VLDLs, IDLs and LDLs:

VLDLs are synthesized in the liver and transport a variety of lipids that are shown in table to other tissues, again majorly skeletal muscle and adipose tissue. As with chylomicrons, the triacylglycerols in VLDLs are acted on through lipoprotein lipase and the released fatty acids taken up through the tissues. The VLDL remnants remain in the blood 1^st as IDLs and then as LDLs.  In the conversion to LDLs, much of the cholesterol is esterified on its hydroxyl group on C-3 by the addition of a fatty acid chain from phosphatidylcholine (lecithin) through the enzyme LCAT (lecithin-cholesterol acyl transferase). Additionally, all of the apoproteins other than apoB-100 are erased.

Through receptor-mediated endocytosis LDLs are then taken up through goal cells. The LDL receptor a transmembrane glycoprotein on the surface of the target cells and specifically binds apoB-100 in the LDL coat. Receptors then cluster into clathrin-coated pits and are internalized. One time in the lysosomes, the LDLs are digested through lysosomal enzymes and with the cholesterol esters being hydrolyzed through a lysosomal lipase to release the cholesterol shown in the figure. This is then incorporated into the cell membrane and any excess is re-esterified for storage through ACAT (acyl CoA cholesterol acyltransferase).

To avoid the buildup of cholesterol and its ester derivatives in the cell into high levels of cholesterol:

-  reduce  the  synthesis  of  the  LDL  receptor,  thus  reducing  the  rate  of uptake of cholesterol through receptor-mediated endocytosis, and

-  through inhibition of HMG CoA reductase inhibit the cellular biosynthesis of cholesterol.