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Block 3; Week 4 Michelle > Valencik Lipid > Flashcards

Valencik Lipid Flashcards

1
Q

What are the 4 pathways of lipid transport?

A

Food–>any tissue
Liver–>other tissues
Other tissues–>Liver (reverse transport)
Adipose tissue –>Other tissues

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2
Q

What are the 5 lipid-like things that are transported around the body?

A 
Free Fatty Acids
Triglycerides
Cholesterol
Cholesterol Esters
Phospholipids
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3
Q

What are free fatty acids attached to as they go around the blood?

A

albumin

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4
Q

What is the storage form of cholesterol?

A

cholesterol esters

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5
Q

Lipids travel via _____.

A

lipoproteins

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6
Q

What makes up lipoproteins?

A

These are assemblies of a bunch of protein & lipid.
Proteins that are involved called apolipoprotein.
Bunch of lipids up in there.
A lot of the stuff is amphipathic w/ the hydrophilic heads on the outside. The hydrophobic stuff is swimming around the inside…including cholesterol esters & triglycerides

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7
Q

What are 2 ways in which lipoproteins can be separated out?

A

Gel electrophoresis

Density gradient centrifugation

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8
Q

If a thing has more lipid than it does protein…is it heavier or lighter?

A

It is lighter.

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9
Q 
In Gel electrophoresis...what would be the order of the following...with those that move the least listed first...
VLDL
HDL
LDL
Chylomicrons
A 
Chylomicrons
LDL
VLDL
HDL
**this means that HDL has the most protein in it. It was the most attracted to the positive charge.
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10
Q

Describe how density gradient centrifugation works.

A

this separates proteins based on their protein/lipid ratio…
When there are more lipids–>it is lighter.

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11
Q

How would the gel electrophoresis sample change if it were collected after fasting 8-12 hours?

A

There wouldn’t be any chylomicrons or VLDLs in the sample. These would be gone after a period of fasting…

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12
Q

What are the 4 major classes of lipids & characteristics of each?

A

Chylomicrons: huge & hydrophobic
VLDL: also hydrophobic
LDL: heavier, has more protein, smaller
HDL: teeny & heavy & full of protein

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13
Q 
8-12 hours after a meal, what are normal levels for the following:
Total Lipid
Triglycerides
Phospholipids
Free Fatty Acids
A

Total Lipid: 400-800
Triglycerides: 40-280
Phospholipids: 125-275
Free Fatty Acids: 8-25

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14
Q

8-12 hours after a meal, what are normal levels for the following:
Total Cholesterol
LDL Cholesterol
HDL Cholesterol

A

Total Cholesterol: 120-280
LDL Cholesterol: 65-200
HDL Cholesterol: 30-90

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15
Q

During fasting, where are most of the triglycerides found?

A

in VLDLs

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16
Q

What does total cholesterol include?

A

cholesterol & cholesterol esters

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17
Q

Where is most cholesterol–that is cholesterol & cholesterol esters found during fasting?

A

70% of this cholesterol is found in LDLs during fasting

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18
Q

What holds 86% of the triglycerides?

A

Chylomicrons

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19
Q

Describe the process of how lipids are handled in the body from consumption to absorption by an enterocyte.

A

Consume lipids.
Gallbladder secretes bile.
Bile salts emulsify the dietary fats in the SI to form micelles.
Intestinal lipases degrade the TAG.
The products of this breakdown are absorbed by the enterocytes.

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20
Q

What happens after lipids are taken up by enterocytes?

A

The breakdown products are reassembled into TAG.
the TAG & cholesterol & apolipoproteins are all assembled into a chylomicron. This is released into the lymph, eventually the blood…

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21
Q

Once the chylomicrons are in the blood…what happens?

A

ApoCII activates the lipoprotein lipase.
This converts the TAG in the blood to fatty acids & glycerol.
Fatty acids enter a variety of cells, especially the myocytes & adipocytes.
When the fatty acids are needed as fuel–>they are oxidized.
When the fatty acids are needed as storage–>they are reesterified.

