Postprandial lipoproteins and atherosclerosis

During the postprandial state, dietary lipid is transported from the intest ine to peripheral tissues by plasma lipoproteins called chylomicrons. In th e capillary beds of peripheral tissues, chylomicron triglycerides are lipol yzed by the enzyme, lipoprotein lipase, allowing the delivery of free fatty acids to the cells. As a result, this produces a new particle of smaller s ize and enriched with cholesteryl ester referred to as chylomicron remnants . These particles are rapidly removed from the blood primarily by the liver . The liver has a complex chylomicron remnant removal system which is compr ised of a combination of different mechanisms that include the low-density- lipoprotein receptor (LDLR) and the LDLR-related-protein (LRP). Furthermore , it has been suggested that there is a sequestration component whereby chy lomicron remnants bind to heparan sulfate proteoglycans (HSPG) and/or hepat ic lipase; this is then followed by transport to one or both of the above r eceptors for hepatic uptake. Over the years, a major concern has arisen abo ut the association of chylomicron remnants and coronary heart disease (CHD) in man. Slow removal of chylomicron remnants, as reflected by a prolonged postprandial state, is now commonly observed in patients with CHD and those that have abnormal lipid disorders such as hypertriglyceridemia, familial hypercholesterolemia, familial combined hyperlipidemia and non-insulin-depe ndent-diabetes-mellitus. The present review will focus on (a) the details o f the metabolic pathway (exogenous pathway) that describes the two-step pro cessing of postprandial lipoproteins, (b) the role of the liver, the recept ors, and the importance of efficient removal of chylomicron remnants from t he blood circulation, and (c) the potential atherogenic effects of chylomic ron remnants on the arterial wall.