Brainscape's Knowledge GenomeTM

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


See full index

Foundational Sciences I-II > Lipoproteins & Cholesterol Homeostasis > Flashcards

Lipoproteins & Cholesterol Homeostasis Flashcards

1
Q

lipoproteins shuttle ____, ____ (so we don’t form plaques)

LDL levels are now determined by ____

A

TAG’s
cholesterol esters
ELISAs

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

Normal Levels

Glucose = ____
Total serum cholesterol = ____
Serum TAG = ____
Serum HDL = ____

A

< 100 mg/dL
200 mg/dL
150 mg/dL
> 40 mg/dL

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

Cholesterol and TAG Rich Lipoproteins

  • Body balance of circulating lipoproteins.
  • Relationship between intracellular cholesterol and circulating cholesterol levels.
  • Role of LDL in formation of ____ and ____
  • Role of HDL in ____ transport
A

fatty streaks
atheroscleoritc plaque

reverse cholesterol

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

Cholesterol and TAG Rich Lipoproteins

relationship bt plasma cholesterol and coronary heart disease mortality rates are NOT ____

as plasma cholesterol elvels increase, you see a ____ in mortality

A

linear

substantial rise

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

Consequences of elevated plasma cholesterol

elevated plasma cholesterol >
elevated ____ > fatty streaks (yellow steaks) > form the basis for the recruitment of additional ____ and proliferation of ____ > formation of a ____ (all that is remaining of the lumen of the endothelium)

A

LDL
cholesterol
smooth muscles
thrombis

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

Lipoproteins

Common Features
 Synthesized in the \_\_\_\_ or \_\_\_\_. 
 Exchange \_\_\_\_ and \_\_\_\_ while in
circulation.
 Nascent or immature vs. mature forms vs remnants
A

intestines
liver
lipids
proteins

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

Lipoproteins

three forms: nascent (immature) form, mature form, remnant form (as it loses ____)

largest = ____ (TAG rich; L/P ratio is very lipid rich) (from ____ TAG/cholesterol)

smallest = ____ (can take cholesterol into itself and remove from the ____)

VLDL = ____ synthesized TAG/cholesterol

A 
lipid
chylomicron
dietary
HDL
plasma membrane
de-novo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Apo-proteins

Role of Apo-proteins
Increase \_\_\_\_
Maintain \_\_\_\_
May act as \_\_\_\_
May serve as ligands for \_\_\_\_
A

hydrophilicity
structure
enzyme activators
endocytosis

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

Apo-proteins

apo-proteins will determine ____ of individual lipoproteins

ApoA-1 > specific for ____
ApoB-48 > ____ (not the ligand for the ____ receptor)
ApoB-100 > ____ (ligand for the ____ receptor)
ApoC-2 > activates ____
ApoeE > involved with ____, involved with clearance > the ____ protein; allows the lipoproteins to be exited through the live

A 
primary functions
HDL
chylomicron
LDL
VLDL
LDL
lipoprotein lipase
all
"exit"
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The fate of a chylomicron
ApoE
• Chylomicrons- Carry ____ after re-esterification and packaging with ____.

A

dietary FA

apoB48

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

The fate of a chylomicron

in core: ____ and ____ (everything in core has FA); ____ is the outer monolayer

as passes through circulation; ApoC2 activates ____; TAG core of chylo is digest (FA used by ____ for energy; or into ____ and stored as TAG)

glycerol backbone > ____; used in syntehsis of phospholipds and TAGs

once TAG core depleted > becomes a ____ at this point; the ____ allows the remnant to bind to receptor on liver, be taken up and whatever is remaining will be broken down in ____ (free FA, cholesterol)

A

TAG
cholesterol ester
cholesterol

lipoprotein lipase
muscle
adipocytes

liver
remnant
ApoE
receptor-mediated endocytosis

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

Cholesterol and TAG Transport

• LDL is made from ____ through an ____ in the circulation
• ____ is the ligand for the LDL receptor.
• LDL has a long ____ and ____ concentration in plasma, hence it carries most ____ as cholesterol and Chol. Esters.

