Understanding postprandial inflammation and its relationship to lifestyle behaviour and metabolic diseases

Abstract

Postprandial hyperlipidemia with accumulation of remnant lipoproteins is a common metabolic disturbance associated with atherosclerosis and vascular dysfunction, particularly during chronic disease states such as obesity, the metabolic syndrome and, diabetes. Remnant lipoproteins become attached to the vascular wall, where they can penetrate intact endothelium causing foam cell formation. Postprandial remnant lipoproteins can activate circulating leukocytes, upregulate the expression of endothelial adhesion molecules, facilitate adhesion and migration of inflammatory cells into the subendothelial space, and activate the complement system. Since humans are postprandial most of the day, the continuous generation of remnants after each meal may be one of the triggers for the development of atherosclerosis. Modulation of postprandial lipemia by lifestyle changes and pharmacological interventions could result in a further decrease of cardiovascular mortality and morbidity. This paper will provide an update on current concepts concerning the relationship between postprandial lipemia, inflammation, vascular function, and therapeutic options.

Figure 1

Concept of the initiation of atherosclerosis by remnant lipoproteins: remnants enter the subendothelial space via nonspecific transcytotic processes. This is often a nonpathologic process, because the remnants leave the subendothelial space again via the vasa vasorum. However, retention of remnants may occur in the presence of proteoglycans and excess extracellular matrices. Remnants can be easily taken up by macrophages, in contrast to LDL, which need to become modified first. Circulating remnants themselves also contribute to the presence of subendothelial macrophages. Monocytes can bind and take up remnants, which stimulates the monocytes to become activated. Subsequently, activated monocytes express adhesion molecules on the outer membrane and stimulate the expression of endothelial cellular adhesion molecules (CAMs), which allows monocytes to home on the endothelium and migrate into the subendothelial space. Finally, the macrophages change into highly atherogenic foam cells when lipid uptake exceeds lipid efflux.

Figure 2

Influence of metabolic diseases and lifestyle factors on postprandial lipemia: factors listed in green circles reduce postprandial lipemia, whereas the factors in red have detrimental effects on postprandial lipemia.