B4-092 Lipoprotein Structure and Metabolism Flashcards
degrades TGs remaining in LDL and chylomicron remnants
hepatic lipase
apoA-1 is found on
HDLs
activates LCAT
apoA1
apoB-100 is found on
LDL, VLDLs
binds LDL receptor
ApoB-100
ApoB-48 is found on
chylomicrons
mediates chylomicron secretion into lymphatics
apoB-48
apoE
ApoC-II is found on
chylomicrons, VLDL, HDL
lipoprotein lipase cofactor that catalyzes cleavage
apoC-II
apoE is found on
chylomicrons
VLDL
HDL
degrades TG in circulating chylomicrons and VLDL
lipoprotein lipase
degrades TGs remaining in IDL and chylomicron remnants
hepatic triglyceride lipase
catalyzes esterification of 2/3 plasma cholesterol
LCAT
- regulation of LDL levels
- redistribution of cholesterol
- utilization of cholesterol
LDL receptors
- uptake of cholesterol loaded chylomicron remnants and HDL
- delivery of cholesterol to liver for excretion
LDL receptor related protein
selective uptake of cholesteryl esters
scavenger receptor
- delivers dietary TGs to peripheral tissues
- secreted by intestinal epithelial cells
chylomicrons
delivers cholesterol to liver in the form of chylomicron remnants
chylomicrons
- delivers hepatic TGs to peripheral tissues
- secreted by liver
VLDL
- delivers TGs and cholesterol to liver
- formed from degradation of VLDL
IDL
- delivers hepatic cholesterol to peripheral tissues
- formed by hepatic lipase modification of IDL in the liver and peripheral tissue
LDL
taken up by target cells via receptor mediated endocytosis
LDL
- mediates reverse cholesterol transport from peripheral tissues to liver
- secreted from both liver and intestine
HDL
plasma HDL is [….] related to risk of CVD
inversely
elevated LDL is a major risk for
atherosclerosis
LDL not taken up by hepatic LDL receptors migrates into
vascular intima
oxidized LDL accumulates in foam cells and can damage intima via
foam cell necrosis
- caused by hepatic overproduction of VLDL
- high TG
primary hyper triglyceridemia
caused by absent or defective LDL receptors
or defective apoB-100 receptors
hypercholesterolemia
high cholesterol with normal TG
primary hypercholesterolemia
- accelerated atherosclerosis
- xanthomas
hypercholesterolemia
- defects in apoE
- increased chylomicrons and IDL-like particles
dysbetalipoproteinemia
- common disorder
- often with obesity, hyperinsulinemia, glucose intolerance, HTN
familial combined hyperlipidemia
complex lipid profiles, elevated total cholesterol
HDL often reduced
mixed hyperlipidemias
caused by defective ABCA1
tangier disease
statins
HMG CoA reductase inhibitors
efflux cholesterol across the canalicular membrane
ABCG5/G8
transport of bile acids into canaliculi
ABCB11
phospholipid floppase
ABCB4
tangier is caused by defective
ABCA1
what happens when ABCA1 is defective
cholesterol accumulates in cells because its not available to efflux it to HDL
reduced HDL, LDL and total cholesterol is characteristic of
Tangier disease
major apolipoprotein of HDL
apoA-1
cholesterol efflux from macrophages
ABCA1
phospholipid floppase in canalicular membranes of hepatocytes
ABCB4
bile salt export pump in canalicular membrane of hepatocytes
ABCB11
cholesterol efflux from hepatocytes
ABCG5/G8
dysfunction ApoA-1 will result in
decreased HDL
no reverse pathway
dysfuctional ApoA-1 is a major risk factor for
CVD
- produced by enterocytes
- carry dietary TGs to liver and periphery
chylomicrons
ligand for LDL receptor
ApoB-100
activates LCAT
ApoA-1
activates lipoprotein lipase
ApoC-II
ligand for SR-B1
apoE
acquires free cholesterol and transports it back to the liver
HDL
carry TGs from intestine
chylomicrons
carry TGs from liver
VLDL
transports cholesterol to peripheral tissues and potentially deposits some in capillaries
LDL
ApoA-1 activates
LCAT
apoB-100 is a ligand for
LDL receptor
apoE is a ligand for
LDL receptor
SR-B1
contains mainly cholesterol esters
HDL
- produced by liver
- important for transport of liver derived TGs
VLDL
made from VLDL loosing fatty acids and apolipoproteins
LDL