Species Human Entrez 3991 | Human Mouse Ensembl ENSG00000079435 | |
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Aliases LIPE, AOMS4, FPLD6, HSL, LHS, lipase E, hormone sensitive type External IDs MGI: 96790 HomoloGene: 3912 GeneCards: LIPE | ||
Hormone-sensitive lipase (EC 3.1.1.79, HSL) also previously known as cholesteryl ester hydrolase (CEH) is an enzyme that, in humans, is encoded by the LIPE gene.
Contents
HSL is an intracellular neutral lipase that is capable of hydrolyzing a variety of esters. The enzyme has a long and a short form. The long form is expressed in steroidogenic tissues such as testis, where it converts cholesteryl esters to free cholesterol for steroid hormone production. The short form is expressed in adipose tissue, among others, where it hydrolyzes stored triglycerides to free fatty acids.
Nomenclature
During fasting-state the increased free fatty acid secretion by adipocyte cells was attributed to the hormone epinephrine, hence the name "hormone-sensitive lipase". Other catecholamines and adrenocorticotropic hormone (ACTH) can also stimulate such responses. Such enzymatic action plays a key role in providing major source of energy for most cells.
Function
The main function of hormone-sensitive lipase is to mobilize the stored fats. Mobilization and Cellular Uptake of Stored Fats (with Animation) HSL functions to hydrolyze the first fatty acid from a triacylglycerol molecule, freeing a fatty acid and diglyceride. It is also known as triglyceride lipase, while the enzyme that cleaves the second fatty acid in the triglyceride is known as diglyceride lipase, and the third enzyme that cleaves the final fatty acid is called monoglyceride lipase. Only the initial enzyme is affected by hormones, hence its hormone-sensitive lipase name. The diglyceride and monoglyceride enzymes are tens to hundreds of times faster, hence HSL is the rate-limiting step in cleaving fatty acids from the triglyceride molecule.
HSL is activated when the body needs to mobilize energy stores, and so responds positively to catecholamines, ACTH. It is inhibited by insulin. Previously, glucagon was thought to activate HSL, however the removal of insulin's inhibitory effects ("cutting the brakes") is the source of activation. The lipolytic effect of glucagon in adipose tissue is minimal in humans.
Another important role is the release of cholesterol from cholesterol esters for use in the production of steroids.
Activation
It may be activated by two mechanisms.