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Association of CETP, APOA5, IL6, and PON1 Gene Variants with Dyslipidemia and Cardiovascular Risk in a Population
Astrid Lorena Urbano-Cano1, Rosa Elvira Álvarez-Rosero2, Yamil Liscano1
1Grupo de Investigación en Salud Integral (GISI), Departamento Facultad de Salud, Universidad Santiago de Cali, Cali 760035, Colombia.
Insights
Genetic variants influence dyslipidemia. The APOA5 rs662799 polymorphism is linked to higher VLDL levels, aiding cardiovascular risk assessment in Colombian adults.
Area of Science:
- Genetics and Cardiovascular Health
- Metabolic Disease Research
- Population Health Studies
Background:
- Cardiovascular disease (CVD) is a leading global cause of mortality.
- Dyslipidemia, a modifiable risk factor, significantly contributes to CVD.
- Understanding genetic influences on lipid metabolism is crucial for CVD prevention.
Purpose of the Study:
- To investigate the association between specific gene polymorphisms (CETP, APOA5, IL6, PON1) and lipid profiles.
- To determine the contribution of these polymorphisms to dyslipidemia.
- To assess their role in overall cardiovascular risk within a Colombian cohort.
Main Methods:
- Cross-sectional observational study of 304 participants (aged 40-69).
- Collection of clinical, anthropometric, and biochemical data.
- Genotyping for CETP (rs3764261), APOA5 (rs662799), IL6 (rs1800796), and PON1 (Q192R) polymorphisms.
- Statistical analysis including non-parametric tests and multivariable logistic regression.
Main Results:
- Dyslipidemia group showed higher total cholesterol, VLDL, and lower HDL levels.
- The APOA5 rs662799 variant was significantly associated with elevated VLDL levels.
- Genotype frequencies differed between dyslipidemic and non-dyslipidemic groups, with APOA5 rs662799 being a potential biomarker.
Conclusions:
- Genetic variants and metabolic factors interact in dyslipidemia development.
- The APOA5 rs662799 polymorphism is a key determinant of VLDL concentration.
- This finding supports personalized cardiovascular risk stratification and management strategies.
Background:
Cardiovascular disease remains the leading cause of death worldwide, and dyslipidemia is a critical, modifiable risk factor.
Aim:
We sought to evaluate the relationship between polymorphisms in CETP (rs3764261), APOA5 (rs662799), IL6 (rs1800796), and PON1 (Q192R) and lipid parameters, and to assess their contribution to dyslipidemia and overall cardiovascular risk in an urban cohort from Cauca, Colombia.
Methods:
In this cross-sectional observational study, 304 participants aged 40-69 years were enrolled. Clinical, anthropometric, and biochemical data were collected, and genotyping was performed for the four target polymorphisms. We used descriptive statistics to characterize the sample, non-parametric tests to compare lipid levels by genotype, and multivariable logistic regression to identify independent predictors of dyslipidemia.
Results:
Individuals with dyslipidemia exhibited significantly higher total cholesterol and VLDL levels, lower HDL levels, and an elevated Castelli II index compared with the non-dyslipidemia group. Although CETP genotype frequencies differed between groups, only the APOA5 rs662799 variant was significantly associated with increased VLDL levels, suggesting its potential role as a genetic biomarker of cardiovascular risk.
Conclusions:
Our findings underscore the interplay between metabolic factors and genetic variants in the pathogenesis of dyslipidemia. Notably, the APOA5 rs662799 polymorphism emerged as a key determinant of VLDL concentration, highlighting its promise for personalized cardiovascular risk stratification and management in this population.
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