A 
VLDL
IDL
ApoB100
residence time
high
plasma cholesterol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cholesterol and TAG Transport

chylo - ____ FA
VLDL - ____ FA from liver; synthesized in the liver, contain an ____; which activate LPL > get a free FA that is used for energy in muscle or stored in adipocytes

VLDL > becomes an ____; half of the IDL is taken up by liver via ____; the other half is going to have that TAG-core cleaved even further > now becomes an ____ (the core is diminished even further; ____)

LDL: deliver choelsterol to ____ (40% to peripheral; 60% taken up by liver via ____)

LDL = ____ cholestroal; the longer it circulates (longer the residence time) > the more likely that the LDL will become ____; when it’s oxidized; it’s taken up by ____ (which makes ____) and stimulates ____ [this is the absolute worst type of lipoprotein]

A

dietary
newly synthesized
ApoC2

IDL
ApoE
LDL
hepatic TAG lipase

peripheral tissues
ApoB100

bad
oxidized
macrophages
foam cells
artherosclerotic plaque formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

High Density Lipoproteins (HDL)

HDL- synthesized in ____; little bit in ____
Transfers Apo E and Apo CII to ____ and ____
Exchanges cholesterol esters for TAG of ____ in a reaction catalyzed by ____

A 
liver
gut
chlyomicrons
VLDL
VLDL
CTEP (cholesterol ester transfer protein)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

High Density Lipoproteins (HDL)

Why is CETP beneficial?
• Catalyzes the transfer of ____ to VLDL which can now become a ____ (via lipoprotein lipase) which is taken up by the liver, hydrolyzed, and converted to ____.

allows HDL to pick up more ____ (and reverse chol trasnport)

decreasing TAG rich of core of VLDL; TAG-rich core is now depelted and can return to ____

(CETP and LPL have ____)

A

cholesterol esters
VLDL remnant
bile acids

cholesterol
IDL
similar functions

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

High Density Lipoproteins (HDL)- exchange of apo-proteins

 HDL deliver ____ and ____ to nascent chylomicrons and nascent VLDL

 After apo-CII activates Lipoprotein Lipase- it is ____ from the mature chylomicron
or the mature VLDL and returns back to ____

HDL in BS > flat structure > lipid ____ structures

give Apo-C2 and ApoE to chylomicrons or to nascent VLDL’s (once it is within, it is now ____)

A 
ApoCII
ApoE
removed
HDL
poor
activated
17
Q

Role of HDL-Reverse Cholesterol Transport
 HDL picks up cholesterol from the ____ and converts it to cholesterol esters with ____.

 LCAT is activated by ____.

 The cholesterol esters are delivered back to the ____ were they are utilized in bile acid formation or repackaged

 ____, scavenger receptor on liver binds HDL

A 
cell surface
LCAT
ApoA1
liver
SRB1
18
Q

Role of HDL-Reverse Cholesterol Transport

HDL can now take up cholesterol from the outer monolayer from msot cells; once it takes up cholesterol > it must ____ it (bc it esterifies within the core) > now a chol ester (using LCAT)

circulating HDL can go to liver > through a scavenger receptor (SRB1) > aren’t ____, the HDL can dump the lipid into the liver (SRB1 high ____ little ____)

A

esterify
endocytosed
capacity
specificity

19
Q

Regulation of Inter and Intra cellular cholesterol

Intracellular cholesterol levels through a balance between ____ and ____ of LDL particles by the LDL receptor.

intracellular cholesterol regualtes ____ cholesterol (the ones associated with LDL’S); this balance leads to an increased ____ of the LDL (of intracellular cholesterol and circulating LDL’s)

LDL-____ (mecahnism in peripheral cells)

A

cholesterol synthesis
receptor mediated endocytosis

extracellular
residence time
receptor-mediated endocytosis

20
Q

Relationship Between Serum and Intracellular Cholesterol Levels

1. Regulation of cholesterol biosynthesis.
A. At level of \_\_\_\_
 \_\_\_\_ dependent
 \_\_\_\_ expression
 Degradation of HMGCoA reductase by
\_\_\_\_
  1. Regulation of LDL receptor number.
    At level of ____ as cholesterol levels increase ____ of LDL receptor expression.

inside the cell: ____

regulated by number of LDLR’s on the cell surace (____ of the cell; regulates how much is taken up)

