Key result
Multilocus genetic variants link to lipid levels, with LPL explaining ~7% of triglyceride variability.
Why the study?
Shared genetic and environmental factors contribute to lipid parameter variability, but the combined effects of multiple polymorphic genes on cardiovascular risk require further elucidation.
Cohort (n=416)
Answers are grounded in this paper and cite their sources.
A multiplex genotyping assay of 35 polymorphic sites on 15 candidate genes is feasible and its allele frequencies align with known Caucasian population data, supporting its use in assessing genetic susceptibility to cardiovascular risk.
Until now, our familial studies have showed that shared genetic and environmental 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 density 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 associated with total cholesterol, high density lipoprotein cholesterol, LDL-Chol, triglycerides and apo B levels genetic variability, d) the lipoproteine lipase (LPL) gene was responsible for 6.5% of the triglycerides variability, e) the apo E and LPL 447 polymorphisms influence in conjunction lipid parameters. These preliminary results on effects and combination effects of polymorphic genes show the interest of a multilocus approach. We have used in a subgroup of 416 individuals of a familial cohort (Stanislas 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 of immobilized, oligonucleotide probes. The frequencies of the rare alleles were in agreement with those reported by others in caucasian populations. The realisation of this multiplex assay in the 1,006 families of the Stanislas Cohort, which is underway, will allow us a better understanding of the inter-individual variability of lipids and will contribute to the determination of the genetic susceptibility of one's individual to cardiovascular risk.
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Pallaud et al. (1999) conducted a cohort in Cardiovascular risk and lipid variability (n=416). Genetic polymorphisms (apo E, apo B, LPL) was evaluated on Lipid parameters variability. Genetic polymorphisms, including the LPL gene which accounted for 6.5% of triglyceride variability, influence lipid parameters, supporting a multilocus genotyping approach for cardiovascular risk.
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