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Drew 922 > 4_2cholesterol > Flashcards

4_2cholesterol Flashcards

(66 cards)

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1
Q

What is the active form of HCR?

A

dephosphorylated (insulin)

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2
Q

How is HCR regulated?

A

feedback (transcription repression by cholesterol and bile) and phosphorylation (de-PO4 = active)

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3
Q

What causes statin side effects?

A

synthesis of HMG-CoA when cholesterol is low

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4
Q

Where is most cholesterol synthesized?

A

liver/intestine

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5
Q

dietary sources of cholesterol

A

egg yolk, red meat, liver

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6
Q

What diseases is cholesterol correlated with?

A

CVD, stroke

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7
Q

What are the characteristics of cholesterol’s structure?

A

1) 27 C; 2) 3’ S-beta-up OH; 3) 5-6 ene; 4) 8C side chain; 5) 3 6-membered and 1 5-membered ring

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8
Q

What are the effects of bile acid sequestrants alone?

A

reduce cholesterol up to 20%

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9
Q

What are the effects of bile acid sequestrants in combo with a statin?

A

55% reduction

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10
Q

Is ezetimibe natural or synthetic?

A

natural

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11
Q

What is the mechanism of ezetimibe?

A

binds to NPC1L1 in brush border

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12
Q

What are ADRs of ezetimibe?

A

growth of plaques in arteries; HA, diarrhea

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13
Q

statin ADRs?

A

dementia, inhibition of CoQ synthesis, cancer, liver damage

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14
Q

pKa of glycine-conjugated bile acids?

A

4

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15
Q

pKa of taurine-conjugated bile acids?

A

2

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16
Q

What are the bile acids?

A

cholic and chenocolid

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17
Q

structure of cholic acid

A

alpha-hydroxy at 3, 7, 12

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18
Q

structure of chenocolic acid

A

alpha-OH at 3, 7

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19
Q

pKa of chenocolid/colic acids?

A

6

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20
Q

What modifications occur from cholesterol to bile acids?

A

1) 7-alpha-down OH, 2) oxidative cleavage of 3 C from side chain (COOH); 3) 3-alpha-down OH, 4) saturated 5-6, 5) maybe alpha-OH-down at C12

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21
Q

What are bacteria’s effects on bile acids?

A

deconjugate and dehyroxylate the 7-alpha-OH

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22
Q

What are the secondary bile acids?

A

deoxycholic acid (from cholic); lithocholic (from deoxycholic)

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23
Q

What does the body do to 2ndary bile acids?

A

reconjugate (do not re-hydroxylate)

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24
Q

Diagnosis of hypercholesteremia.

A

200+ mg/dL

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25
How is hypercholesteremia caused?
1) familial (defective LDL receptor synthesis; hyperactive PCSK9); 2) high-cholesterol diet (down-regulates LDL receptor)
26
What contributes most to diabetic hypercholesteremia?
LDL receptor glycosylation
27
What proteins are in HDL?
1) apoCII, 2) apoE, 3) apo AI
28
function of apoc2
stimulate LPL degradation of TGs
29
function of apoE
ligand for liver receptor (CM remnants and HDL, not LDL)
30
function of apoA1
stimulates LCAT to form CE
31
function of CETP
HDL protein that exchanges CE for TG and PLs in VLDL
32
proteins in nascent CM
apoB48
33
what are the proteins in LDL?
apoB100; transfers apoC2 and apoE back to HDL
34
What causes LDL oxidation?
superoxide radicals, NO, H2O2
35
What substances are antioxidants?
vitamin C, E, carnitine, resveratrol, CoQ
36
What is the depository form of cholesterol?
bile acids
37
purpose of lipoproteins
transport FATS for storage and energy
38
describe contents of VLDL
10% cholesterol; 15% CE; some phospholipids; mostly TG
39
Describe location of cholesterol and CE in a lipoprotein.
cholesterol at membrane; CE at core
40
What is LCAT and where is it located?
lecithin:cholesterol acyltransferase, blood
41
What is ACAT and where is it located?
acyl:cholesterol acyltransferase, cells
42
How is CE formed?
esterification of 3'OH
43
What do statins look like?
mevalonate (competitive inhibitors)
44
How many carbons in squalene?
30
45
How many carbons in farnesyl Ppi?
15
46
How many carbons in isopentenyl Ppi and demethylallyl Ppi?
5
47
How many carbons in geranyl Ppi?
10
48
What is HTGL?
hepatic TAG lipase
49
What are the fates of LDL?
1) can enter LDL receptors on target cells; 2) can enter liver for cholesterol recycling; 3) can be oxidized
50
Functions of HDL
1) exchanges lipids/proteins with CM and VLDL; 2) takes up cholesterol from cell surfaces and lipoproteins; 3) converts cholesterol to CE; 4) returns CE to liver by reverse cholesterol transport
51
What proteins does the LDL receptor recognize?
apoE, apoB100
52
How is cholesterol metabolism regulated?
1) primarily by HCR; 2) rate of LDL receptor synthesis; 3) rate of ACAT esterification
53
Describe the specificity of the LPL receptor?
specific for blood lipoproteins relative to the other receptors
54
What does cholesterol do after uptake?
1) increases membrane rigidity; 2) decreases HCR and LDLr synthesis; 3) stimulates ACAT for CE storage
55
What does PCSK9 do?
binds to LDL receptor to initiate degradation
56
When is the LDLr downregulated and how?
hi [cholesterol] and by PCSK9
57
Describe the relative structure and specifity of LRP.
similar looking to LDL, but less specific for lipoproteins
58
What proteins does LRP recognize?
alpha2-macroglobulin and TPA; apoE
59
Where is LRP abundant?
liver, brian, placenta
60
How is LRP regulated?
synthesis stimulated by insulin; otherwise unaffected by [cholesterol]
61
Where are SR's prevalent?
macrophages
62
What things does the SR bind?
oxLDL; SRB1 binds cholesterol-loaded HDL
63
What are fatty steaks?
foam cells formed by macrophage uptake of oxLDL, early sign of atherosclerosis
64
How are SRs regulated?
not downregulated according to [cholesterol]
65
Why does apoE not really contribute to hypercholesteremia in t2dm?
1) apoE inside HDL and for short timeframe; 2) LDL doesn't use apoE
66
How does an MI develop?
foam cells stimulate proliferation of smooth muscle; smooth muscle migrates to intimal layer; intimal cells release lipids and collagen/elastin to form fibrous cap; necrosis, calcification, hemorrhage, cap rupture leads to embolism

Drew 922 (12 decks)

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