Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Biochem > Cholesterol > Flashcards

Cholesterol Flashcards

1
Q

cholesterol is a precursor to

A

aldosterone
cortisol
vitamin D
sex hormones; estosterone & estradiol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

structure of cholesterol

A

4 fused rings
branched hydrocarbon tail attached to C-17 of ring D
hydroxyl grp at C3 of A => Sterol

cell membrane cholesterol -> free -OH grp at C3 of A
plasma cholesterol -> has a FA esterified there = cholesteryl ester (even more hydrophobic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

cell membrane cholesterol vs.

plasma cholesterol

A

difference at C-3 of ring A

membrane - free -OH grp
plasma - FA esterified = Cholesteryl ester

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

specialized transport system for cholesterol?

why is this necessary?

A

lipoproteins

highly hydrophobic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

sources of cholesterol

A

diet - animal products
(plants do not contain cholesterol, and sterols are poorly absorbed)
de novo synthesis - mainly in liver, intestine, adrenal cortex, and repro tissues
(accounts for 70% of cholesterol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

subcellular location of de novo cholesterol synthesis

A

cytoplasm and rough ER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

carbon atoms for cholesterol come from

A

acetyl CoA

just like FA synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

reducing equivalents for de novo synthesis

A

NADPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

where does the energy driving de novo synthesis come from

A

hydrolysis of the high energy bonds in acetyl CoA and ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

the first two steps of cholesterol synthesis are similar to what other synthesis? how so? whats the diff?

A

ketone body synthesis

condensations of 2 acetyl CoA -> acetoacetyl Co A + (3rd) acetyl CoA -> 3-hydroxy-3-methylglutaryl CoA (HMGCoA)
enz: HMGCoA synthase

Different isozymes of HMGCoA Synthase
cytosolic -> cholesterol
mito -> ketone bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

HMGCoA Reductase

A

HMGCoA -> mevalonate

rate limiting, regulated step

target for statin drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q 
dolichol
ubiquinone (CoQ)
prenylated proteins

are all made from what intermediate in cholesterol synthesis?

A

farnesyl PP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

vitamin D is made from what intermediate in cholesterol synthesis?

A

7-dehydrocholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

regulation of cholesterol biosynthesis

A 
Regulation of HMGCoA Reductase
3 ways:
1. transcriptional control
2. proteosomal degradation
3. covaelent modification
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

transcription of the HMGCoA reductase gene is controlled by the transcription factor::

A

SREBP-2 (sterol regulatory element binding protein-2) binds to the sterol regulatory element (SRE) of the reductase gene.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

location of SREBP-2 and its associations

A

SREBP-2 integral to ER membrane
associated w:
SCAP (SREBP-2 cleavage activating protein)
- sterol-sensing domain
- high sterol => binds to Insig (insulin-induced gene product) = retention in the ER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

when sterol levels are low…

A 
Increase Chol Syn:
SCAP no longer interacts w Insig
SREBP-2/SCAP complex -> Golgi
Proteases (S1P & S2P) cleave SREBP-2 = soluble amino-terminal domain that enters the nucleus and acts as a transcription factor for;
HMGCoA reductase gene
HMGCoA synthase
LDL-R
PCSK9
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what about SREBP-1?

A

controls genes assoc w FA synthesis
reg by similar pathway
insulin (increase) glucagon (decrease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

proteosomal degradation

A

high sterol;
HMGCoA reductase interacts with Insig in the ER mem ->
ubiquitination and proteosomal degradation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

phosphorylation / deP of HMGCoA reductase

A

controlled by AMPK

HMGCoA reductase:
deP = Active -> insulin dec cAMP
P’lated = Inactive -> inc glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

AMPK regulates what other enzyme from a diff metabolic process

A

Acetyl CoA carboxylase

FA synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

in what form is cholesterol removed? why?

A

bile salts
excreted as intact cholesterol in bile

fused ring -> can’t completely break down to CO2 and H2O

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the components of bile? the use of bile?

A

mainly phosphatidylcholine & bile salts

surfactant to emusify fat in foods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

primary bile acids, what makes them into bile salts?

A

cholic acid
chenodeoxycholic acid

conjugation w/ glycine or taurine => bile salts
(makes them more amphipathic)

