Obestity is associated with a range of metabolic abnormalities including fasting and postprandial
dyslipidemia, both of which may contribute to increased atherosclerotic risk. Male obese subjects have a decreased level of
low-density lipoprotein (
LDL) receptor binding in mononuclear cells, the level of which reflects binding in the liver, compared with lean controls. In this study, we investigated whether the implementation of a
weight loss regimen in viscerally obese subjects improves
LDL receptor binding level. We examined
apolipoprotein B(48) (
apo B(48)) and
retinyl palmitate (RP) metabolism following an oral fat challenge to determine whether
weight loss improves postprandial
dyslipidemia in viscerally obese subjects. Male obese, mildly dyslipidemic, and
insulin-resistant subjects were randomly assigned to either a
weight loss (n = 12) or control weight maintenance (n = 10) group. In response to
weight loss of 10 kg,
insulin sensitivity improved as evidenced by decreased fasting
insulin and homeostatic model assessment (HOMA) score. In addition,
LDL receptor binding in mononuclear cells increased significantly by 27.5% and
LDL-cholesterol was significantly reduced. However, despite the increased
LDL receptor levels, fasting
apo B(48) levels did not fall. Postprandially, the area under the curve (AUC) for RP was significantly reduced after
weight loss, but the incremental and total AUCs for
apo B(48) were not altered.
Apo B(48) is an unequivocal marker of
chylomicron particle number; hence, the reduction in RP metabolism achieved with
weight reduction may reflect decreased
lipid incorporation into nascent
chylomicrons or improved hydrolysis of
triglyceride-rich
chylomicrons resulting from a decreased competition with hepatic
lipoproteins for
lipoprotein lipase. Our findings suggest that the improvement in
LDL receptor binding following
weight reduction of 10 kg in
insulin-resistant male obese subjects is insufficient to reduce the elevated
chylomicron remnant levels.