Understanding Postprandial Inflammation and Its Relationship to Lifestyle Behaviour and Metabolic Diseases

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.