VLDL stands for very low density lipoprotein, and it delivers endogenous lipids (mainly triglycerides) throughout the body. It is synthesized in the liver, and its synthesis begins with MTP’s lipidation of the structural protein Apo B-100. The lipidated Apo B-100 is now called VLDL, which can now be secreted into the bloodstream. Next, Apo C-II on the VLDL particle binds to lipoprotein lipase in capillary beds. Together, they release triglycerides from VLDL and deliver them to tissues as free fatty acids.
Once VLDL loses some of its triglycerides, it is now termed IDL (intermediate density lipoprotein, which is also known as a VLDL remnant). IDL is then either taken up by Apo E in the liver, or it is converted into LDL by hepatic lipase.
LDL (low density lipoprotein) is rich in cholesterol, and LDL’s main function is to deliver endogenous cholesterol to the rest of the body. To do this, LDL’s Apo B-100 binds to the LDL receptor. This facilitates the endocytosis of the LDL particle, and hence the delivery of its endogenous cholesterol contents.
“Low” vs “high” density refers to triglyceride content. Low density = high triglycerides and high density = low triglycerides. Low density lipoproteins contain relatively less triglycerides and relatively more cholesterol.
– Mutations in MTP can cause Abetalipoproteinemia.
– Homozygous mutations in LPL / Apo C-II can cause Familial Hyperchylomicronemia.
– Heterozygous mutations in LPL / Apo C-II or overproduction of VLDL can cause Familial Hypertriglyceridemia.
– Mutations in Apo E can cause Familial Dysbetalipoproteinemia.
– Mutations in the LDL receptor / Apo B-100 can cause Familial Hypercholesterolemia.