The goal of the present study was to assess the influence of mealtime
on postprandial lipemia. Thirteen healthy subjects aged 19-32 y were g
iven the same meal at night (0100) or during the day (1300) in random
order; the meal contained 40% of estimated daily energy expenditure. B
lood samples were drawn at baseline and hourly for 8 h after the meal.
Serum total cholesterol, very-low-density-lipoprotein cholesterol (VL
DL-C), low-density-lipoprotein cholesterol (LDL-C), high-density-lipop
rotein cholesterol (HDL-C), triacylglycerols, VLDL-triacylglycerols, a
polipoprotein (ape) A-I, and apo B were measured at each time point. I
n a subgroup of seven subjects a control fasting reference line was me
asured according to the same nocturnal and diurnal time schedule. The
mean postprandial concentrations of triacylglycerol (P < 0.001), VLDL-
triacylglycerol (P < 0.001), and VLDL-C (P < 0.001) were higher at nig
ht than during the day. In contrast, mean cholesterol (P < 0.01), LDL-
C (P < 0.01), HDL-C (P < 0.001), apo A-I (P < 0.001), and apo B (P < 0
.001) concentrations were lower after the night meal than after the da
y meal. The magnitude of the postprandial response was estimated by th
e area between the fasting and postprandial curves. The triacylglycero
l and VLDL-triacylglycerol responses were not significantly different
between night and day. The VLDL-C (P < 0.01) response was greater and
LDL-C (P < 0.0001) and HDL-C (P < 0.01) responses were lower at night
than during the day. These results indicate that circadian factors spe
cifically affect serum cholesterol transport. Apo B (P < 0.01) and apo
A-I (P < 0.01) responses followed LDL-C and HDL-C changes during the
day but were dissociated from lipoprotein responses at night, suggesti
ng that circadian apolipoprotein regulation is dissociated from that o
f serum lipids. The results of the present study indicate that postpra
ndial lipid, lipoprotein, and apolipoprotein concentrations are affect
ed by circadian factors.