To examine the relation between postprandial lipemia and high density lipoprotein (HDL) concentrations, we measured the plasma triglyceride and retinyl palmitate responses to SO-g fat meals of 1) 25 men with low HDL cholesterol concentrations (<36 mg • dl" 1 ) and normal fasting triglyceride concentrations, 2) 25 men with normal HDL cholesterol (>40 mg • dl" 1 ) and normal fasting triglyceride concentrations, and 3) 20 men with mild to moderate fasting hypertriglyceridemia (250-347 mg • dl" 1 ). The average magnitude of postprandial lipemia induced by the fat meals was markedly higher in the hypertriglyceridemic men (593 ±311 mg -dl" 1 • 8 hr) than in either of the normolipidemic groups. In nonnotriglyceridemic men with low HDL cholesterol, mean postprandial lipemia (303±158 mg • dl" 1 • 8 hr) was similar to the corresponding value of men with normal HDL (283±130 mg -dl"' • 8 hr). Postprandial plasma retinyl palmitate concentrations, which reflect chylomicron remnant metabolism, also were similar in normal-HDL and low-HDL groups. These data suggest that defects in chylomicron-triglyceride clearance that give rise to excess postprandial lipemia are not a common occurrence in normolipidemic men with low HDL cholesterol concentrations. Accordingly, the low HDL cholesterol concentrations measured in the normotriglyceridemic men in this study must be attributable to factors other than an exaggerated postprandial lipemia. ( . Because coronary heart disease remains a primary cause of morbidity in Western populations, the factors that determine the plasma concentrations of HDL have become a subject of considerable medical interest. Observations in patients with genetic deficiency states of hepatic lipase, 2 lipoprotein lipase, 3 cholesterol ester transfer protein, 4 -5 and lecithin cholesterol acyltransferase 6 have revealed an important role for each of these enzymes in HDL metabolism, but the extent to which HDL concentrations are modulated by physiological variations in the activities of these enzymes is not known.The metabolism of HDL is closely linked to the intravascular processing of the trigryceride-rich lipoproteins. 7 This relation is illustrated by the lipoprotein profiles of people with hypertriglyceridemia, which are characterized by low HDL cholesterol concentrations, 8 and by epidemiological studies, which have consistently indicated a negative correlation between HDL and fasting plasma triglyceride concentrations. In most studies the correlation coefficient between these parameters is too low to indicate triglyceride levels as the primary determinant of HDL concentrations. 9 However, because most people spend much of each day in a postprandial state, measurements of fasting plasma triglyceride concentrations may not be an accurate reflection of the average 24-hour triglyceride level. Indeed, considerably stronger correlation coefficients have been reported between HDL concentrations (particularly HDL 2 ) and measurements of triglyceride levels in the postprandial state. 1011 Accordingly, it has been post...