Health Dictionary
Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.
Very low-density lipoprotein
Introduction
Overview
Historical Perspective
Classification
Biochemistry
Overview
Biochemistry
Structure
| Lipoprotein | Density | Size | % Protein | % Cholesterol | % Triglyceride | Major Lipid | Apolipoprotein |
| VLDL |
For more information about the biochemistry of all lipoproteins, click here.
VLDL Receptors
Enzymes Associated with VLDL
References
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Physiology
Overview
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.
Function
VLDL transports endogenous triglycerides, phospholipids, cholesterol and cholesteryl esters. It functions as the body’s internal transport mechanism for lipids.
Changes during circulation
Nascent VLDL circulates in blood and picks up apolipoprotein 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 storage 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 lose 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 and disease
VLDL levels have been correlated with accelerated rates of atherosclerosis, and are elevated in a number of diseases and metabolic states.
The uniqueness of this correlation is disputed by Harchaoui and Boekholdt http://www.medscape.com/viewarticle/551425
See also
de:Very low density lipoprotein
he:VLDL
fi:Very low density lipoprotein
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Clinical Correlation
Clinical Correlation
Epidemiology and Demographics | Pathophysiology | Causes | Prognosis and Complications
Epidemiology and Demographics | Pathophysiology | Causes | Prognosis and Complications
Treatment
Treatment
Medical Therapy | Primary Prevention | Secondary Prevention | Landmark Trials | Future or Investigational Therapies
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]; Raviteja Guddeti, M.B.B.S. [3]