Lipoprotein structure and function Flashcards

1
Q

3 types of lipid complexes and their cores

A
  1. vesicle - aqueous core
  2. micelle - no core
  3. microemulsion - hydrophobic core
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2
Q

what is structure of lipoprotein

A
  1. phospholipid shell with apolipoproteins embedded

2. filled with triglycerides and cholesterol esters

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3
Q

order of lipoproteins from least to most dense

A

CM<HDL

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4
Q

apolipoproteins in HDL

A

A,C,E

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5
Q

apolipoproteins in LDL

A

B100

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6
Q

order of lipoproteins from least to most protein

A

CM<HDL

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7
Q

order of lipoproteins from most to least triglcerides

A

CM<HDL

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8
Q

3 non-exchangable lipoproteins

A

Apo(a), B100, B48

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9
Q

feat of apoA-1

A

main HDL - activates LCAT

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10
Q

feat of apoB

A

key structural protein of all but HDL

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11
Q

what is exogenous lipoprotein metabolism path

A
  1. lipids from diet
  2. abs. by small intestine
  3. come out as CM
  4. CM to capils.
  5. LPL breaks down to give FFAs
  6. left with CM remnant which goes to liver to bing with LDL-R
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12
Q

endogenour path

A
  1. liver produces VLDL
  2. VLDL to capils
  3. LPL makes FFAs
  4. IDL left over and goes to liver or become LDL
  5. LDL then meets LDL receptor for pick-up
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13
Q

what is LDL-receptor

A

present in liver adrenal some tissues, not heart, skeletal muscle - binds apo-B

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14
Q

what is LDL receptor-like protein

A

like LDL-r but recognizes others besides just apo-B

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15
Q

what is LPL

A

hydrolyzes TG of CMs and VLDL

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16
Q

what is heptic lipase

A

functions as both lipase and phospholipase with IDL and HDL

17
Q

how does cholesterol come into small intestine

A

chol. transporter

18
Q

how is chol. excreted back into lumen

A

ABCA or ABCG transporter

19
Q

how much chol. is synthesized vs. consumed

A

syn. 900 mg/day
consume 300 mg/day
1200 fecally excreted

20
Q

what happens of problem in LDL-r

A

doesn’t get taken up and get hypercholesterolemia - FH

21
Q

3 causes of hypercholesterl

A
  1. mutation of LDL-r
  2. mutation of apo-B ligand - can’t grab LDL-r
  3. mutation in PCSK9 - limits bind and endocytosis
22
Q

2 common disorders of LDL or VLDL metabolism

A
  1. poor clearance due to LDL rec

2. VLDL overproduction in diabetes of metabolic syndrome

23
Q

how is HDL raised

A

can’t pharma - excercise

24
Q

how much do men and women benefit from HDL

A

women - 3%

men - 2%

25
Q

where does apo-A1 come from

A

liver 70%

intest. 30%

26
Q

how does HDL protect atherosclerosis

A

reverse chol. transport- takes it out of cells in peripheral tissue and bring back to liver

27
Q

what turns HDL to VLDL and LDL

A

CETP - choleteryl ester transfer protein - have tried unsuccessfully to block in past