Recent large-scale clinical trials indicate that
hypertriglyceridemia is a risk factor in
coronary artery disease; however, the mechanism has not yet been completely clarified. We are currently studying the metabolism of
triglyceride-rich
lipoproteins and their role in
atherosclerosis. Remnants, one of atherogenic
lipoproteins, showed a marked increase and remained high even 8 hours after fat loading, especially in patients with
coronary artery disease or
diabetes mellitus. This shows that the postprandial state persists almost the whole day in these patients. Accordingly, it may be important to assess post-prandial remnant concentrations when evaluating risk factors for
atherosclerosis. We identified apo B100 expression in the epithelial cells of the small intestine by immunoblotting with anti-apo B100
monoclonal antibody and dot-blotting of PCR-amplified
cDNA. This indicates that not only apo B48, but also apo B100 is expressed in human small intestinal epithelium. The expression of apo B100 suggests that dietary VLDL may be synthesized in human small intestinal epithelium and converted into
LDL, which may play an important role in
atherosclerosis. A new receptor, apo B48, which binds and internalizes
triglyceride-rich
lipoproteins via a domain in apo B48, was identified in human monocyte-macrophages. The receptor differs from the
scavenger receptor family and
LDL receptor family because it does not bind
acetyl LDL and it does bind VLDL devoid of
apo E. Immunohistochemical studies indicate colocalization of anti-
apo B48 receptor antibody in human atherosclerotic lesion foam cells, suggesting that
apo B48 receptor may contribute to foam cell formation and
atherosclerosis.