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(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

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