Very-low-density lipoprotein (VLDL), density relative to extracellular water, is a type oflipoprotein made by theliver.[1] VLDL is one of the five major groups of lipoproteins (chylomicrons, VLDL,intermediate-density lipoprotein,low-density lipoprotein,high-density lipoprotein) that enable fats andcholesterol to move within the water-based solution of the bloodstream. VLDL is assembled in theliver fromtriglycerides,cholesterol, andapolipoproteins. VLDL is converted in the bloodstream tolow-density lipoprotein (LDL) andintermediate-density lipoprotein (IDL). VLDL particles have a diameter of 30–80nanometers (nm). VLDL transportsendogenous products, whereaschylomicrons transportexogenous (dietary) products. In the early 2010s both the lipid composition[2] and protein composition[3] of this lipoprotein were characterised in great detail.
Very-low-density lipoprotein size is variable, with diameters ranging from approximately 35 to 70 nm.[4] Some researchers further classify VLDL particles into VLDL1 and VLDL2 based on size (as measured bySvedberg flotation units), where VLDL1 particles are larger and contain more triglycerides, while other researchers create a tripartite system by subdividing VLDL1 into larger VLDL1 and smaller VLDL2 and relabeling VLDL2 as VLDL3.[4]
Very-low-density lipoproteins transport endogenoustriglycerides,phospholipids,cholesterol, andcholesteryl esters. They function as the body's internal transport mechanism for lipids. In addition they can assist in long-range transport of hydrophobic intercellular messengers, like the morphogenIndian hedgehog (protein).[5]
Nascent VLDL released from the liver containsapolipoprotein B100,apolipoprotein C1 (apoC1),apolipoprotein E (apoE),cholesterol,cholesteryl esters, andtriglycerides. As it circulates in blood, it picks upapolipoprotein C-II (apoC-II) and additional apoE donated fromhigh-density lipoprotein (HDL). At this point, nascent VLDL becomes a mature VLDL. Once in circulation, VLDL will come in contact withlipoprotein lipase (LPL) in the capillary beds in the body (adipose, cardiac, and skeletal muscle). LPL will remove triglycerides from VLDL for storage or energy production. VLDL now meets back up with HDL where apoC-II is transferred back to HDL (but keeps apoE). HDL also transfers cholesteryl esters to the VLDL in exchange for phospholipids and triglycerides viacholesterylester transfer protein (CETP). As more and more triglycerides are removed from the VLDL because of the action ofLPL and CETP enzymes, the composition of the molecule changes, and it becomes intermediate-density lipoprotein (IDL).[6]
Fifty percent of IDLs are recognized by receptors in the liver cells because of theapolipoprotein B-100 (apoB-100) and apoE they contain and areendocytosed. The other 50% of IDL lose apoE; when their cholesterol content becomes greater than the content of triglyceride, they become LDL, with apoB-100 as the primary apolipoprotein. The LDL is taken into a cell via the LDL receptor via endocytosis, where the contents are either stored, used for cell membrane structure, or converted into other products such as steroid hormones or bile acids.[7]
Lipids:lipoprotein particle metabolism | ||
|---|---|---|
| Lipoprotein particle classes and subclasses |
|  |
| Apolipoproteins | ||
| Extracellularenzymes | ||
| Lipid transfer proteins | ||
| Cell surface receptors | ||
| ATP-binding cassette transporter | ||
