Abstract
The recent discovery that fibrinogen binds to chylomicrons in gastrointestinal lymph has prompted a new rationale regarding the arterial deposition of postprandial lipids, i.e., dietary fat. According to this new rationale, fibrinogen bound to chylomicrons in the gastrointestinal lymph renders those lipid particles and/or their remnants an adhesive potential, even before the particles reach the arterial system. It is proposed that such an adhesive potential, if realized in the vicinity of the arterial wall, can contribute to the nucleation and growth of atherosclerotic plaques, especially during and immediately following a fat-rich meal. Arguments in support of this proposal are made based on the proximity of the lymph outflow tract to the arteries most susceptible to atherosclerosis, and on the tissue distributions and activities of heparin, diamine oxidase, and lipoprotein lipase. This new rationale reconciles existing theories on atherosclerosis, and it also suggests novel means by which to prevent/treat the disease.
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