A

HMGCoA Reductase
hormone
gene
proteolysis

gene expression
down-regulate

HMG CoA Reductase
outside

21
Q

Regulation of Inter and Intra cellular cholesterol

1. When cells require cholesterol take up ____ via LDL-receptor

  1. LDL-Receptor complex is ____- and intracellular cholesterol increases
  2. Cholesterol is stored as a ____ (via ACAT).
  3. Increase intracellular cholesterol inhibits
    – ____ and down regulates ____ either via recycling or at level of synthesis. Will also decrease ____ levels
  4. As cholesterol levels inside cell decrease, cholesterol synthesis is ____ and LDL-receptor expression and cells surface localization ____
A 
LDL
endocytosed
cholesterol ester
cholesterol biosynthesis
LDL-receptor on cell surface
HMG CoA Reductase
stimulated
increases
22
Q

Esterification of intracellular cholesterol

The fatty acyl chain that is attached to the cholesterol is often ____
or ____

A

palmitate

oleate

23
Q

When you just have bad genes…

familial hyperalphlipoporteinemia > increases your ____ > ____, longer life

____ classes of mutations of LDL receptor

LDL receptor has a ligand binding domain; EGF precursor homology (maintains ____); cytoplasmic domain (helps in ____)

mutations in any one of these regions > various levels of ____ (depending on whether you’re homo/hetero for that mutation)

genetic predispositions to ____ circulating LDL’s

A 
HDL
beneficial
4
structure
RM endocytosis

hypercholesteroemia

increased

24
Q

Familial hypercholesterolemia: half the normal amount of LDL receptor isn’t enough!

  • ____ inherited disease due to mutations in LDL receptor gene
  • ____ have elevated cholesterol and early onset of cardiovascular disease (age 30-40)
  • ____ have very high cholesterol and often suffer heart attacks in childhood
A

dominantly
heterozygotes
homozygotes

25
Q

Arteriosclerosis (____ of the arteries)-is the physical manifestation of the underlying pathologic process called atherosclerosis.

Atherosclerosis -the pathologic process resulting in ____, peripheral vascular disease, and ____.

CHOLESTEROL IMPLICATED BECAUSE
1. The lesion in arterial ____ is loaded with C and its ester, CE.

  1. High blood C correlates with incidence of ____.
  2. Lowering C (with statins, inhibitors of C synthesis) decreases the incidence of ____.
  3. Feeding C to susceptible animals produces ____.
A 
hardening
heart attacks
stroke
intima
CHD
CHD
atherosclerosis
26
Q

Production of foam cells by phagocytosis of oxidized LDL

HDL are able to move freely within BS
in presence of ____ (all are generated cigarette smoke/viral infections)

oxidizing agents > oxidize the ____ > allow them to go through endothelial cell layer (where it has been disrupted)

also recruits monocytes (which then become ____) > underneath cell layer the macrophages take up the oxidized LDL’s through ____ > formation of a ____

foam cells > secrete ____ that end up altering the ____ muscle that is underneath the endothelial layer

____ soluble vitamins (E,A) and ____ soluble (C) > are all potent ____ > help prevent the oxidation of LDL (overall they are beneficial)

A 
oxidizing agents
LDL
macrophages
scavenger receptors
foam cell
GF/cytokines
smooth
lipid
water
anti-oxidants
27
Q

Evolution of an atherosclerotic plaque

  1. ApoB-containing lipoproteins, mostly ____, penetrate the subendothelial space of large arteries.
  2. ____ and ____ modification of LDL occurs
  3. Uptake of Ox-LDL in the ____ by scavenger receptors in ____-these are now foam cells. Scavenger receptors have high ____ and low ____
    Lesion is a ____
  4. Recruitment and proliferation of ____ muscle cells from the media. Lesion now has a fibrous cap- a ____
A

LDL

lipid oxidation
covalent

intima
macrophages
capacity
specificty
fatty streak

smooth
plaque

28
Q 
ACAT = \_\_\_\_ cholesterol ester formation
LCAT = forms cholesterol esters in lipid core of \_\_\_\_

____ chemical reaction

A

intracellular
HDL
identical

Foundational Sciences I-II (14 decks)

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