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.
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: HDL, LDL, IDL, VLDL and chylomicrons.
The proteins included in the external shell of these particles, called apolipoproteins, are synthesized and secreted into the extracellular water by both the small intestine and liver cells.
The outer shell of lipoprotein particles have the hydrophilic groups of phospholipids, cholesterol, and apolipoproteins directed outward.
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[3] Lipoproteins are complex particles that have a central hydrophobic core of non-polar lipids, primarily cholesteryl esters and triglycerides.
This hydrophobic core is surrounded by a hydrophilic membrane consisting of phospholipids, free cholesterol, and apolipoproteins.
Bile emulsifies fats contained in the chyme, then pancreatic lipase cleaves triglyceride molecules into two fatty acids and one 2-monoacylglycerol.
Via apolipoprotein C-II, mature chylomicrons activate lipoprotein lipase (LPL), an enzyme on endothelial cells lining the blood vessels.
The liver is the central platform for the handling of lipids: it is able to store glycerols and fats in its cells, the hepatocytes.
Apolipoprotein C-II activates LPL, causing hydrolysis of the VLDL particle and the release of glycerol and fatty acids.
Absorption occurs through endocytosis, and the internalized LDL particles are hydrolyzed within lysosomes, releasing lipids, chiefly cholesterol.
[6] This property is due to the crystalline hydrophobic structure of lipids, providing a suitable environment for O2 solubility compared to an aqueous medium.
This is a useful response by the immune system when the body is exposed to pathogens, such as bacteria in locations that will prove harmful, but can also have detrimental effects if left unregulated.
[8] When the body is functioning under normal, stable physiological conditions, HDL has been shown to be beneficial in several ways.
[8] In fact, this altered composition of HDL is associated with increased mortality and worse clinical outcomes in patients with sepsis.
[14] High levels of lipoprotein(a) are a significant risk factor for atherosclerotic cardiovascular diseases via mechanisms associated with inflammation and thrombosis.