Key result
Chylomicron remnant clearance half-times were prolonged in endogenous hypertriglyceridemia and Type 3 hyperlipoproteinemia compared to normal subjects.
Why the study?
Does chylomicron remnant clearance differ between normal subjects, those with endogenous hypertriglyceridemia, and those with apoE E2/2 phenotype?
Observational (n=24)
Does chylomicron remnant clearance differ between normal subjects, those with endogenous hypertriglyceridemia, and those with apoE E2/2 phenotype?
Chylomicron remnant clearance is delayed in endogenous hypertriglyceridemia and severely impaired in subjects with apoE E2/2 phenotype, likely due to VLDL overproduction and structural apoE abnormalities, respectively.
Answers are grounded in this paper and cite their sources.
Impaired remnant clearance may elevate cardiovascular risk in hypertriglyceridemia; leaves open whether enhancing clearance improves outcomes.
The kinetics of chylomicron metabolism have been studied by measuring retinyl palmitate in chylomicrons and their remnants for 10-12 hr following oral administration of vitamin A and Lipomul in three groups of adult male subjects: A) normal plasma triglyceride levels (n = 7); B) endogenous hypertriglyceridemia (n = 12); C) apolipoprotein E (apoE) phenotype E2/2, with Type 3 hyperlipoproteinemia (n = 4) or normal plasma lipids (n = 1). A multicompartmental model was developed using SAAM 27 to characterize the appearance, intravascular metabolism, and clearance from the plasma of retinyl palmitate-labeled dietary lipoproteins. The half-times for retinyl palmitate clearance from the chylomicron remnant fraction (T1/2 REMNANT) were 14.1 +/- 9.7 min in Group A; they were prolonged in Group B (50.7 +/- 20.8 min) and were extremely prolonged for Type 3 subjects in Group C (611.9 +/- 419.9 min). One subject with the apoE 2/2 phenotype and normal plasma triglycerides had a T1/2 REMNANT of 66.8 min. T1/2 REMNANT was highly correlated with fasting plasma triglycerides in Group A and B (r = 0.77, slope = 0.15), and in Group C (r = 0.97, slope = 0.85). These results support the interpretation that delayed chylomicron remnant clearance in subjects with endogenous hypertriglyceridemia may be largely secondary to overproduction of VLDL particles, whose remnants compete with chylomicron remnants for removal by the liver via apoE receptor-mediated endocytosis. The subjects with apoE 2/2 have an additional defect in the removal of chylomicron remnants presumably due to the structural abnormality in their apoE.
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Cortner et al. (1987) conducted an observational in Hyperlipoproteinemia (n=24). Endogenous hypertriglyceridemia or apoE phenotype E2/2 vs. Normal plasma triglyceride levels was evaluated on Half-times for retinyl palmitate clearance from the chylomicron remnant fraction (T1/2 REMNANT). Chylomicron remnant clearance half-times were prolonged in endogenous hypertriglyceridemia and Type 3 hyperlipoproteinemia compared to normal subjects.
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