Very Low Density Lipoprotein (VLDL) is a lipoprotein subclass. It is assembled in the liver from cholesterol and apolipoproteins. It is converted in the bloodstream to low density lipoprotein (LDL). VLDL particles have a diameter of 30-80 nm. VLDL transports endogenous products where chylomicrons transport exogenous (dietary) products.
VLDL transports endogenous triglycerides, phospholipids, cholesterol and cholesteryl esters. It functions as the body's internal transport mechanism for lipids.
Nascent (young) VLDL is released into the blood from the liver with the apolipoprotein B-100 (ApoB-100) marker. At this point, the VLDL consists of ~50% triglycerides, ~18% phospholipids, ~20% cholesterol and 10% protein (hence the name, very low density lipoprotein).
Nascent VLDL circulates in blood and picks up apoliprotein C-II and apolipoprotein E donated from High Density Lipoprotein (HDL). At this point, the nascent VLDL becomes a mature VLDL. Once in circulation, the VLDL will come in contact with Lipoprotein Lipase (LPL) in the capillary beds in the body (adipose, cardiac and skeletal muscle). The LPL will remove triglycerides from the VLDL for storages or energy production.
The VLDL now meets back up with HDL where apoC-II is transferred back to the HDL (but keeps apoE). In addition to this, the HDL transfers cholesteryl esters to the VLDL in exchange for phospholipids and triglycerides (via cholesteryl ester transfer protein).
As more and more triglycerides are removed from the VLDL because of the action of the LPL enzyme, the composition of the molecule changes, and it becomes intermediate density lipoprotein (IDL).
50% of IDL are recognized by receptors in the liver cells (because of the apoB-100 and apoE they contain) and are endocytosed.
The other 50% of IDL loose their apoE. When their cholesterol content becomes greater than the triglyceride content, they become low-density lipoprotein (LDL), with the primary apolipoprotein being apoB-100. The LDL is taken into a cell via the LDL receptor (endocytosis) where the contents are either stored, used for cell membrane structure, or converted into other products (steroid hormones or bile acids).
VLDL is prone to accelerate atherosclerosis, and is elevated in a number of diseases and metabolic states.
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