Product Code Database
(the largest lipoprotein).
ApoA, Apolipoprotein B, Apolipoprotein C, Apolipoprotein E are ; green particles are ; T is triglyceride; C is cholesterol ester.]]
A lipoprotein is a biochemical assembly whose primary function is to transport hydrophobic lipid (also known as fat) molecules in water, as in blood plasma or other extracellular fluids. They consist of a triglyceride and cholesterol center, surrounded by a phospholipid outer shell, with the hydrophilic portions oriented outward toward the surrounding water and lipophilic portions oriented inward toward the lipid center. A special kind of protein, called apolipoprotein, is embedded in the outer shell, both stabilising the complex and giving it a functional identity that determines its role.
Plasma lipoprotein particles are commonly divided into five main classes, based on size, lipid composition, and apolipoprotein content. They are, in increasing size order: HDL, LDL, IDL, VLDL and . Subgroups of these plasma particles are primary drivers or modulators of atherosclerosis.
Many , transporters, structural proteins, , adhesins, and are sometimes also classified as lipoproteins, since they are formed by lipids and proteins.
All cells use and rely on fats and cholesterol as building blocks to create the multiple cell membrane that cells use both to control internal water content and internal water-soluble elements and to organize their internal structure and protein enzymatic systems. The outer shell of lipoprotein particles have the hydrophilic groups of phospholipids, cholesterol, and apolipoproteins directed outward. Such characteristics make them soluble in the salt-water-based blood pool. and cholesteryl esters are carried internally, shielded from the water by the outer shell. The kind of apolipoproteins contained in the outer shell determines the functional identity of the lipoprotein particles. The interaction of these apolipoproteins with enzymes in the blood, with each other, or with specific proteins on the surfaces of cells, determines whether triglycerides and cholesterol will be added to or removed from the lipoprotein transport particles.
Characterization in human plasma
| + | !Chylomicrons !VLDL !LDL !HDL | |||
| Electrophoretic mobility | Origin | Pre-Beta | Beta | Alpha |
| Density | less than 0.96 | 0.96-1.006 | 1.006-1.063 | 1.063-1.21 |
| Diameter (nm) | 100-1000 | 30-90 | 20-25 | 10-20 |
| Apolipoproteins | B48, Al, All | B100 CI, CII | B100 | AI, AII, CI |
| Composition (% of total content) | ||||
| · Protein | 2 | 10 | 20 | 40 |
| · Lipid | 98 | 90 | 80 | 60 |
| Lipid component (% of total lipid content) | ||||
| · Triglycerides | 88 | 55 | 12 | 12 |
| · Cholesteryl esters | 4 | 24 | 59 | 40 |
| · Phospholipids | 8 | 20 | 28 | 47 |
| · Free fatty acids | - | 1 | 1 | 1 |
The are the main platform for the handling of triglycerides and cholesterol; the liver can also store certain amounts of glycogen and triglycerides. While are the main storage cells for triglycerides, they do not produce any lipoproteins.
In the blood stream, nascent chylomicron particles interact with HDL particles, resulting in HDL donation of apolipoprotein C-II and apolipoprotein E to the nascent chylomicron. The chylomicron at this stage is then considered mature. Via apolipoprotein C-II, mature chylomicrons activate lipoprotein lipase (LPL), an enzyme on lining the blood vessels. LPL catalyzes the hydrolysis of triglycerides that ultimately releases glycerol and from the chylomicrons. Glycerol and fatty acids can then be absorbed in peripheral tissues, especially Adipose tissue and Muscle tissue, for energy and storage.
The hydrolyzed chylomicrons are now called chylomicron remnants. The chylomicron remnants continue circulating the bloodstream until they interact via apolipoprotein E with chylomicron remnant receptors, found chiefly in the liver. This interaction causes the endocytosis of the chylomicron remnants, which are subsequently hydrolyzed within . Lysosomal hydrolysis releases glycerol and fatty acids into the cell, which can be used for energy or stored for later use.