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22
Q

What are 2 tissue types that do NOT have lipoprotein lipase & therefore do NOT take up the fatty acids?

A

Brain & Liver

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23
Q

When pancreatic lipase eats up the lipids…what is the most common product?

A

2-monoacylglycerol.

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24
Q

2MAG passes into enterocytes & it reassembled into TAGs. What can pass thru the enterocyte & then into lymph/blood w/o reassembly?

A

medium & short chain fatty acids

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25
Q

Where would medium & short chain fatty acids go after getting into the blood?

A

probably the muscle–>b/c it loves to use little fatty acids for energy.

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26
Q

What happens in the enterocyte during the process of reassembly of TAGs w/ long chain fatty acids?

A

There is a process that these fatty acids are fed into that involved acyl coA synthetase.
In the ER, they are made into TAGs.
They are then packaged into chylomicrons & put into the lymph!

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27
Q

What do enterocytes need to make the glycerol phosphate for TAGs? What do they lack?

A

Need glucose.

Lack glycerol kinase

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28
Q

What is the lifespan of chylomicrons? Of TAGs?

A

Chylomicrons: less than an hour
TAGs: 5-10minutes
**after fasting your blood looks clear…

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29
Q

How do the chylomicrons transition from blood to lymph?

A

First they are in lymph after the intestinal mucosa

@ the left subclavian vein…they get into blood! How exciting!

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30
Q

What is the name of the apolipoprotein that is ONLY found on the chylomicrons?

A

ApoB-48

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31
Q

What are the apolipoproteins that predominate before the chylomicrons make it into circulation?

A

ApoB-48
ApoA-I
ApoA-II
Apo-IV

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32
Q

What are the 3 roles of apolipoproteins?

A
  1. Regulate plasma lipid metabolizing enzymes.
  2. Facilitate lipid transfer.
  3. Mediate endocytosis
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33
Q

In the blood chylomicrons acquire more apolipoproteins from another source. Which source? Which proteins?

A

HDL
apoE
apoCII

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34
Q

Once the chylomicrons are chilling in the capillaries equipped w/ the apolipoproteins from the HDL…what happens next?

A

They bump into lipoprotein lipase attached to capillary endothelial cells of muscle or adipose tissue…the apo C-II activates the LPL.
the LPL hydrolyzes 80-90% of the TAGs inside.
Then the A & C apolipoproteins & some phospholipids & cholesterol peel off & go onto HDL. This transfer requires phospholipid transfer protein.
What is left behind is considered the chylomicron remnant & can’t be further broken down by LPL b/c it now lacks Apo C-II.

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35
Q

What apolipoprotein can inhibit the LPL activity?

A

Apo C-III

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36
Q

What detaches LPL from the capillary membrane?

A

heparin

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37
Q

Once again, which 2 organs lack LPL?

A

brain & liver

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38
Q

What activity increases the amount of LPL on adipocytes & decreases the amount on skeletal & cardiac muscle?

A

Food consumption increases the amount on adipocytes & decreases it elsewhere. This insures that in a well-fed state, the food is being stored properly.

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39
Q

Describe the features of the chylomicron remnant.

A

It is smaller than the original chylomicron.
Its apolipoproteins are B-48 & E.
Inside, there aren’t many TAGs. Now, there are a bunch of cholesterol esters.

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40
Q

What put the cholesterol esters into the chylomicron remnant?

A

HDL

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41
Q

Where does dietary cholesterol end up overall?

A

the liver!

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42
Q

What happens when a chylomicron remnant ends up next to a hepatocyte?

A

the apo E on the chylomicron remnant binds the LDL receptor on the hepatocyte.
Receptor-mediated endocytosis is initiated
The chylomicron remnant is funneled to lysozyme degradation. Sad end to your journey, buddy. Hope you enjoyed the ride!

