Genetic variants of apolipoprotein A5 T-1131C and apolipoprotein E common polymorphisms and their relationship to features of metabolic syndrome in adult dyslipidemic patients
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
24709297
DOI
10.1016/j.clinbiochem.2014.03.015
PII: S0009-9120(14)00157-X
Knihovny.cz E-resources
- Keywords
- Apolipoprotein A5, Apolipoprotein E, Dyslipidemia, Genetic polymorphism, Metabolic syndrome, Triglycerides,
- MeSH
- Apolipoprotein A-V MeSH
- Apolipoproteins A genetics MeSH
- Apolipoproteins E genetics MeSH
- Adult MeSH
- Dyslipidemias genetics MeSH
- Gene Frequency MeSH
- Middle Aged MeSH
- Humans MeSH
- Metabolic Syndrome genetics MeSH
- Polymorphism, Genetic * MeSH
- Triglycerides blood MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- APOA5 protein, human MeSH Browser
- Apolipoprotein A-V MeSH
- Apolipoproteins A MeSH
- Apolipoproteins E MeSH
- Triglycerides MeSH
OBJECTIVES: The aim was to evaluate the relationships of the T-1131C (rs662799) polymorphism variants of apolipoprotein A5 (Apo A5) gene and variants of apolipoprotein E (Apo E) gene common polymorphism (rs429358, rs7412) to signs of metabolic syndrome (MetS). DESIGN AND METHODS: We examined 590 asymptomatic dyslipidemic patients divided into MetS+ (n=146) and MetS- (n=444) groups according to criteria of NCEP ATPIII Panel. We evaluated genotype frequencies and differences in MetS features between individual groups. Logistic regression analysis was used for the evaluation of Apo A5/Apo E variants as possible risk factors for MetS. RESULTS: We found no statistical differences between genotype and allele frequencies for both Apo A5 and Apo E polymorphisms between MetS+ and MetS- groups. In all subjects and MetS- group, we confirmed well-known association of the -1131C Apo A5 minor allele with elevated triglycerides (TG, p<0.001). The Apo E gene E2 and E4 variants were associated with higher levels of TG (p<0.01) in comparison to E33 common variant. However, no statistical differences were observed in MetS+ subjects, regardless of significantly higher TG levels in this group. Apo A5/Apo E variant analysis in all dyslipidemic patients revealed significant increase of TG levels in all subgroups in comparison to common -1131T/E3 variant carriers, the most in -1131C/E4 variant subgroup. Logistic regression analysis models showed no association of Apo A5, Apo E and all Apo A5/Apo E variants with metabolic syndrome, even after adjustment for age and sex. CONCLUSION: Our study refined the role of Apo A5 and Apo E genetic variants in the group of adult dyslipidemic patients. We demonstrate that except of TG, Apo A5 T-1131C (rs662799) and Apo E (rs429358, rs7412) polymorphisms have no remarkable effect on MetS characteristics.
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