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Biochem 385 Unit 2 > Lectures 21-22 Cholesterol Metabolism > Flashcards

Lectures 21-22 Cholesterol Metabolism Flashcards

(59 cards)

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1
Q

Cholesterol

A

membrane
made in liver from acetyl-CoA
transported by large lipoproteins
used to make steroids

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2
Q

Eicosanoids

A

fatty acid derivitaives
precursors to other blood clotting molecs and stuff
NOT DERIVED FROM CHOLESTEROLS

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3
Q

What is cholesterol derived from

A

ALL from acetyl-CoA

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4
Q

What IS cholesterol?

A

a lipid

its hydrophoibic

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5
Q

Generation of cholesterol: major points

A

rate limiting step: enzyme HMG-CoA reductase makes HMG-CoA into mevalonate
uses two NADPHs and releases a conezyme A
carbons come from acetyl CoA
regulation happens early!
its a complicated process

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6
Q

what enzyme does statin drugs target?

A

HMG CoA reductase

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7
Q

Is cholesterol metabolism hard or easy

A

LOTS OF STEPS

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8
Q

Compound… we start with a 2 carbon compound (acetyl CoA)…

A 
go to a 6 C
to a 5 C
put two together to get 10C then add 5C so we get 15C
then 2 of those makes 30C
lose a few carbons: end up with 27C
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9
Q

3 fates of cholesterol

A
  1. combined with fatty acid to make cholesterol ESTER
    esters can be stored or exported
  2. Cholesterols can become bile acids (less hydrophobic!)
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10
Q

Bile Acids can…

A

Solubelilze dietary fats
reabsorbed so they can can lower cholesterol
be excreted as waste

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11
Q

one way to lower cholesterol levels

A

use bile acid resins
bile acid resisn bind to bile acids
bile acids secreted instead of reabsorbed

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12
Q

Explain how eating bile acid resins can deplete the body of cholesterol

A

you need to make more bile acids from cholesterol
if we excrete them, more cholesterol will be used up in creating bile acids

resins bind up the bile acids to break down and excrete them

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13
Q

What do bile acid RESINS do?

A

aid in binding up and excreting bile acids

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14
Q

particles that choleseterols are solublized into so they can circulate

A

chylomocrions
LDL
VLDLs
HDL

all have hydrophobic core
surfaces have at least one apolipoprotein

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15
Q

Why do we solubilize cholesterol into things like VLDLs, HDLs, etc

A

so that they can circulate in the blood!

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16
Q

chylomicrons

A

very few cholesterol esters (3)

lots of triacylglycerols (85)

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17
Q

LDL

A 
some cholesterol esters (12)
some triacylglycerols (50)
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18
Q

VLDL

A 
Lots of cholesterol esters (37)
little triacylglycerols (10)
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19
Q

HDL

A

More cholesterols esters (15)

VERY little triacylglycerols (4)

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20
Q

How do we ID good and bad cholesterols???

A

amount of cholesterol esters

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21
Q

Consider that circulating plasma cholesterol is probably bad, then is it better to have high or low levels of LDL? HDL?

A

LOW levles of LDL good

HIGH levels of HDL good

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22
Q

structure of the cholesterol lipoproteins

A

cholesterols inside w/ triacylglycerols
lipid bilayer
protiens on outside

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23
Q

Which class of lipoproteins are responsible for the gross blood plasma that appears w/in one hour of eating the triple burger

A

chylomicrons

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24
Q

Chylomicrons in circulating and disributing fatty acids…

Study These Flashcards
A

form in intestines
can deliver fatty acids elsewhere
lipases: removal of fatty acids carried by them
remaining praticles go back to liver to be reused (can make VLDLs)

