Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CV > 6. Part B lipo biochem > Flashcards

6. Part B lipo biochem Flashcards

1
Q

What is responsible for esterifing free cholesterol to CE

~ for example, excess free cholesterol can be stored~

A

ACAT (Acyl-CoA Acyctrasferase)

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

regulates absorption of dietary cholesterol in liver, thus makes good pharmK target
esterifies free cholesterol–> CE

A

ACAT-2 (found in intestine and liver)

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

Where is ACAT-1 and what is it’s role

A

in macrophages, foam cells, adrenocortico, skin&raquo_space;> key for foam cell formation and cholesterol homeostais in extra-hepatic tissues

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

Fate of VLDL remants

A

once LPL shrinks VLDL–> goes back to circulation and withing 30 mins will either
-get cleared by liver via liver LDL receptors and LRP
OR
-LPL and hpatic lipase convert–> to LDL by removing TGs

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

Virtually all LDL particles in plasma come from

A

VLDL

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

LDL is enriched in:

LDL major apo is:

A

cholesterol and CE

apoB 100

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

rate of removal of VLDL remnants is a derterminant of:

A

LDL production

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

How is LDL made from VLDL

A

removal of residual TG via hepatic lipase facilitated by ApoE

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

What ligand binds to LDL-R

A

apo100

**liver removes 75% of all LDL from plasma

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

What else has LDL-Rs besides liver

A

muslces and adipocytes: they can also take up LDL thus cholesterol via receptor-mediated endocytosis

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

Half life of:
chylomicron
VLDL
LDL

A

5-20 mins
30 mins to 1 hour
2.5 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where in cell is LDL-R made

A

made on the RER and then moves to plasma membrane via golgi apparatus
otherwise it is segregated into a vesicle post endocytosis and recycled back to surface

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

What is the cause of autosomal dominant hypercholesterolemia?

A

mutation of LDL receptor (over 900 kinds)

see elevated plasma LDL

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

What effect does throxine and estrogen have on LDL-R

A

they enhance LDL-R gene expression; thus ahve LDL lowering effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do cells regulate LDL-R expression?

A

via TFs: SREBPs and SREBP cleavage activating protein called Scap

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

A serine protease that decreases steady state level expression of LDL-R on hepatocyte

A

PCSK9

PCSK9/LDLr complex is internalized and targeted for lysosomal degredation —> end up with increased LDL

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

what is better a GOF or LOF PCSK9 mutation

A

LOF mutation: then we get higher levels of LDL-R thus lower LDL-C levles = protects from CHD
(GOF makes more PCSK9 binding and internalizing and ddestroying LDL-R = bad)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

is Lp(a) good or bad?

A

its bad; risk factor for CVD

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

an LDL-like particle where apoB is covalently bound to apolipoportein(a)

A

Lp(a)

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

We see a ____ releationship btwn size of apo(a) isorform and Lp(a) plasma conc

A

inverse

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

is anti-oxidant, anti-thrombic, reduces vascular adhesion molecules on endothelium, stims endothelial repair, lowers inflammation

A

HDL

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

carries out reverse cholesterol transport

A

HDL

picks up cholesterol from peripheral cells–> takes to liver for excreation via bile

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

Most and second most abundant protein in HDL

A

apoA-I most abundant
apoA-II second most
***made in liver and inetestine and necessary for normal HDL production

24
Q

***made in liver and inetestine and necessary for normal HDL production

A

ApoA-I and apoA-II

25
Q

Mutation in apoA-I lead to:

A

HDL deficiency and accerleated atherosclerosis

–> mutation reduce capacity of ApoA-I to activate LCAT

26
Q

Membrane transporter expressed in liver, intestine, macros to promote efflux of cellular phospholipd adn cholesterol to lipid-free apoA-I

A

ATP binding casset transporter (ABCA1)

27
Q

helps release free cholesterol to apoA-I to make DISCOIDAL HDL

A

ABCA1

28
Q

Result of defective ABCA1

A

reduced choesterol efflux to apoA1 and aquisition of cholesterol by HDL is decreased; reduced HDL levels

29
Q

Loss of function of ABCA1; thus low levels of HDL and CE accumulation in liver, intestines, spleen, tonsils
can’t form spherical or discoidal HDL with LOW plasma cholesterol

A

Tangier disease

30
Q

How is preB HDL or discoidal HDL formed?

