20 - Antihyperlipidemics Flashcards
most dense =
HDL
the least dense would be a chylomicron
dietary triglycerides and cholesteryl esters
chylomicron
endogenous triglycerides and cholesteryl esters
VLDL
cholesteryl esters and endogenous triglycerides
IDL
apoprtns associated with chylomicron
B-48
C
E
A
apoprtns associated with VLDL
C
B-100
E
apoprtns associated with LDL
B-100
apoprtns associated with HDL
A-I A-II C E D
3 roles of lipoprtns
- serve as cofactors for enzymes involved in lipoprtn metabolism
- serve as ligands for receptors
- structual stabillity of lipoprtns
Chylomicron metabolism
- nascent TAG rich chylomicrons with apoB48 leave the small intestine
- Apo C and Apo E added to chylomicron from HDL
- lipoprtn lipase degrades TAG in CM at adipose tissue
- Apoc C is returned to HDL
- CE rick CM remnant bind through apoE to receptors on liver where endocytosed
what activates lipoprtn lipase?
apo C
metabolism of hepatic origin lipoprtns
- liver secretes nascent TAG rich VLDLs with Apo B100
- Apo C and Apo E transferred to VLDL from HDL
- Liportn lipase activated by apoC degrades TAG in VLDL
- Apo C and Apo E returned to HDL (NOW AN IDL)
- LDL binds to specific receptors and are endocytosed
the only place where cholesterol can be eliminated
liver
___ of bile acids/salts are excreted in feces daily
5%
95% reabsorbed and returned to liver
accepts excess cholesterol from peripheral tissues
HDL
HDL is transported to the liver where it binds to SRB1 through ApoA and CE are selectively delivered to hepatocytes
what enzyme turns a nascent HDL into a CE full mature HDL
LCAT
lecithin:cholesterol acyltransferase
what apoprtn activates LCAT
apoA-I
which apoprtn is a cofactor for lipoprtn lipase
Apo C-II
Major goals of clinical management of dyslipidemia
- prevent acute pancreatitis
(severe hypertriglyceridemia) - preventionof cardiovascular disease (reduce LDL reduces CVD risk)