25
VLDLs in circulating and distributing fatty acids
can be made from left overs of chylomicrons circulate leave fatty acids in other tissues remnants are IDLs, can go back to liver or make LDLs again... BAD
26
LDLs in circulating and distributing fatty acids
can be made from left overs of VLDLs distribute cholesterol to other tissues this is why they're BAD
27
HDLs in circulating and distributing
picks up cholesterol left in tissues (likely by LDLs) brings found cholesterol back to liver "cholesterol scavenger" made in liver
28
How does HDL do cholesterol scavenging??
apolipoproteins on surface! activate serum protein LCAT LCAT pulls cholesterol out of cell membranes, esterifies it
29
How do we take the cholesterol out?
cell membranes made from phospholipids | LCAT takes a fatty acid tail from a phospholipid and attaches it to the cholesterols, takes this part away
30
Cardiovascular Diseases (CVD) due to...
cholesterol plaque buildup in arteries where walls are a little bit damaged can block blood flow or break off and cause stroke/heart attack
31
LDL... how they enter cells?
LDL interacts with cell receptors, brought in as a vescile vesciles divide, cholesterol esters and LDL brough in (in lysosome), receptors go back to surface cholesterol esters broken down, contribute to cellular cholesterol pool
32
What pathway is activated when cholesterol levels are low inside liver cells
LDL receptor protein production | nucleus says MAKE MORE
33
when cholesterol levels are high, what happens?
ACAT enzyme activated: cholesterols esterified Lipid droplets filled with cholesterol esters
34
How does having more LDL receptors on the cell increase the cholesterol pool?
receptors grab more LDL particles to bring into cell
35
Statin drugs!
inhibit cholesterol biosynth
36
How do statin drugs inhibit cholesterol biosynth??
block HMG-CoA reductase bind to enzyme active site to do so because its structure is similar to HMG-CoA reductase
37
How do statin drugs lower serum LDL levels and thereby reduce the risk of cardiovascular disease??
target intercellular pathway Blocking HMG-CoA reductase=lower cholesterol pool Then we active the LDL receptor protein production=more surface receptors so we bring in more LDL particles from SERUM then they won't be deposited in arteries!!!! YAY!!!
38
Blocking dietary cholesterol uptake. what drug?
Ezetimibe
39
How does Ezetimibe work?
block uptake of cholesterol from diet targets transporters from intestines from bringing cholesterols into cells reduce LDL serum levels by 20%, inc HDL levels by 5% WHY HDL inc???? liver says cholesterol levels are low, so HDL takes more cholesterol back to it
40
What if we hit both the dietary uptake and the biosynthetic process??
LDL levlels continue to decrease, but CVD doesnt decrease
41
Why doesn't combo drug work to lower rate of CVD? (it DOES decrease serum cholesterol though)
maybe LDL isn't the only thing that causes CVD we don't know everything, serum choleterols isnt the only factor in CVD
42
Steroids: synthesized from cholesterol. Where? | brief (very) pathway?
``` adrenal glands (produces testosterone for women) testes ovaries ``` Cholesterol-->progesterone--> steroids
43
Steriods and gene expression
very hydrophobic, so brouth into nucleus of cell | binding which causes conf changes which controls gene expression
44
Steroid Agonists
activate steroid receptor signaling | can turn on OR off gene expression
45
Steroid Antagonists
inhibit steroid receptors signaling, turn of RECEPTOR signaling
46
Eicosandoids
``` fatty acid derivitives paracrine signalers (inside cell) short term signals Prostaglandins Thromboxanes Leukotrienes ```
47
Prostaglandins
stim inflammatory response | control secretion of mucins that protect stomach lining from low pH
48
Thromboxanes
regulate blood vessel constriction and platelet aggregation
49
Leukotrienes
pro-inflammatory molecs | associated with asthma
50
Eicosandoids Production
ligand binding to GCPRs activates G proteins phospholipase A2 cleaves a tail of a membrane phospholipid, used to make eicosanoids from arachidonate by COX1 and 2, other things etc.
51
COX-1
in stomach generates prostaglandins from arachidonate to protect stomach lining EVERYWHERE in body
52
COX-2
generated at inflammation sites to CONTINUE inflammatory response to go from arachidonate to prostaglandin
53
Prostacyclin Synthase
prevent platelet aggregation | go from arachidonate to prostacyclin
54
What do aspirin and ibuprogen do?
inhibit COX 1 and COX2: Inhibit inflammatory response
55
Vioxx and Celebrex
inhibit COX-2, but also prostacyclin synthase a little bit
56
Aspirin
acetylsalicylic acid
57
COX-2 Inhibitors (to block inflammatory response)
Non-selective inhibitors (aspirin, Motrin): fit into enzyme active sites of COX 1 and 2 Selective: fit into enzyme active site of COX-2, inhibit prostocyclin synthase
58
What explains the side effect of aspirin and ibuporten in causing stomach bleeding
it inhibits production of mucins, which protect stomaching lining
59
What explains the side effect of Vioxx and Celebrex causing heart attacks
also inhibit prostocyclin synthase this leads to not being able to stop platelet agregation/decrease blood clotting you get a heart attack

Biochem 385 Unit 2 (13 decks)

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