome-wide association studies have recently expanded the number of genetic susceptibility loci for type 2 diabetes and obesity. Transcription factor 7-like 2 (TCF7L2) gene seems to be one of the most predictive identifiable factors promoting T2DM development. It has been suggested that TCF7L2 influences pancreatic β-cell function butthe effect of genetic variants of TCF7L2 on metabolic syndrome development is not well characterized among subjects with obesity. The aim of our study was to analyze whether genetic variants of the TCF7L2 gene influence fasting leptin levels and insulin sensitivity in nondiabetic obese/overweight subjects.

Methods: We genotyped previously identified TCF7L2 SNPs: rs7901695 and rs7903146 in 944 subjects (463 women and 481 men), who underwent anthropometry (BMI) and body composition analysis: percent of body fat, visceral, and subcutaneous abdominal adipose tissue by multi-frequency bio-impedance method.

Results: In the present study we found that subjects with TT rs7903146 TCF7L2 homozygotes presented significantly higher fasting levels of leptin (29.7 vs 19.7 ng/ml, P=0.035) and higher HOMA-IR (3.9 vs 2.6, P=0.009), despite the lack of differences in BMI, body fat content, and body fat distribution. Moreover in the logistic regression analysis presence of CC genotype of rs7901695 TCF7L2 predicted higher IR independently from BMI, gender and caloric intake (P<0.01).

Conclusions: We believe that our study may help to understand the pathways that TCF7L2 gene influence the risk of T2DM and provide personalized treatments and prevention strategies to fight against type 2 diabetes.