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Kabagambe EK, Glasser SP, Ordovas JM, et al. TCF7L2 polymorphisms and inflammatory markers before and after treatment with fenofibrate. Diabetol Metab Syndr. 2009;1(1):16doi: 10.1186/1758-5996-1-16.
Kabagambe, E. K., Glasser, S. P., Ordovas, J. M., Warodomwichit, D., Tsai, M. Y., Hopkins, P. N., Borecki, I. B., Wojczynski, M., & Arnett, D. K. (2009). TCF7L2 polymorphisms and inflammatory markers before and after treatment with fenofibrate. Diabetology & metabolic syndrome, 1(1), 16. https://doi.org/10.1186/1758-5996-1-16
Kabagambe, Edmond K, et al. "TCF7L2 polymorphisms and inflammatory markers before and after treatment with fenofibrate." Diabetology & metabolic syndrome vol. 1,1 (2009): 16. doi: https://doi.org/10.1186/1758-5996-1-16
Kabagambe EK, Glasser SP, Ordovas JM, Warodomwichit D, Tsai MY, Hopkins PN, Borecki IB, Wojczynski M, Arnett DK. TCF7L2 polymorphisms and inflammatory markers before and after treatment with fenofibrate. Diabetol Metab Syndr. 2009 Oct 12;1(1):16. doi: 10.1186/1758-5996-1-16. PMID: 19825152; PMCID: PMC2766367.
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Diabetol Metab Syndr. 2009 Oct 12;1(1):16. doi: 10.1186/1758-5996-1-16.

TCF7L2 polymorphisms and inflammatory markers before and after treatment with fenofibrate.

Diabetology & metabolic syndrome

Edmond K Kabagambe, Stephen P Glasser, Jose M Ordovas, Daruneewan Warodomwichit, Michael Y Tsai, Paul N Hopkins, Ingrid B Borecki, Mary Wojczynski, Donna K Arnett

Affiliations

  1. Department of Epidemiology, School of Public Health and Clinical Nutrition Research Center, University of Alabama, Birmingham, AL 35294, USA. [email protected].

PMID: 19825152 PMCID: PMC2766367 DOI: 10.1186/1758-5996-1-16

Abstract

BACKGROUND: 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.

METHODS: 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.

RESULTS: 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-alpha 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.

CONCLUSION: 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.

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