G-->A substitution at position -75 of the apolipoprotein A-I gene promoter. Evidence against a direct effect on HDL cholesterol levels

Arterioscler Thromb Vasc Biol. 1995 Oct;15(10):1740-5. doi: 10.1161/01.atv.15.10.1740.

Abstract

The present study sought to resolve the contradictory evidence as to whether the G-->A 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Alleles
  • Apolipoprotein A-I / genetics*
  • Base Sequence
  • Canada
  • Cholesterol, HDL / blood*
  • Female
  • Genetic Linkage
  • Humans
  • Hyperlipoproteinemias / genetics*
  • Hyperlipoproteinemias / metabolism*
  • Male
  • Middle Aged
  • Molecular Sequence Data
  • Pedigree
  • Point Mutation
  • Polymorphism, Genetic
  • Promoter Regions, Genetic / genetics

Substances

  • Apolipoprotein A-I
  • Cholesterol, HDL