Much of our knowledge about the relationship between lipid, lipoprotein metabolism, and the development of atherosclerosis and cardiovascular disease is based on measurements in the fasting state. Although such measurements remain the foundation of clinical assessment and an important basis for decisions regarding hypolipidemic interventions, it should be acknowledged that we spend a considerable amount of time in a nonfasting, postprandial state. Based on typical Western eating patterns, most people consume three or more meals a day, with each containing 20–70 g of fat (Cohn et al., 1988). Aside from breakfast, each of these meals is most likely consumed before plasma triacylglycerols (TGs) have returned to baseline levels from the lipemic conditions resulting from the previous intake. Thus, humans spend the majority of their day in a postprandial (fed) state, with a continual fluctuation in the degree of lipemia throughout the day. The postprandial state is a dynamic, nonsteady-state condition, with rapid remodeling of lipoproteins compared with the relatively stable fasting condition. Determination of the postprandial response is complex, and it is, therefore, more challenging to assess the cardiovascular risk associated with postprandial lipemia than during fasting conditions. In spite of this, it is becoming increasingly evident that future efforts to study and treat lipids related to atherogenesis should include postprandial parameters. The aim of this chapter is to consider the regulatory pathways of postprandial lipoproteins and the major factors including nutrition, life style, pathophysiology, and genetics which may contribute to interindividual variability in postprandial lipaemia, and thereby, susceptibility to atherosclerosis.
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