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Volume 41, Issue 1, Pages 19-25.e1 (January 2010)


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Associations for Lipoprotein Lipase and Peroxisome Proliferator-activated Receptor-γ Gene and Coronary Artery Disease in an Indian Population

Manickaraj AshokKumara, Navaneethan Gnana Veera Subhashinia, Sekar Kanthimathia, Ramineni SaiBabua, Arabandi Rameshc, Kotturathu Mammen Cheriana, Cyril EmmanuelbCorresponding Author Informationemail address

Received 29 July 2009; accepted 22 October 2009.

Background and Aims

Peroxisome proliferator activated receptor-γ (PPARγ) and lipoprotein lipase (LPL) genes are important in pathways of triglyceride metabolism, insulin resistance and adipogenesis. We hypothesized that polymorphisms of PPARγ Pro12Ala, LPL HindIII and LPL Ser447X influence severity of coronary artery disease (CAD) in an Indian population.

Methods

PPARγ Pro12Ala, LPL HindIII and LPL Ser447X polymorphisms were genotyped in 414 patients with CAD and matched with 424 controls. The study subjects were inducted after standard diagnostic procedures and analyzed statistically for the association of polymorphisms with clinical characteristics.

Results

We found that PPARγ alleles were not associated with CAD among Indians although proline carriers had significantly higher levels of HDL-cholesterol (p = 0.03) among CAD patients. The LPL HindIII also had no significant correlations for CAD or for any clinical characteristics. The Ser447X polymorphism (p = 0.015) influenced lower triglyceride levels among CAD patients with significant associations (OR = 0.66, 95% CI 0.483–0.915, p = 0.012). This protective effect of the 447X allele was more pronounced among the CAD patients without the risk factor of diabetes (OR = 0.60, 95% CI 0.403–0.907, p = 0.014) along with less progression of a severe atherosclerotic disease.

Conclusions

PPARγ and LPL have intractable roles in pathways that lead to CAD, but their gene polymorphisms associate differently. Our results imply a significant correlation of Ser447X polymorphism and its protective effect on Indians against severity of CAD modified by the risk of diabetes, than LPL HindIII and PPARγ Pro12Ala.

(ARCMED-D-09-00365)

a International Centre for Cardiothoracic and Vascular Diseases, Frontier Lifeline, Chennai, India

b Global Hospitals and Health City, Chennai, India

c Department of Genetics, Dr. A. L. Mudaliar Postgraduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, India

Corresponding Author InformationAddress reprint requests to: Dr. Cyril Emmanuel, Ph.D., Director, Research and Academics, Global Hospitals and Health City, Perumbakkam, Chennai-600100, India; Phone: +914422777000, +919444206238; Fax: +914422777100

PII: S0188-4409(10)00006-8

doi:10.1016/j.arcmed.2010.01.005


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