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43
Q

What is the overall function of chylomicrons?

A

to deliver dietary TAGs to adipocytes & muscle & to deliver dietary cholesterol to the liver.

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44
Q

How & where are VLDLs made?

A

They are made in the liver w/ the excess carbs & fats that are there. These excess materials are made into TAGs & lipids.
The TAGs, lipids & cholesterol are packaged into VLDLs in the ER/Golgi.

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45
Q

What happens to the VLDLs once they are made in the liver?

A

They are excytosed directly into the blood.
This allows them to get to extra hepatic tissues.
Once the tissues take up the TAGs they use the free fatty acids to store energy or produce energy thru beta oxidation.

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46
Q

What is the extracellular lifespan of VLDLs?

A

less than 1 hour

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47
Q

What are VLDLs born with? What do they soon acquire in the blood from HDLs?

A

Born with: ApoB-100

Quickly acquire: ApoCs & ApoEs & cholesterol esters from HDL

48
Q

What is the difference b/w the ApoB48 of chylomicrons & the ApoB100 of VLDLs?

A

They are the same & coded for by the same gene. The only difference is that the ApoB48 is shorter by about half the length.
In intestinal cells, the RNA from this gene is post-transcriptionally modified to have a stop codon about halfway thru. When the ribosome makes it, it stops appropriately.

49
Q

Is the fact that ApoB48 is half the length of ApoB100 a result of proteolytic processing?

A

NO
it doesn’t happen once the protein is made…it happens when it is in the RNA form…
example of: tissue-specific RNA editing.

50
Q

So…this is where our VLDLs are in their journey…they have just been booted out of the liver, their warm & loving home. They now have to prove themselves. What is their first stop?

A

They bump into HDLs & acquire the tools they need for their adventure, including ApoCs, ApoEs, & cholesterol esters.

51
Q

So…now the VLDLs are equipped with their weapons–>their ApoCs, ApoEs, & cholesterol esters… Where is their next mission?

A

Their ApoC-II activates the lipoprotein lipase on the extra-hepatic tissues. The free fatty acids are pushed into the tissue.Then HDL reclaims the ApoCs. But wait, there’s more! The VLDLs take something from HDL this time. Cholesterol esters. They get a bunch with the help of a little friend.

52
Q

What is the little friend that helps the VLDLs get a bunch of cholesterol esters from HDL?

A

CETP: cholesterol ester transfer protein

53
Q

Sadly…this mission has changed the idealistic, youthful attitude of VLDL. Now, it must be called a VLDL remnant. What is a part of this remnant?

A 
ApoB-100 (its birthright)
Cholesterol Esters (thanks HDL)
Phospholipids
Some TAG & Cholesterol
ApoE (glad HDL didn't take that back too!)
54
Q

So, now that things have changed…the VLDL remnants must reevaluate themselves & make a choice. They can become 2 types.
One will return home…
The other will die trying to deliver more fat to tissues.
Describe what happens to the family guys.

A

1/2 the VLDL remnants are larger ones that will go back to the liver. These are ones that still have a lot of ApoE. They will experience receptor-mediated endocytosis.

55
Q

Describe what happens to the warriors.

A

1/2 the VLDL remnants are smaller. These are called IDLs. They bump into the hepatic lipase on a hepatocyte. This turns the IDL into a LDL. It sheds its ApoE, giving it to HDL…the last ticket home to the liver…gone forever.

56
Q

What happens to the IDL turned LDL now?

A

It attaches to LDL receptors on hepatic or extra hepatic tissues. It then experiences receptor mediated endocytosis.

57
Q

What exactly does hepatic lipase do?

A

hydrolyzes TAGs & phospholipids

this is independent of ApoC-II

58
Q

What things does hepatic lipase work on?

A

only IDLs & HDLs

59
Q

What attaches the hepatic lipase to the hepatocyte? What could compromise this attachment?

