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Apolipoprotein E4 phenotype increases non-fasting serum triglyceride concentration in infants - the STRIP study
A Tammi1, T Rönnemaa, J Viikari
1Cardiorespiratory Research Unit, University of Turku, Kiinamyllynkatu 10, FIN-20520, Turku, Finland. anne.tammi@utu.fi
Atherosclerosis
|September 21, 2000
Summary
Apolipoprotein E (apo E) phenotypes affect infant triglyceride levels. Infants with apo E4/4 or apo E3/4 phenotypes have higher triglyceride values than those with apo E3/3, suggesting increased atherosclerosis risk.
Area of Science:
- Pediatrics
- Genetics
- Cardiovascular Health
Background:
- Apolipoprotein E (apo E) phenotypes are known to influence serum cholesterol.
- Understanding factors affecting infant lipid profiles is crucial for early cardiovascular risk assessment.
Purpose of the Study:
- To investigate the association between apo E phenotypes and non-fasting serum triglyceride values in infants.
- To determine if apo E genotype influences triglyceride metabolism in early childhood.
Main Methods:
- Analysis of non-fasting serum triglyceride concentrations in 1062 infants aged 7 and 13 months from the STRIP project.
- Stratification of infants based on apo E phenotypes (E4/4, E3/4, E3/3, E2/3).
- Statistical comparison of triglyceride levels across different apo E phenotypes, controlling for weight, milk type, and feeding interval.
Main Results:
- Infants with apo E4/4 and apo E3/4 phenotypes exhibited significantly higher non-fasting serum triglyceride concentrations compared to those with the apo E3/3 phenotype at both 7 and 13 months.
- These differences were independent of infant weight, milk type, and time since the last meal.
- The apo E varepsilon4 allele was associated with elevated triglyceride levels in infants.
Conclusions:
- Apolipoprotein E phenotypes regulate non-fasting serum triglyceride levels in healthy infants.
- The apo E3/4 and apo E4/4 phenotypes predispose infants to higher triglyceride values than the apo E3/3 phenotype.
- The varepsilon4 allele may contribute to atherosclerosis risk through its impact on postprandial triglyceride metabolism in infants.