High density lipoprotein physiology: Difference between revisions
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====Synthesis and Uptake of Cholesterol==== | ====Synthesis and Uptake of Cholesterol==== | ||
* HDL consists majorly of apo A-I and/or apo A-II. Both organs synthesize apo A-I while only the liver synthesizes apo A-II. HDL is normally synthesized consisting of composed mainly of [[phospholipids]] and [[apolipoproteins]]. | * HDL consists majorly of apo A-I and/or apo A-II. Both organs synthesize apo A-I while only the liver synthesizes apo A-II. HDL is normally synthesized consisting of composed mainly of [[phospholipids]] and [[apolipoproteins]]. | ||
* Free apo A-I is released into the plasma as nascent HDL. This readily takes up excess free cholesterol (FC) from peripheral tissues such as [[fibroblast]]s and [[macrophage]]s mediated by either ATP-binding cassette A1 ([[ABCA1]]), G1/G4, [[Scavenger receptor#Types |scavenger receptor class B type 1 (SR-B1)]], [[Cyp27A1]], caveloin, and [[Passive transport|passive diffusion]], leading to the formation of discoid HDL. | * Free apo A-I is released into the plasma as nascent HDL. This readily takes up excess free cholesterol (FC) from peripheral tissues such as [[fibroblast]]s and [[macrophage]]s mediated by either ATP-binding cassette A1 ([[ABCA1]]), G1/G4, [[Scavenger receptor#Types |scavenger receptor class B type 1 (SR-B1)]], [[Cyp27A1]], caveloin, and [[Passive transport|passive diffusion]], leading to the formation of discoid HDL (a.k.a. pre-βHDL). | ||
* Apo A-I activates lecithin:cholesteryl acetyltransferase (LCAT) which catalyses the esterification of the free cholesterol bound to the discoid HDL. The [[Apolipoprotein A1]] acts as a signal protein in mobilizing cholesterol esters from within the cells. | * Apo A-I activates lecithin:cholesteryl acetyltransferase (LCAT) which catalyses the esterification of the free cholesterol bound to the discoid HDL. The [[Apolipoprotein A1]] acts as a signal protein in mobilizing cholesterol esters from within the cells. | ||
<font color="white">aaaaavvvvvvccccccattttttttttttttttttttttttaaaaaaaaaa</font><font color="red">LCAT</font> | <font color="white">aaaaavvvvvvccccccattttttttttttttttttttttttaaaaaaaaaa</font><font color="red">LCAT</font> | ||
<font color="white">aaaaavvvvvvaaaaaaaaaaa</font>Lecithin + Cholesterol ———-> Lysolecithin + Cholesterol ester | <font color="white">aaaaavvvvvvaaaaaaaaaaa</font>Lecithin + Cholesterol ———-> Lysolecithin + Cholesterol ester | ||
====Maturation and Transfer of Cholesterol==== | ====Maturation and Transfer of Cholesterol==== | ||
Revision as of 18:18, 13 September 2013
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ayokunle Olubaniyi, M.B,B.S [2]
Overview
Physiology
HDL Metabolism
The metabolism of HDL can also be described as the Reverse Cholesterol Transport System. HDL serves a mode of transportation for the excess cholesterol from peripheral tissues to the liver.
Synthesis and Uptake of Cholesterol
- HDL consists majorly of apo A-I and/or apo A-II. Both organs synthesize apo A-I while only the liver synthesizes apo A-II. HDL is normally synthesized consisting of composed mainly of phospholipids and apolipoproteins.
- Free apo A-I is released into the plasma as nascent HDL. This readily takes up excess free cholesterol (FC) from peripheral tissues such as fibroblasts and macrophages mediated by either ATP-binding cassette A1 (ABCA1), G1/G4, scavenger receptor class B type 1 (SR-B1), Cyp27A1, caveloin, and passive diffusion, leading to the formation of discoid HDL (a.k.a. pre-βHDL).
- Apo A-I activates lecithin:cholesteryl acetyltransferase (LCAT) which catalyses the esterification of the free cholesterol bound to the discoid HDL. The Apolipoprotein A1 acts as a signal protein in mobilizing cholesterol esters from within the cells.
aaaaavvvvvvccccccattttttttttttttttttttttttaaaaaaaaaaLCAT
aaaaavvvvvvaaaaaaaaaaaLecithin + Cholesterol ———-> Lysolecithin + Cholesterol ester
Maturation and Transfer of Cholesterol
- The esterified cholesterol moves into the hydrophobic core of the HDL, changing the HDL particle from discoid to spherical (mature HDL). This process also prevents the re-uptake of cholesterol by cells. LCAT is responsible for the maturation of HDL particle.
- The esterified cholesterol can be delivered back to the liver through a number of routes:
- By the action of cholesterylester transfer protein (CETP) - CETP, secreted in the liver, transfers cholesterol from HDL to the apo B–containing lipoproteins e.g., very low-density lipoprotein (VLDL) or intermediate-density lipoprotein (IDL) to be taken up by the liver. Mutations of this transport protein gene causes familial HDL deficiencies and Tangier disease
- HDL particles may be taken up directly by the liver
- Free cholesterol may be taken up directly by the liver
- HDL cholesterol esters may be selectively taken up via the scavenger receptor SR-B1, which is expressed in the liver.
Catabolism
- Triglyceride lipases degrade these cholesterol-deplete HDL particles into small, dense HDL which after dissociation, release apo A-I (nascent HDL). The apo A-1 then either rapidly reuptakes cholesterol again by ABCA1 to form discoid HDL or it is endocytosed in the kidney tubule or cleared via glomerular filtration.