TCF7L2 polymorphisms and inflammatory markers before and after treatment with fenofibrate
1 Department of Epidemiology, School of Public Health and Clinical Nutrition Research Center, University of Alabama, Birmingham, AL 35294, USA
2 Division of Preventive Medicine, Department of Medicine, University of Alabama, Birmingham, AL 35294, USA
3 Nutrition and Genomics Laboratory, JM-USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111, USA
4 Department of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok 10400 Thailand
5 Department of Laboratory Medicine and Pathology, University of Minnesota, 420 Delaware Street SE, Minneapolis, MN 55455, USA
6 Department of Internal Medicine, University of Utah, 410 Chipeta Way, Salt Lake City, UT 84108, USA
7 Division of Statistical Genomics, Department of Genetics, Washington University, School of Medicine, 4444 Forest Park Boulevard - Box 8506, St Louis, MO 63108, USA
8 Department of Biostatistics, Section on Statistical Genetics, University of Alabama, Birmingham, AL, 35294, USA
Diabetology & Metabolic Syndrome 2009, 1:16 doi:10.1186/1758-5996-1-16Published: 12 October 2009
Inflammation is implicated in causing diabetes. We tested whether transcription factor 7 like-2 (TCF7L2) gene polymorphisms (rs12255372 and rs7903146), consistently associated with type 2 diabetes, are associated with plasma concentrations of inflammatory markers before and after three weeks of daily treatment with fenofibrate.
Men and women in the Genetics of Lipid-Lowering Drugs and Diet Network study (n = 1025, age 49 ± 16 y) were included. All participants suspended use of lipid-lowering drugs for three weeks and were then given 160 mg/day of fenofibrate for three weeks. Inflammatory markers and lipids were measured before and after fenofibrate. ANOVA was used to test for differences across TCF7L2 genotypes.
Under the additive or dominant model, there were no significant differences (P > 0.05) in the concentrations of inflammatory markers (hsCRP, IL-2, IL-6, TNF-α and MCP-1) across TCF7L2 genotypes in the period before or after treatment. For both rs12255372 and rs7903146, homozygote T-allele carriers had significantly higher (P < 0.05) post-fenofibrate concentrations of MCP-1 in the recessive model. No other significant associations were detected.
Overall these data show no association between TCF7L2 polymorphisms and the inflammatory markers suggesting that the effects of TCF7L2 on diabetes may not be via inflammation.