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.
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