A

heparan sulfate proteoglycan

heparin could ruin this…

60
Q

Once the LDLs are about to be taken up by other tissues…what percentage of them is composed of cholesterol esters? Describe the rest of their composition.

A

40% Cholesterol Esters
20% phospholipids
only have ApoB-100
Also have some TAGs

61
Q

What is the lifespan of LDL?

A

3 days

62
Q

Explain how LDLs get into extra-hepatic tissues.

A

The ApoB100 on their surface binds to LDL receptors on the membrane of the extra hepatic tissue. Receptor mediated endocytosis ensues.

63
Q

What fraction of LDLs go to the extra hepatic tissues like this?

A

2/3

1/3 do not…these are the ones that are roaming around & put us at greater risk for plaque formation

64
Q

What do the extra hepatic tissues do with the LDL?

A

It goes to a lysosome, & the apoproteins are degraded & the cholesterol esters are converted into cholesterol. The cholesterol is used for the plasma membrane or ER.

65
Q

Which 2 things increase the binding of LDL to LDL receptors on extrahepatic tissues?

A

insulin

T3

66
Q

What decreases the binding of LDL to LDL receptors on extra hepatic tissues?

A

glucocorticoids

67
Q

When there is excess cholesterol in extra hepatic cells b/c of LDL uptake…what happens?

A
  • the enzyme ACAT converts the cholesterol to create cholesterol esters for storage
  • the transcription of HMG CoA reductase is repressed via SREBP
  • the transcription of LDL receptors is repressed
68
Q

What happens to the LDLs that don’t attach to the LDL receptors?

A

they are cleared by scavenger receptors

69
Q

What are scavenger receptors?

A

macrophages or endothelial cells that have a lower affinity for LDL than LDL receptors.
the spleen & intestine make a lot of them…

70
Q

When HDLs give LDLs old TAGs or whatever that are oxidized or acetylated…what happens to the likelihood that scavenger receptors will take them up?

A

It increases! The scavenger receptors’ affinity for LDL increases when they appear “aged.”

71
Q

What are the 3 ways to get lipids from other tissues back to the liver? Which of these ways is the most used?

A

Most Used Way: ApoE mediated endocytosis of remnant particles containing CE
Way #2: HDL transfers CE to hepatocytes via SR-BI
Way #3: Large HDL w/ plenty of ApoE are endocytosed into the liver cells…

72
Q

What are the remnant particles that we are talking about that transfer CE into the liver?

A

chylomicron remnant

VLDL remnant

73
Q

How do the remnant particles that transfer CE to the liver cells get the CE?

A

Remember: HDL gives it to them! this is helped w/ CETP.

74
Q

What are nascent HDLs? What are their characteristics? Where are they released from?

A

These are the HDLs that are first born/released from the liver & intestines. They are small & disc-shaped & they have a bunch of phospholipids. They lack cholesterol & cholesterol esters. They have various apolipoproteins based off of where they were formed.

75
Q

What apolipoproteins do HDLs that came from the liver have?

A 
ApoA-I
ApoA-II
ApoC-I
ApoC-II
ApoE
76
Q

What apolipoproteins do HDLs that came from the intestines have?

A

ApoA-I only

77
Q

What are the nascent HDLs converted into?

A

As the nascent HDLs accumulate cholesterols & cholesterol esters they get bigger & bigger.
HDL3: 5-9nm
HDL2: 9-12 nm (biggest size)

78
Q

What does HDL do primarily?

A

Well, it didn’t seem like it before when it was giving things to chylomicrons & VLDLs & then taking them back again…but HDLs are nice guys. They go door to door & get rid of people’s old stuff. They dock to the cell surface via ApoA-1 or Apo-E.
ABCA1 in the cell’s cell membrane pumps old cholesterol (acetylated etc) into the HDL & exchanges it for healthy cholesterol stored in HDL.

79
Q

What does ABCA1 stand for?

