Figure 1.

Atherogenic potential of intestinally-derived lipoproteins. This schematic illustrates two mechanisms through which the entry of chylomicron cholesterol (CM-C) into the circulation can potentially play a role in atherosclerotic plaque formation. (1) The uptake of CM-C by the liver can lead to a shift in intrahepatic cholesterol metabolism that in turn causes either a downregulation of low density lipoprotein receptor (LDL-R) activity, or/and an increase in hepatic very low density lipoprotein-cholesterol (VLDL-C) secretion. Either of these events can lead to a rise in the steady-state plasma low density lipoprotein-cholesterol (LDL-C) concentration. (2) Upon entering the circulation, CM’s lose much of their triacylglycerol content, resulting in the formation of a much smaller, cholesterol rich remnant particle (CMr) that can permeate the vessel wall. Ordinarily, CMr particles are rapidly cleared from the circulation by the liver but in Type 2 diabetes and other disorders this clearance rate can be markedly delayed.