This Article Full Text Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Minnich, A. Articles by Davignon, J. Search for Related Content PubMed PubMed Citation Articles by Minnich, A. Articles by Davignon, J.

(Arteriosclerosis, Thrombosis, and Vascular Biology. 1995;15:1740-1745.)
© 1995 American Heart Association, Inc.

Articles

GA Substitution at Position -75 of the Apolipoprotein A-I Gene Promoter

Evidence Against a Direct Effect on HDL Cholesterol Levels

Anne Minnich; Ghislaine DeLangavant; Jacques Lavigne; Ghislaine Roederer; Suzanne Lussier-Cacan; Jean Davignon

From the Clinical Research Institute of Montreal, Montreal, Canada.

Correspondence to Dr Anne Minnich, Clinical Research Institute of Montreal, 110 Pine Avenue, West, Montreal, PQ, Canada H2W 1R7. E-mail minnica@ircm.umontreal.ca.

Abstract The present study sought to resolve the contradictory evidence as to whether the GA substitution at position -75 of the apoA-I gene promoter raises HDL cholesterol (HDL-C) levels by examining the effect of this polymorphism in French Canadians, a relatively genetically homogeneous population. Among 308 women, carriers of the A allele displayed 12% and 10% higher mean plasma HDL-C and apoA-I concentrations, respectively, than did noncarriers. Among 345 men, no effect of the A allele was noted. The frequency distribution of HDL-C levels in women carrying the A but not the G allele appeared bimodal, with one peak corresponding to the mean of the noncarriers and a second to higher HDL-C. Thus it appears that only a subset of A alleles confers high HDL-C levels. This hypothesis was supported by data from four kindreds within which some but not all A alleles segregated with hyperalphalipoproteinemia. The data suggest that the A substitution in the apoA-I gene promoter does not directly confer high HDL-C levels but may be in linkage disequilibrium with other sequence polymorphism(s) at this locus in a subset of alleles that raise HDL-C levels.

Key Words: hyperalphalipoproteinemia • genetic polymorphism • HDL cholesterol • apoA-I gene

This article has been cited by other articles:

				J. M Ordovas Genetic interactions with diet influence the risk of cardiovascular disease Am. J. Clinical Nutrition, February 1, 2006; 83(2): 443S - 446S. [Abstract] [Full Text] [PDF]

				Q. Yang, C.-Q. Lai, L. Parnell, L. A. Cupples, X. Adiconis, Y. Zhu, P. W. F. Wilson, D. E. Housman, A. M. Shearman, R. B. D'Agostino, et al. Genome-wide linkage analyses and candidate gene fine mapping for HDL3 cholesterol: the Framingham Study J. Lipid Res., July 1, 2005; 46(7): 1416 - 1425. [Abstract] [Full Text] [PDF]

				J. M Ordovas, D. Corella, L A. Cupples, S. Demissie, A. Kelleher, O. Coltell, P. W. Wilson, E. J Schaefer, and K. Tucker Polyunsaturated fatty acids modulate the effects of the APOA1 G-A polymorphism on HDL-cholesterol concentrations in a sex-specific manner: the Framingham Study Am. J. Clinical Nutrition, January 1, 2002; 75(1): 38 - 46. [Abstract] [Full Text] [PDF]

				W. Huang, J. Sasaki, A. Matsunaga, H. Nanimatsu, K. Moriyama, H. Han, M. Kugi, T. Koga, K. Yamaguchi, and K. Arakawa A Novel Homozygous Missense Mutation in the Apo A-I Gene With Apo A-I Deficiency Arterioscler Thromb Vasc Biol, March 1, 1998; 18(3): 389 - 396. [Abstract] [Full Text] [PDF]