Postprandial lipemia: relevance to atherosclerosis
It was suggested by Zilversmit in 1979 that atheroscle-rosis was a postprandial phenomenon. This concept was based on the finding that patients either with or at high risk of developing coronary heart disease (CHD) showed an impaired capacity to remove TAG-rich lipoproteins from the circulation after a meal. This resulted in enhanced postprandial lipemia, which also became known as the TAG intolerance hypothesis. At about the same time, evidence emerged that TAG-rich lipoproteins, and especially remnants of chylomi-crons, were directly atherogenic, meaning that they can damage the endothelial lining of arteries and promote the deposition of cholesterol in coronary arteries. For this reason, there is considerable research interest in the metabolic determinants of postprandial lipemia. This includes the mechanisms that underlie the production and removal of TAG-rich lipoproteins, not only in the intestine but also in the liver, since the production and removal of VLDL can clearly influ-ence postprandial events. The quality and, to a lesser extent, quantity of dietary fat are extremely important in this respect and have a major role to play in modu-lating lipid-mediated atherosclerosis.