Lipoprotein structure and function Flashcards
3 types of lipid complexes and their cores
- vesicle - aqueous core
- micelle - no core
- microemulsion - hydrophobic core
what is structure of lipoprotein
- phospholipid shell with apolipoproteins embedded
2. filled with triglycerides and cholesterol esters
order of lipoproteins from least to most dense
CM<HDL
apolipoproteins in HDL
A,C,E
apolipoproteins in LDL
B100
order of lipoproteins from least to most protein
CM<HDL
order of lipoproteins from most to least triglcerides
CM<HDL
3 non-exchangable lipoproteins
Apo(a), B100, B48
feat of apoA-1
main HDL - activates LCAT
feat of apoB
key structural protein of all but HDL
what is exogenous lipoprotein metabolism path
- lipids from diet
- abs. by small intestine
- come out as CM
- CM to capils.
- LPL breaks down to give FFAs
- left with CM remnant which goes to liver to bing with LDL-R
endogenour path
- liver produces VLDL
- VLDL to capils
- LPL makes FFAs
- IDL left over and goes to liver or become LDL
- LDL then meets LDL receptor for pick-up
what is LDL-receptor
present in liver adrenal some tissues, not heart, skeletal muscle - binds apo-B
what is LDL receptor-like protein
like LDL-r but recognizes others besides just apo-B
what is LPL
hydrolyzes TG of CMs and VLDL
what is heptic lipase
functions as both lipase and phospholipase with IDL and HDL
how does cholesterol come into small intestine
chol. transporter
how is chol. excreted back into lumen
ABCA or ABCG transporter
how much chol. is synthesized vs. consumed
syn. 900 mg/day
consume 300 mg/day
1200 fecally excreted
what happens of problem in LDL-r
doesn’t get taken up and get hypercholesterolemia - FH
3 causes of hypercholesterl
- mutation of LDL-r
- mutation of apo-B ligand - can’t grab LDL-r
- mutation in PCSK9 - limits bind and endocytosis
2 common disorders of LDL or VLDL metabolism
- poor clearance due to LDL rec
2. VLDL overproduction in diabetes of metabolic syndrome
how is HDL raised
can’t pharma - excercise
how much do men and women benefit from HDL
women - 3%
men - 2%
where does apo-A1 come from
liver 70%
intest. 30%
how does HDL protect atherosclerosis
reverse chol. transport- takes it out of cells in peripheral tissue and bring back to liver
what turns HDL to VLDL and LDL
CETP - choleteryl ester transfer protein - have tried unsuccessfully to block in past
