Lipoprotein Classification
The five main classes of lipoproteins based on their size and density. The higher the ratio of protein to lipid content the higher the lipoprotein density.
1. Chylomicrons
The largest and least dense lipoproteins. Chylomicrons mainly transport triacylglycerols to adipose tissue and muscle as fatty acids, but also deliver some dietary cholesterol to the liver. Once most of the triacylglycerols have been delivered to the adipose tissue and muscle, the remnants of the lipoprotein, including cholesterol, apoE, and apo-B48 are then delivered to, and taken up by, the liver through interaction with the chylomicron remnant receptor.
2. Very low density lipoproteins (VLDL)
Produced by the liver and consist of:
- an outer core composed of apolipoproteins; apo-B100, apo-CI, apo-CII, apo-CIII, and apoE surrounding
- an inner core of phospholipids, triacylglycerols, cholesterol, and cholesteryl esters.
Very low density lipoproteins (VLDL) are smaller and more dense than chylomicrons. The role of VLDLs is to remove triacylglycerols and cholesteryl esters from the liver and distribute them throughout the body.
As VLDLs move into the circulating plasma they are converted first to intermediate density lipoproteins (IDL) and then into low density lipoproteins (LDL). Lipoprotein lipase removes the majority of fatty acids from both the VLDL and IDL, thus increasing the density of the lipoproteins while maintaining cholesterol and cholesteryl ester concentrations. In the blood, VLDL transfers apolipoprotein-CII to high density lipoprotein (HDL).
3. Intermediate density lipoproteins (IDL)
About 50% of IDL particles are removed from the circulation by the liver. The remaining IDLs are transformed to low density lipoprotein particles by the loss of apolipoprotein E and the further reduction of triglyceride content until it is exceeded by the content of cholesteryl esters. The removal of fatty acids and the loss of all apolipoproteins except apoB-100 results in LDL.
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4. Low density lipoproteins (LDL)
Te so-called "bad" cholesterol, LDL, delivers lipids to the body's cells via LDL receptor-mediated endocytosis. LDLs are the primary plasma carriers of cholesterol for delivery to all tissues. All peripheral cells express the LDL receptor and translocate it to the cell surface upon need of the cell for cholesterol. Cholesterol is delivered to these cells through binding of LDL to LDL receptor, which triggers endocytosis (internalization) of both species.The ligand binding domain of the LDL receptor on the target cell recognizes apo-B100 on LDL, resulting in the formation of a clathrin-coated vesicle in the cell that buds from the inner surface of the cell membrane. After loss of the clathrin coat, the vesicles fuse with lysosomes resulting in peptide and cholesteryl ester enzymatic hydrolysis. The LDL receptor can be recycled back to the cell membrane.
When the need for cholesterol is satisfied, the recycling of LDL receptor is discontinued. Normally, an LDL particle stays in circulation for no more than a few days before being consumed by a cholesterol needing cell. However, under conditions of sustained cholesterol excess, the particle stays in circulation for longer periods of time, and becomes more vulnerable to undesired modifications (e.g. oxidation). As high levels of oxidized LDL are commonly found in atherosclerotic plaques, they are thought to be the major inducer of atherosclerotic lesions. Hence, LDL became known as bad cholesterol.
5. High density lipoproteins (HDL)
The so-called "good" cholesterol, HDL, is composed of apolipoproteins A, C and E surrounding a lipid core. HDL contains mostly proteins, phospholipids, cholesteryl esters, and cholesterol. High density lipoproteins (HDL) are the smallest of the lipoproteins and most dense.
HDL is produced as a protein rich particle in the liver and intestine, and serves as a circulating source of Apo A, Apo C and ApoE for other lipoproteins.
Unlike LDL, HDL is not recognized by LDL receptor, and cannot deliver cholesterol to cells. Instead, it has the ability to remove excess peripheral cholesterol and return it to the liver for recycling and excretion. This process, called reverse cholesterol transport, is thought to protect against atherosclerosis. Thus, HDL serves as a scavenger of free cholesterol. Cholesterol returned to the liver by HDL is synthesized into bile acids. Bile acids facilitate the digestion of lipids by acting as emulsifying agents and also aid in the absorption of fat-soluble vitamins.
|
Lipoprotein |
Size (nm) |
Density (g/ml) |
Major Associated Lipoprotein |
|
Chylomicron |
1000 |
<0.95 |
Apo B-48 |
|
VLDL |
70 |
0.98 |
Apo E |
|
IDL |
40 |
1.01 |
Apo E |
|
LDL |
20 |
1.04 |
Apo B-100 |
|
HDL |
10 |
1.13 |
Apo A-I, Apo C, Apo E |
The functional difference between LDL and HDL results primarily from the different character of their major apoproteins, apoB-100 and apoA-I, respectively. ApoB-100, which is found in VLDL, IDL, and LDL, but not in HDL, serves as a ligand for LDL receptor, and provides LDL with the means to deliver cholesterol to tissue cells. On the other hand, apoA-I, which is found exclusively in HDL, has a unique ability to capture and solubilize free cholesterol. This apoA-I ability enables HDL to act as a cholesterol scavenger.
Cholesterol is ultimately excreted from the body as bile salts.
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