Until now, our familial studies have showed that shared genetic and environ
mental factors are involved on lipid parameters variability. More precisely
, being working on 119 families we have showed that: a) The apolipoprotein
E (apo E) common polymorphism is involved in the total cholesterol, low den
sity lipoprotein cholesterol (LDL-Chol), apo E, apo B levels variability, b
) the apolipoprotein A-IV gene had no effect on lipid metabolism parameters
variability, apo A-IV levels included, c) the apolipoprotein B gene was as
sociated with total cholesterol, high density lipoprotein cholesterol, LDL-
Chol, triglycerides and apo B levels genetic variability, d) the lipoprotei
ne lipase (LPL) gene was responsible for 6.5 % of the triglycerides variabi
lity, e) the apo E and LPL 447 polymorphisms influence in conjunction lipid
parameters. These preliminary results on effects and combination effects o
f polymorphic genes show the interest of a multilocus approach.
We have used in a subgroup of 416 individuals of a familial cohort (Stanisl
as Cohort) a prototype assay that genotypes a panel of 35 polymorphic sites
on 15 candidate genes of Cardiovascular diseases. Each sample is amplified
by two multiplex polymerase chain reactions, then hybridized to an array o
f immobilized, oligonucleotide probes. The frequencies of the rare alleles
were in agreement with those reported by others in caucasian populations. T
he realisation of this multiplex assay in the 1 006 families of the Stanisl
as Cohort, which is underway, will allow us a better understanding of the i
nterindividual variability of lipids and will contribute to the determinati
on of the genetic susceptibility of one's individual to cardiovascular risk
.