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Human Molecular Genetics Advance Access originally published online on February 27, 2008
Human Molecular Genetics 2008 17(11):1695-1704; doi:10.1093/hmg/ddn060
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Variants in the CD36 gene associate with the metabolic syndrome and high-density lipoprotein cholesterol

Latisha Love-Gregory1,*, Richard Sherva3, Lingwei Sun3, Jon Wasson2, Timothy Schappe1, Alessandro Doria6, D.C. Rao4, Steven C. Hunt5, Samuel Klein1, Rosalind J. Neuman3,4, M. Alan Permutt2 and Nada A. Abumrad1

1 Department of Medicine, Center for Human Nutrition 2 Division of Diabetes and Lipid Metabolism 3 Department of Psychiatry 4 Department of Human Genetics, Division of Biostatistics, Washington University School of Medicine, St Louis, MO 63110, USA 5 Cardiovascular Genetics Division, University of Utah School of Medicine, Salt Lake City, UT 84108, USA 6 Joslin Diabetes Center, Genetics and Epidemiology, Boston, MA 02215, USA

* To whom correspondence should be addressed at: Department of Medicine, Center for Human Nutrition, Washington University School of Medicine, Campus Box 8031, St Louis, MO 63110, USA. Tel: ++1 3143628672; Fax: +1 3143628230; Email: lgregory{at}im.wustl.edu

Received December 28, 2007; Accepted February 25, 2008

A region along chromosome 7q was recently linked to components of the metabolic syndrome (MetS) in several genome-wide linkage studies. Within this region, the CD36 gene, which encodes a membrane receptor for long-chain fatty acids and lipoproteins, is a potentially important candidate. CD36 has been documented to play an important role in fatty acid metabolism in vivo and subsequently may be involved in the etiology of the MetS. The protein also impacts survival to malaria and the influence of natural selection has resulted in high CD36 genetic variability in populations of African descent. We evaluated 36 tag SNPs across CD36 in the HyperGen population sample of 2020 African-Americans for impact on the MetS and its quantitative traits. Five SNPs associated with increased odds for the MetS [P = 0.0027–0.03, odds ratio (OR) = 1.3–1.4]. Coding SNP, rs3211938, previously shown to influence malaria susceptibility, is documented to result in CD36 deficiency in a homozygous subject. This SNP conferred protection against the MetS (P = 0.0012, OR = 0.61, 95%CI: 0.46–0.82), increased high-density lipoprotein cholesterol, HDL-C (P = 0.00018) and decreased triglycerides (P = 0.0059). Fifteen additional SNPs associated with HDL-C (P = 0.0028–0.044). We conclude that CD36 variants may impact MetS pathophysiology and HDL metabolism, both predictors of the risk of heart disease and type 2 diabetes.


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