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FOM 3 wks 1-6 > lipoprotein metabolism - biochem > Flashcards

lipoprotein metabolism - biochem Flashcards

1
Q

cholesterol is a precursor for what

A

steroid hormones, bile acids, vit. D

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2
Q

what is the rate-limiting step of de novo cholesterol synthesis

A

HMG-CoA
–(HMGCR)–>
mevalonate
->
->
->
cholesterol

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3
Q

what enzyme is the target of cholesterol-lowering statin drugs

A

HMGCR

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4
Q

what is SREBP

A

a TF that activates HMGCR

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5
Q

how is HMGCR inhibited through negative feedback

A

SREBP is inhibited by cholesterol

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6
Q

liver is distribution hub of _____

A

cholesterol

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7
Q

reaction for cholesterol ester synthesis in cells

A

free cholesterol
–(ACAT)–>
cholesterol ester

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8
Q

reaction for cholesterol ester synthesis in plasma

A

free cholesterol
–(LCAT)–>
cholesterol ester

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9
Q

free cholesterol

-polarity
-function

A

amphipathic
membrane structure

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10
Q

cholesterol ester (CE)

-polarity
-function & where
-transported how

A

hydrophobic
storage
in lipid droplets within cells
transported in plasma inside lipoprotein particles

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11
Q

how do lipoprotein particles transport cholesterol

A

in the core of lipoprotein particles in the form of cholesterol ester

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12
Q

lipoprotein composition

A
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13
Q

integral apoproteins

-definition
-function

A

structural component of lipoproteins (can’t be removed)

gives “identity” to the lipoprotein

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14
Q

peripheral apoproteins

-definition
-function

A

transferable between lipoproteins

controls activity of lipoprotein-metabolizing enzymes

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15
Q

TG-rich lipoproteins

A
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16
Q

cholesterol-rich lipoproteins

A
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17
Q

lipoprotein CM is _____ & contains _____

A

TG-rich

ApoB-48
ApoE
ApoC-II

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18
Q

integral apoproteins

A

ApoB-48
ApoB-100
Apo(a)
ApoA-I

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19
Q

peripheral apoproteins

A

ApoE
ApoC-II

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20
Q

lipoprotein VLDL is _____ & contains _____

A

TG-rich

ApoB-100
ApoE
ApoC-II

21
Q

lipoprotein CMR is _____ & contains _____

A

cholesterol-rich

ApoB-48
ApoE

22
Q

lipoprotein IDL is _____ & contains _____

A

cholesterol-rich

ApoB-100
ApoE

23
Q

lipoprotein LDL is _____ & contains _____

A

cholesterol-rich

ApoB-100

24
Q

lipoprotein Lp(a) is _____ & contains _____

A

cholesterol-rich

ApoB-100
Apo(a)

25
lipoprotein HDL is _____ & contains _____
cholesterol-rich ApoA-I ApoE ApoC-II
26
lipoprotein Lp(a) has high _____, contributes to _____, & how is it shown in labs
high heterogeneity contributes to atherosclerosis in labs it is lumped in with LDL
27
why does hydrolysis of remaining TG not occur in CMR (which would produce additional smaller lipoproteins)
bc ApoB-48 is too short to bind an LDL receptor
28
how are cholesterol-rich lipoproteins produced from TG-rich lipoproteins
CM, VLDL --(LPL hydrolyzes TG)--> CMR, IDL
29
how is LDL produced from IDL
hydrolysis of remaining TG in IDL occurs
30
what Apo protein does the liver express
only ApoB100
31
general pathway of cholesterol in the body
dietary cholesterol -> absorbed in intestines -> delivered to liver -> excess hepatic cholesterol (as bile acids) is transported back to intestine for fecal excretion
32
detailed pathway of cholesterol absorption into chylomicrons
dietary cholesterol + plant sterols (sitosterols) taken into enterocytes via NPC1L1 (cholesterol transport protein) -> cholesterol esterified by ACAT to form cholesterol ester -> chylomicron formed -> chylomicron exocytosed from enterocyte to the lymph and into the circulation -> plant sterols leave enterocyte & back to where they started via ABCG5/8 (sterol efflux protein)
33
components of a chylomicron
cholesterol ester TAG PL (phospholipid) fat-soluble vitamins -> MTTP loads all of them onto ApoB-48
34
what is a deficiency in ABCG5/8 called
sitosterolemia
35
what happens if NPC1L1 (Ezetimibe) is inhibited
decreased cholesterol absorption -> decreased plasma cholesterol
36
how is dietary cholesterol delivered to the liver
by CM remnants
37
LDLR pathway
LDL binds to LDLR through AopB-100 -> this complex taken in by endocytosis -> LDL & LDLR separate in endosome -> LDLR recycled back to plasma membrane -> LDL goes to lysosomes & enters cellular cholesterol pool
38
v intracellular cholesterol = ___ LDLR = ___ LDL-c
^ LDLR, v LDL-c
39
^ intracellular cholesterol = ___ LDLR = ___ LDL-c
v LDLR, ^ LDL-c
40
what are the main bile acids that cholesterol is converted into
cholic & chenodeoxycholic acids
41
what is the rate-limiting enzyme of bile acid synthesis
CYP7A1
42
how is bile acid synthesis regulated
negative feedback of bile acids inhibits CYP7A1 via transcription factor
43
how are bile acids delivered to duodenum
via bile
44
% of excreted bile acids that are reabsorbed, & how are they reabsorbed
95% reabsorbed to liver through portal vein
45
reverse cholesterol transport mechanism
LDL enters intima layer of artery -> LDL oxidized by free radicals -> gobbled up by macrophages, makes foam cells -> HDL causes reverse cholesterol transport from artery to liver
46
what does HDL protect against by initiating reverse cholesterol transport
atherosclerosis
47
mechanism if foam cells accumulate in artery
atherosclerotic plaque build up -> blood vessels narrow -> ischemia, MI
48
mechanism of how bile acid reabsorption inhibition lowers cholesterol
bile acid reabsorption inhibition -> less bile acid in liver -> CYP7A1 no longer inhibited -> more cholesterol converted to bile acid -> less cholesterol in liver -> causes more expression of LDLR on surface -> more LDL uptake -> lower plasma LDL

FOM 3 wks 1-6 (27 decks)

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