Its function is to hydrolyze triacylglycerol to diacylglycerol and carboxylate (free fatty acids) with the addition of water.

[7] These remaining remnants of LDL can be sent back to the liver, where it can be stored for later use or broken down to harness its energy.

[8] This process creates HDL3 (High density lipoprotein 3), a mature HDL molecule that has been esterified by another enzyme known as LCAT.

When HDL takes up free fatty acids from cells to prevent plaque build-up, it begins to increase its overall negative charge and instead stimulates HL to catalysis the triacylglycerides inside of VLDL (very low density lipoprotein).

It has been shown that women contain lower levels of ApoE along with an increased amount of free HL enzymes in their circulatory system when compared to men.

The production of estrogen in women is also believed to reduce the activity of HL by serving as an inhibitor of gene transcription.

[7] Secretion of HDL from the liver into the circulatory system regulates the release of HL into the body's bloodstream.

Another lipoprotein, ApoA-I, which increases release of HDL was shown to have a similar effect by mutating the gene that coded it.

Thus, the inability of endothelial cells to take up free fatty acids becomes higher and more IDL gets stored in the liver.