A
  1. ABCA-1 adds phospholips + FC to apoA-I= discoidal HDL
    -mostly happens in intestine
    OR
  2. Chylomicrons or VLDL–> TGs hydrolzed + loss of apoA-I and phospholipids–> forms preB HDL
31
Q

What must preBHDL aquire before LCAT helps form it’s CE core?

A

preBHDL gets free unesterified cholesterol from cell membranes of tissues

32
Q

What is the enZ that forms the CE core of HDL by esterifying free chosterol?

A

LCAT: from liver and circulates in blood

33
Q

How does HDL become spherical instead of discoidal

A

LCAT keeps esterifying cholesterol–> CE moves to core and gets more spherical

34
Q

What activates LCAT?

A

apoA-I

35
Q

role of ABCG1 in HDL

A

promotes cholesterol efflux to HDL

alters distribution of cholesterol on cell membane so that HDL can remove it

36
Q

What exchanges lipids betwen LDL and HDL

A

Cholesteryl ester transfer protein (CETP)

37
Q

What does CETP do?

A

transfers CE from HDL to VLDL/LDL/IDL in exchange for TGs

38
Q

what catalyzes transfer of phospholipids between lipoprotein classes

A

phospholipid transfer protein (PLTP)

39
Q

PLTP takes excess FC and phospholipds from surface of chylomicrons and VLDL following hydrolysis of TG to___

A

HDL

40
Q

What is needed for maximal activity of LCAT

A

PLTP

–> bc plays key role in generating preB-HDL the major acceptor of cellular cholesterold

41
Q

When is HDL a good substrate for hepatic lipase?

A

once CETP and PLTP mediate lipid exchange and HDL is rich in TGs

42
Q

What does HL do?

A

hydrolyzes TG and PL to make smaller HDL particles that recirculate and aquire more FC from tissues

43
Q

Androgens ____ HL activity, thus will overall _____ HDL-C values

A

increase HL activity

decrease HDL-C

44
Q

Estrogen ____ HL activity but doesn’t have as much of an effects as androges do

A

decrease HL activity

45
Q

hydrolyzes HDL phospholipds and makes smaller HDL particles that are catabolized faster

A

endothelial lipase

46
Q

over expression of Endothelial lipase reduced ____ and ____ levels to almost zezo

A

apoA-I and HDL

47
Q

What may inhibit EL activity?

A

apoAII

48
Q

What is our HDL receptor

A

Scavenger receptor BI (SR-BI)

seen in liver, ovaries, testes and adrenals

49
Q

mutations in SR-BI in humans confirmed:

A

SR-BI is key in maintaining plasma cholesterol levels and plays protective role against atherosclerosis

50
Q

During HDL catabolism, what is transferred to cells via SR-BI in ‘selective uptake?

A

CE core so ONLY LIPD uptake
entire HDL is NOT INTERNALIZED
–> lipid depleated particle will re-enter circulation to pick up more cholesterol

51
Q

Where are apoA I and apoA II from HDL taken up and degraded

A

removed synchronously via liver and kidney

52
Q

When AMP rises; kinase phosphorylates HMG-CoA reductase which will:

A

decrease activity and decrease cholesterol synthesis

-

53
Q

Glucagon and epinephrine cascade leads to:

A

phosphoryaltion of HMG-CoA reductase to decrease activity and decrease cholesterol synthesis

54
Q

Insulin cascase lead to DEphosphorylation cascade causing:

A

increased activity of HMG CoA reductase = increased cholesterol synthesis

55
Q

At low sterol levels; SREB-Scap is cleaved and moves to nucleus–>

A

increases HMGCoA reducatse and increaes LDL-R synthesis

CV (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions