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Apolipoprotein E polymorphism influences postprandial retinyl palmitate but not triglyceride concentrations
E Boerwinkle1, S Brown, A R Sharrett
1Genetics Center, University of Texas Health Science Center, Houston 77225.
American Journal of Human Genetics
|February 1, 1994
Summary
The apolipoprotein E (apo E) polymorphism influences postprandial lipemia, specifically delaying the clearance of vitamin A in individuals with the epsilon 2 allele. This genetic variation significantly impacts retinyl palmitate response but not triglyceride levels after a high-fat meal.
Area of Science:
- Genetics
- Metabolic Studies
- Nutritional Science
Background:
- Apolipoprotein E (apo E) polymorphism is a known factor influencing lipid metabolism.
- Understanding its role in postprandial lipemia is crucial for assessing cardiovascular disease (CAD) risk.
- Previous studies have established apo E's effect on fasting lipid levels.
Purpose of the Study:
- To quantify the effect of apo E polymorphism on postprandial lipemia.
- To determine the role of apo E in the metabolic response to a high-fat meal.
- To investigate the impact of apo E genotypes on specific lipid and lipoprotein profiles.
Main Methods:
- Analysis of a large cohort (N=474) from the Atherosclerosis Risk in Communities Study.
- Monitoring plasma triglyceride, TGRL-triglyceride, apo B-48/apo B-100 ratio, and retinyl palmitate over 8 hours post-meal.
- Determination of apo E polymorphism via DNA amplification and digestion.
Main Results:
- Postprandial retinyl palmitate response was significantly different among apo E genotypes, with delayed clearance in epsilon 2 carriers.
- The apo E polymorphism explained 7.1% of the interindividual variation in postprandial retinyl palmitate response.
- No significant differences in postprandial triglyceride response were observed among apo E genotypes.
Conclusions:
- The apo E polymorphism significantly affects postprandial vitamin A clearance, indicating delayed remnant particle removal in epsilon 2 carriers.
- While apo E influences postprandial lipemia, its direct link to coronary artery disease (CAD) via the epsilon 2 allele remains unproven.
- These findings provide mechanistic insights into apo E's role in postprandial lipemia and its potential implications for cardiovascular health.