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PPAR Research
Volume 2009 (2009), Article ID 543746, 11 pages
Research Article

Peroxisome Proliferator-Activated Receptor Gamma Polymorphisms and Coronary Heart Disease

1Service d'Epidémiologie et de Santé Publique, Institut Pasteur de Lille, Lille; INSERM, U744, Lille; Université Nord de France, Lille; UDSL, 59019 Lille, France
2Kaiser Permanente Division of Research, Oakland, CA 94612, USA
3INSERM, U558, Toulouse, Department of Epidemiology, Paul Sabatier-Toulouse Purpan University, 31073 Toulouse, France
4The Department of Epidemiology and Public Health, Queen’s University Belfast, Belfast BT71NN, Northern Ireland, UK
5Department of Epidemiology and Public Health, EA 3430, University of Strasbourg, Faculty of Medicine, 67085 Strasbourg, France
6Stanford Prevention Research Center, Stanford University School of Medicine, Stanford, CA 94305-5705, USA
7INSERM, U780, 94807 Villejuif, Hôpital Kremlin-Bicêtre, France
8Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA 94305, USA
9Stanford Human Genome Center, Stanford, CA 94304, USA
10Falk Cardiovascular Research Center, Stanford Falk Cardiovascular Research Building, Stanford, CA 94305-5406, USA

Received 11 June 2009; Accepted 26 August 2009

Academic Editor: Mostafa Badr

Copyright © 2009 Jean Dallongeville et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Single nucleotide polymorphisms (SNPs) in the peroxisome proliferator-activated receptor (PPARG) gene have been associated with cardiovascular risk factors, particularly obesity and diabetes. We assessed the relationship between 4 PPARG SNPs (C-681G, C-689T, Pro12Ala, and C1431T) and coronary heart disease (CHD) in the PRIME (249 cases/494 controls, only men) and ADVANCE (1,076 cases/805 controls, men or women) studies. In PRIME, homozygote individuals for the minor allele of the PPARG C-689T, Pro12Ala, and C1431T SNPs tended to have a higher risk of CHD than homozygote individuals for the frequent allele (adjusted OR [95% CI] = 3.43 [0.96–12.27], , 3.41 [0.95–12.22], and 5.10 [0.99–26.37], , resp.). No such association could be detected in ADVANCE. Haplotype distributions were similar in cases and control in both studies. A meta-analysis on the Pro12Ala SNP, based on our data and 11 other published association studies (6,898 CHD cases/11,287 controls), revealed that there was no evidence for a significant association under the dominant model ( [0.92–1.07], ). However, there was a borderline association under the recessive model ( [0.99–1.67], ) that became significant when considering men only ( [1.20–2.48], ). In conclusion, the PPARG Ala12Ala genotype might be associated with a higher CHD risk in men but further confirmation studies are needed.