Lipid Transport Flashcards
What is an apolipoprotein?
Proteins attached to a phospholipid layer of a lipoprotein. That can be integral (passing through the bilayer) or peripheral (resting on top of the bilayer) and are important in lipoprotein functions.
What is the lifecycle of a chylomircon?
Loaded in the small intestine, where apop B48 is added, before entering the lympatic system, travelling to the thoraic duct and entering the left subclavian vein, where apop C and apop E are aquired within the blood, apop c binds to lipoprotein lipase which realses the fatty acids, apop c dissociates and the chylomicron remnant returns to the liver, where apop E binds and is taken up by receptor mediated endocytosis.
How is a VLDL metabolised?
ApopB 100 is added during formation, apopC and ApopE are added from HDL in blood, binds to lipoprotein lipase on endothelial cells and becomes depleted of trigylercol.
How are IDLs and LDLs produced?
When VLDL trigylercol concentration reduces to 30%, it becomes a short lived iDL particle and when carbon depletes to 10%, apop C and apop E are released and a LDL is produced.
How do LDLs become foam cells?
LDLs do not have apopC or apopE so are not recognised by the liver, so have a longer half life and are more suspecible to oxidative damage, oxidised LDLs are taken up by macrophages which can transform them into foam cells.
How do LDLs provide cholesterol to the tissues?
Cells which need cholesterol express LDL receptors and can uptake cholesterol by receptor mediated endocytosis.
What do HDLs do?
The transfer of cholesterol back to the liver from the tissues.
How is nascent HDL synthesised?
It can be produced in the liver and intestine, and can bud off from chylomircons
How does reversal cholesterol transport work?
ABCA1 protein facilitates cholesterol transfer by LCAT.
Why is reverse cholesterol transport important?
Reduces the risk of macrophages forming foam cells
What is the fate of mature HDL?
Cells that require cholestrol can use scavenger receptors to obtain it from HDL, and it can be taken up using specific receptors.
What are the clinical signs of hypoloporteinamemias?m
High level of cholestrol in blood, cholestrol depostions in various areas of the body (xathenlesma, yellow patches on eyes) tendon xanthoma, nodules on tendons, corneal arcus where there is an obvious white circle around the eyes.
How are artherosleroctic plaques formed?
Oxidised LDL is recognised and engulfed by marcophages, foam cells acclimate in the initma of blood vessel walls to for, a fatty streak and a fatty streak can grow to form an artheroscelortic plaque.
What are the potential impacts of an athreosceloric plaque?
It can grow and enchroach on the lumen of an atery, causing angina, and it can also rupture, triggering thrombosis by activating platlets and the clotting cascade.
How do statipns work?
They inhibit the enzyme acetyl CoA reductase.
