The following material is largely taken from references (1) and (2).

Our bodies make essentially three types of lipoproteins: chylomicrons, very low density lipoproteins (VLDLs), and high density lipoproteins (HDLs or "good cholesterol"). As these particles unload their lipid cargo, the chylomicrons change into chylomicron remnants, and the VLDLs become VLDL remnants, also known as intermediate density lipoproteins (IDLs), some of which eventually turn into low density lipoproteins (LDLs or "bad cholesterol").

Lipids are less dense than the proteins on the particle surfaces, the so-called apolipoproteins. The size of the lipid load therefore determines the particle density. Chylomicrons carry the largest lipid load and are the least dense. The names of the rest of the lipoproteins reflect their relative lipid loads and densities.

Chylomicrons are assembled in the cells of the small intestine and carry dietary lipids to the tissues. As they pass through the capillaries, they discharge their cargo of triglycerides (TGs), but not their cholesteryl esters. The TG-depleted particles, called chylomicron remnants, are rapidly taken up whole by liver cells and dismantled. Some of the dietary cholesterol is used for bile acid synthesis.

Three proteins control the fate of chylomicrons. The defining apolipoprotein is apo B48. HDLs provide two additional freely exchangeable proteins, apo C-II and apo E. These proteins control the discharge of the triglycerides and the uptake of the lipoprotein remnants by the liver.

Apo C-II binds to the enzyme lipoprotein lipase (LPL) bound to capillary walls and serves as LPL cofactor in the hydrolysis of TGs to free fatty acids (FFAs) and glycerol. The free fatty acids cross the capillary walls and most are taken up by the tissues. Any leftover FFAs bind to albumin and eventually return to the liver.

As long as apo C-II is present, it prevents the uptake of the chylomicron particle by the liver. The transfer of apo C-II back to an HDL particle exposes apo E and permits its binding to an hepatic apo E receptor, followed by endocytosis of the complete lipoprotein.

VLDLs (very low density lipoproteins)

VLDLs are assembled in the liver and carry lipids from the liver to the tissues. These may be lipids synthesized by the liver or returned to the liver by remnants of other VLDLs or chylomicrons, or albumin-bound free fatty acids.

Like chylomicrons, VLDLs initially unload their TG cargo and become TG-depleted remnants, called intermediate density lipoproteins (IDLs). However, unlike chylomicron remnants, VLDL remnants can turn into a new type of lipoprotein - LDLs.

The defining protein of VLDLs is apo B-100. In addition, VLDLs also get apo C-II and apo E from HDLs; these apolipoproteins play the same roles here as they do on chylomicrons. Apo C-II is the lipoprotein lipase cofactor required for TG hydrolysis and release of free fatty acids. In addition, it blocks the premature elimination of VLDLs.

The IDLs have discharged most of their triglycerides and essentially carry only cholesteryl esters. They have also lost their apo C-IIs. If they keep their apo Es, they bind to apo E receptors and are taken up by the liver. If they lose their apo E apoproteins as well, they can no longer bind to apo E receptors and remain in circulation. This new type of particle is called LDL.

LDLs (low density lipoproteins)

LDLs deliver cholesterol from the liver to the tissues. This cholesterol load is made up of molecules synthesized by the liver, dietary cholesterol delivered to the liver via chylomicrons, and cholestryl esters transferred in plasma from HDLs. These LDLs rich in cholesteryl esters only carry one type of apolipoprotein, namely apo B100.

Most tissues are able to synthesize all the cholesterol they need and do not rely on the liver or on dietary sources. However, growing tissues and organs synthesizing steroidal hormones require large amounts of cholesterol. Cells in those tissues display LDL receptors on their plasma membranes; the number of LDL receptors is related to a cell's need for cholesterol. When an LDL particle binds to an LDL receptor via the apo B100 protein, the whole lipoprotein is taken up by the cell.

Liver cells also express LDL receptors, and LDL particles that weren't taken up by extra-hepatic tissues are removed in this way.

HDLs (high density lipoproteins)

HDLs are synthesized in the liver and, to a lesser extent, the small intestine. They have two functions. First, HDLs are involved in triglyceride transport by supplying apo C-II and apo E proteins to TG-carrying lipoproteins. Secondly, they collect excess cholesterol from tissues and transfer it either to cholesterol-hungry cells for use or to the liver for disposal.

HDLs are excreted empty or in a lipid-poor form, in which state they are collapsed disk-shaped bags. Apo A-I is the defining apo protein of HDLs. It is their only apolipoprotein at the initial stage, and it is present throughout the life cycle of an HDL particle. It binds to hepatic HDL receptors and serves as cofactor for lecithin:cholesterol acyltransferase (LCAT).

Excess cholesterol mainly comes from cellular debris, including damaged lipoproteins, taken up by macrophages and incorporated into their plasma membranes. Lipoproteins can suffer oxidative damage to the lipid or protein components. In addition, elevated blood glucose levels can damage the apolipoproteins by glycating lysyl residues. Damaged lipoproteins are disfunctional and are quickly eliminated by macrophages.

The uptake of cholesterol by HDLs requires the conversion to cholesteryl esters. which is catalyzed by the HDL-bound enzyme lecithin:cholesterol acyltransferase (LCAT). As its name implies, the source of the fatty acid used to esterify cholesterol is the lecithin part of a phospholipid.

The collection and disposal of surplus cholesterol is called reverse cholesterol transport (RCT). Reverse cholesterol transport can occur directly or indirectly.

In the direct route the HDLs themselves deliver the cholesterol to the target cells. Either they bind to a so-called scavenger receptor class B type I (SR-BI) and transfer only their cholesterol load, or the HDL particle binds via apo A-I to an hepatic HDL receptor and is taken up whole and dismantled.

In the indirect route the HDLs transfer cholesterol to VLDLs, many of which become LDLs. The LDL apo B-100 binds to an LDL receptor on a cell that need cholesterol; the cell then takes up the whole lipoprotein.

The transfer of cholesteryl esters between HDLs and VLDLs is catalyzed by the plasma enzyme cholesteryl ester transfer protein (CETP).

To summarize, both chylomicrons and VLDLs deliver their triglyceride cargo directly to their destination cells in muscle and adipose tissue. The transport and delivery of cholesterol is a different matter. Dietary cholesterol ends up in the liver via endocytosis of the chylomicron particles. The liver controls the cholesterol export via VLDLs and the elimination of any excess via bile formation.

Only LDLs have the necessary apolipoprotein, apo B100, for binding to LDL receptors and delivering cholesterol to cells that need it. Only HDLs can salvage excess cholesterol and recycle it via LDLs. Cholesterol distribution is essentially controlled by HDLs and LDLs.

Cholesterol is clearly more than just a risk factor for atherosclerosis. It is a vital substance, an important component of cell and lipoprotein membranes, and the starting material for the synthesis of all steroidal hormones. Its distribution is carefully orchestrated by the interplay of lipoproteins and enzymes.