In the hepatocytes, triglycerides and cholesteryl esters are assembled with apolipoprotein B-100 to form nascent VLDL particles. Nascent VLDL particles are released into the bloodstream via a process that depends upon apolipoprotein B-100.
In the blood stream, nascent VLDL particles bump with HDL particles; as a result, HDL particles donate apolipoprotein C-II and apolipoprotein E to the nascent VLDL particle. Once loaded with apolipoproteins C-II and E, the nascent VLDL particle is considered mature. VLDL particles circulate and encounter LPL expressed on . Apolipoprotein C-II activates LPL, causing hydrolysis of the VLDL particle and the release of glycerol and fatty acids. These products can be absorbed from the blood by peripheral tissues, principally adipose and muscle. The hydrolyzed VLDL particles are now called VLDL remnants or intermediate-density lipoproteins (IDLs). VLDL remnants can circulate and, via an interaction between apolipoprotein E and the remnant receptor, be absorbed by the liver, or they can be further hydrolyzed by hepatic lipase.
Hydrolysis by hepatic lipase releases glycerol and fatty acids, leaving behind IDL remnants, called low-density lipoproteins (LDL), which contain a relatively high cholesterol content (). LDL circulates and is absorbed by the liver and peripheral cells. Binding of LDL to its target tissue occurs through an interaction between the LDL receptor and apolipoprotein B-100 on the LDL particle. Absorption occurs through endocytosis, and the internalized LDL particles are hydrolyzed within lysosomes, releasing lipids, chiefly cholesterol.
When the body is functioning under normal, stable physiological conditions, HDL has been shown to be beneficial in several ways. LDL contains apolipoprotein B (apoB), which allows LDL to bind to different tissues, such as the artery wall if the glycocalyx has been damaged by high blood sugar levels. If oxidised, the LDL can become trapped in the proteoglycans, preventing its removal by HDL cholesterol efflux. Normal functioning HDL is able to prevent the process of oxidation of LDL and the subsequent inflammatory processes seen after oxidation.
Lipopolysaccharide, or LPS, is the major pathogenic factor on the cell wall of Gram-negative bacteria. Gram-positive bacteria has a similar component named Lipoteichoic acid, or LTA. HDL has the ability to bind LPS and LTA, creating HDL-LPS complexes to neutralize the harmful effects in the body and clear the LPS from the body. (2025). 9783319096643, Springer. ISBN 9783319096643 HDL also has significant roles interacting with cells of the immune system to modulate the availability of cholesterol and modulate the immune response.
Under certain abnormal physiological conditions such as system infection or sepsis, the major components of HDL become altered, The composition and quantity of lipids and apolipoproteins are altered as compared to normal physiological conditions, such as a decrease in HDL cholesterol (HDL-C), phospholipids, apoA-I (a major lipoprotein in HDL that has been shown to have beneficial anti-inflammatory properties), and an increase in Serum amyloid A. This altered composition of HDL is commonly referred to as acute-phase HDL in an acute-phase inflammatory response, during which time HDL can lose its ability to inhibit the oxidation of LDL. In fact, this altered composition of HDL is associated with increased mortality and worse clinical outcomes in patients with sepsis.
For young healthy research subjects, ~70 kg (154 lb), these data represent averages across individuals studied, percentages represent % dry weight:
| Density (g/mLitre) | Class | Diameter (nm) | % protein | % cholesterol & cholesterol ester | % phospholipid | % triglyceride |
| >1.063 | HDL | 5–15 | 33 | 30 | 29 | 4-8 |
| 1.019–1.063 | LDL | 18–28 | 25 | 46-50 | 21-22 | 8-10 |
| 1.006–1.019 | IDL | 25–50 | 18 | 29 | 22 | 31 |
| 0.95–1.006 | VLDL | 30–80 | 10 | 22 | 18 | 50 |
| <0.95 | Chylomicrons | 75-1200 | 1-2 | 8 | 7 | 83-84 |
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