25
rate-lim step in bile acid production
cholesterol-7-alpha-hydroxylase into of -OH grp at C-7 of ring B; cholesterol -> cholic acid + Cholesterol - Cholic acid
26
fate of bile salts
secreted into intestine | excreted (5%) or reabsorbed (70%); enterohepatic recirculation
27
cholesterol is precursor to all classes of steroid hormones, name classes + examples
glucocorticoids - cortisol mineralcorticoids - aldosterone sex hormones - estradial, testosterone
28
apolipoproteins
specific proteins that are a part of plasma lipoproteins along with lipids lipids; TG, phospholipids, chol, chol e
29
whats different about HDL in terms of lipoprotein classes
``` its the only lipoprotein class that lacks B apoproteins migrates the farthest on electrophoretic mobility ```
30
chylomicron
transport fr intestine -> periphery TG is 98% of lipids Apo B-48 unique to chylomicrons - due to post-trans RNA editing of Apo B-100 in intestine -> smaller protein Short half life (hours) should be no CMs after an overnight fast
31
microsomal triaclyglycerol transfer protein (MTP) role
loads apo B-48 w/ lipid in the ER, then particle is moved out into golgi and sec into lymphatic system -> blood as nascent chylomicron
32
nascent vs. mature chylomicron
just apo B-48 = nascent chylomicron | + apo E & apo C-II (both from HDL) = mature
33
lipoprotein lipase
mem of endothelial cells everywhere EXCEPT LIVER recog; apo C-II hydrolyzes TAG -> glycerol + FA apo C-II returned to HDL removes 90% of TAG CM remnant cleaned up by liver (apo E receptors) (FA -> fuel, FA-albumin, adipose Glycerol -> lipid syn, glycolysis, gluconeogen)
34
accumulation of CM particles in plasma is due to a deficiency in
lipoprotein lipase or apo C-II = hyperlipoproteinemia Type I
35
function of VLDL, production
transport triaclyglycerol to periphery produced in liver nascent = apo B-100 microsomal triglyceride transfer protein (MTP) aids in the assembly of nascent VLDL secreted -> pickts up apo C-II & apo E from circ HDL
36
LDL have a higher concentration of ___ than ___ . Their main function is to carry
conc of cholesterol and cholesteryl esters > TAG, than VLDLs carry cholesterol to peripheral tissues Apo B-100 recog by LDL-Receptors (also recog apo E on IDLs and have a higher affinity for apo E = shorter plasma time for apo E)
37
LDL-Receptor binds to
LDL - apo B-100 and apo-E (IDL, higher affinity)
38
process of LDL-R recycling
after binding, localized to clathrin coated pits, forms endosome, proton pumps decrease the pH, causing lipoprotein to dissociate from receptor, receptor recyled to the surface cholesterol -> ER
39
increases in cellular cholesterol can reduces cellular cholesterol synthesis by
1. end prod inhibition of HMGCoA reductase 2. inc chol -> inc proteosomal degradation of red 3. transcription of LDL-R & HMG reductase genes decreased by inc chol 4. enzy acyleCoA:cholesterol acyltransferase (ACAT) esterifies chol w FA for storage, inc chol -> inc ACAT activity 5. serine protease PCSK9 blocks LDL-R recycling
40
ACAT
acylCoA:cholesterol acyltransferase (ACAT) esterifies chol to FA for storage inc chol increases its activity
41
PCKS9
a serine protease | blocks LDL-R recycling -> greater internalization of LDL -> reduced plasma LDL
42
familial hypercholesterolemia (FH)
genetic defect in LDL pathway atherosclerosis -> angina, MI genes mutated - LDL-R (most common), apo B, PCSK9 heterzygotes - serum chol 2-3x normal, MI age 30-50 tx statins homozygotes - serum chol 4-6x normal, MI age 20-25 tx much more difficult, LDL apheresis, liver transplant
43
HDL
formed in blood = lipid + apo A -1 (produced by liver and intestine) chol released from non hepatic tissue via ABCA1 transporter (aka chol efflux regulatory protein - CERP -> tangier disease) chol is esterified by LCAT (lecithin:cholesterol acyltransferase) which is activated by apo A-1 on the HDL => cholesterol ester cholesteryl esters make it more spherical / mature taken up by scavenger receptor class B type 1 (SR-B1)
44
what makes HDL "good"
reverse cholesterol transport - removal of chol from periphery and transport to the liver
45
Lipoprotein a / Lp(a)
= LDL and glycoprotein apoprotein a covalently attached to apo B-100 function unknown high livels assoc w increased reisk of coronary heart disease
46
apos associated with HDL
apo A 1 (unique to HDL) apo E apo C (donates apo E and apo C)
47
apo's associated with LDL
ONLY apo B - 100
48
apo's associated with VLDL
apo B -100 apo E apo C
49
what is Cholestyramine? what does it do?
bile acid sequesterant inc excretion of bile salts inc synthesis of bile acids by liver inc # of LDL-R on liver
50
Niacin tx
inhibits HSL lowers Lp (a), TG, LDL-C decreases clearance of apo A-1 from blood -> raises HDL
51
moderate alcohol consumption may protect against coronary artery disease by
increasing serum conc of HDL
52
lipoprotein that req apo A-1
HDL
53
aspirin may be helpful in preventing development of atherosclerosis bc it inhibits
COX 2 -> syn of TXA2 also inhibits COX1 but effect more imp on COX2 bc the platlets that produce clotting factors are anucleated and thus can't produce more protein
54
CETP
Cholesteryl ester transfer protein (CETP) | HDL exchanges cholesteryl ester for TAGs from VLDL via this enzyme
55
main function of VLDL
transports TG from liver to adipose and mm
56
main function of LDL
primary carrier of cholesterol in blood
57
main role of HDL
transport cholesterol from peripheral tissues to liver
58
ABCA-1 and SR-B1
ABCA-1 releases cholesterol from tissues SR-B1 is the hepatic scavenger that picks up the cholesterol HDL is the carrier
59
how do you calc total cholesterol?
TC = LDL-C + HDL-C + VLDL- C with, VLDL-C = TG / 5 (fasting)

Biochem (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions