Cholesteryl Ester Transfer Protein Gene and Effectiveness of Lipid Lowering of Atorvastatin
Genovefa Kolovou1, *, Constantinos Mihas2, Katherine Anagnostopoulou3, Vana Kolovou3, Vasiliki Giannakopoulou1, Peggy Kostakou1, Marianna Stamatelatou1, Sophie Mavrogeni1, Dimitrios Degiannis3, Dimitri P. Mikhailidis4
Identifiers and Pagination:Year: 2010
First Page: 297
Last Page: 301
Publisher ID: TOCMJ-4-297
Article History:Received Date: 22/10/2010
Revision Received Date: 26/10/2010
Acceptance Date: 28/10/2010
Electronic publication date: 10/12/2010
Collection year: 2010
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
Cholesteryl ester transfer protein (CETP) plays a key role in lipid metabolism. Thus, variations in the CETP gene may be clinically relevant.
Newly started atorvastatin users (n=212) were genotyped for CETP genetic variants (TaqIB and I405V). Homozygotes for B1 allele of TaqIB polymorphism had lower plasma high density lipoprotein cholesterol (HDL-C) compared with B1B2 or B2B2 genotypes (p=0.03, for each). Homozygotes for I allele of I405V polymorphism had lower plasma HDL-C compared with IV or VV genotypes (p=0.001, for each). In the whole population, the B1 carriers increased HDL-C levels by 4% after atorvastatin treatment, compared with B2 carriers, where a 4% decrease occurred (p=0.03). Also homozygotes for B1 allele decreased triglyceride levels to a lesser, though not significant, degree compared to B1B2 or B2B2 genotypes.
CETP TaqIB or I405V polymorphisms seem to modify the lipid lowering response to atorvastatin treatment. This knowledge may help design more effective hypolipidaemic treatment.