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Papers In Press, published online ahead of print March 16, 2003
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Cardiovascular and Metabolic Diseases, Pfizer Global Research and Development, Groton, CT 06340
Corresponding Author: john_f_thompson{at}groton.pfizer.com
Since the identification of CETP, its role in the modulation of HDL levels and cardiovascular disease has been debated. With the early detection of genetic variants followed by the finding of families deficient in CETP, genetic studies have played a large role in the attempts to understand the association of CETP with lipids and disease. However, results of these studies have often led to disparate conclusions. With the availability of a greater variety of genetic polymorphisms and larger studies in which disease has been examined, it is now possible to compare the breadth of CETP genetic studies and draw better conclusions. The most broadly studied polymorphism is TaqIB for which over 10,000 individuals have been genotyped and HDL levels determined. When these studies are subjected to a meta-analysis, the B2B2 homozygotes are found to have higher HDL levels than B1B1 homozygotes (0.12 mmol/l, 95% CI = 0.11-0.13, p<0.0001). A similar analysis of the I405V polymorphism yields 0.05 mmol/l higher HDL levels in 405VV homozygotes than in 405II homozygotes (95% CI = 0.03-0.07, p<0.0001). The implications of these studies for cardiovascular disease will be addressed.
Revised on March 6, 2003
Accepted on March 10, 2003
Natural genetic variation as a tool in understanding the role of CETP in lipid levels and disease
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