DELAYED POSTPRANDIAL RETINYL PALMITATE AND SQUALENE REMOVAL IN A PATIENT HETEROZYGOUS FOR APOLIPOPROTEIN A-I-FIN MUTATION (LEU 159-]ARG) AND LOW HDL CHOLESTEROL LEVEL WITHOUT CORONARY-ARTERY DISEASE

A low HDL cholesterol level is frequently but not consistently associa ted with inefficient postprandial fat clearance. We studied triglyceri des, retinyl palmitate and squalene and apolipoprotein B-48 after a fa t loading test in one subject heterozygous for a novel point mutation of apolipoprotein A-I (A-I-FIN, Leu 159 --> Arg) and low HDL cholester ol level without coronary artery disease, and in 16 healthy controls w ith the same apolipoprotein E phenotype, 3/3, as the proband. HDL chol esterol and apolipoprotein A-I levels were 0.32 mmol/l and 57 mg/dl in the proband, and 1.29 +/- 0.12 mmol/l (mean +/- S.E.) and 126 +/- 4 m g/dl in the controls. The peak concentration for triglycerides in plas ma, chylomicrons and VLDL occurred at 4 h both in the case and control s. However, the peak concentrations for retinyl palmitate and squalene in chylomicrons and VLDL were delayed to 12 h in the proband compared with 4 and 9 h in the controls. The peak of apolipoprotein B-48 occur red at 6 h in the proband and at 4 h in the controls, so that triglyce rides, apolipoprotein B-48 and retinyl palmitate and squalene peaked d ifferently. After 24 h, retinyl palmitate, squalene, and apolipoprotei n B-48 had returned to the baseline levels. The results show for the f irst time an impaired postprandial lipoprotein removal in a case heter ozygote with moderately low HDL cholesterol due to an apolipoprotein A -I mutation not associated with coronary artery disease.