A

ATP-binding cassette protein-1

80
Q

So…when the HDL acquires all of this old cholesterol from cells…how does it make it into cholesterol esters?

A

an enzyme called LCAT catalyzes the esterification of the cholesterol

81
Q

What does LCAT stand for?

A

lecithin cholesterol acyl transferase

82
Q

Where is LCAT synthesized? How does it get into business w/ HDL?

A

It is synthesized in the liver.
It binds to the surface of the HDL.
ApoA-1 on the surface of HDL activates the LCAT.

83
Q

What is transferred in the rxn of LCAT?

A

a fatty acid @ the C2 position of the lecithin is transferred to the C3 OH position of the cholesterol

84
Q

Write out the rxn of LCAT.

A

Cholesterol + Phosphatidylcholine –>Cholesterol Ester + 2-lysophosphatidylcholine (aka lysolecithin)
**as a result nascent HDL–>HDL3 (a little bigger)
& the lysolecithin is transferred in the blood via albumin

85
Q

What is another name for CETP? Once again, what is its role?

A

CETP: cholesterol ester transfer protein
aka ApoD
**this helps transfer CE from HDL to a chylomicron remnant or VLDL remnant or LDL.

86
Q

When does CETP transfer the CEs?

A

…when everything is docked @ a cell

when the chylomicron or whatever is in contact w/ LPL.

87
Q

Explain the process of reverse cholesterol transport.

A

Cholesterol-rich HDLs go to the liver.
Hepatic lipase removes TAGs & phospholipids from them…this makes them smaller (HDL2–>HDL3)
SR-BI transfers CEs into the hepatocyte.

88
Q

What are 4 diseases caused by lipoprotein deficiency?

A

Abetalipoproteinemia
Tangier Disease
Apo CIII Deficiency
CETP Deficiency

89
Q

Abetalipoproteinemia

What is it deficient in?

A

Deficiency in a triglyceride transfer protein

**no ApoB lipoproteins, such as chylomicrons, VLDLs, LDLs are assembled

90
Q

Abetalipoproteinemia

What does this cause?

A

a reduction in plasma C & TAG of 75-80%

makes it hard for fat soluble vitamins, like Vitamin E to make it into tissues

91
Q

Abetalipoproteinemia

What does this cause clinically?

A

severe fat malabsorption
steatorrhea
TAG accumulation in intestinal mucosa & liver

92
Q

Tangier disease

What is deficient?

A

ABCA1 protein

therefore mature HDLs don’t form!

93
Q

What are the results of Tangier disease?

A

cholesterol ester deposits in reticuloendothelial cells, bone marrow, & Schwann cells
Orange Tonsils! From dietary carotene
early onset cardiovascular disease

94
Q

What happens w/ ApoCIII deficiency?

A

ApoCIII is an LPL inhibitor…so more LPL activity…decreased plasma TAGs & LDLs. There is also increased HDL.
Probably a good thing…1/4 of people who live into their 100s have this deficiency.

95
Q

What happens w/ CETP deficiency?

A

cholesterol esters can’t be transferred to other remnants…
LDL is low, HDL is high & CEs get to the liver directly via HDL
benign condition…but not a good pharmacological target–>doesn’t help.

96
Q

What are the apolipoproteins that don’t get transferred around?

A

ApoB-48

ApoB-100

97
Q

Review: what does Apo-A-I activate?

A

LCAT

98
Q

What things are ApoA-I & ApoA II found on? What is their ultimate source?

A

HDL & chylomicrons

Liver & intestine

99
Q

What is ApoB-48 found on? What is its source?

A

chylomicrons

intestine

100
Q

What is ApoB-100 found on? What is its source?

A

VLDL, LDL

Liver

101
Q

What are C lipoproteins found on? Their source?

A

almost all lipoproteins

liver

102
Q

Review: What does ApoC-II activate?

A

LPL

103
Q

Where is ApoD found?

A

HDL–functions like CETP?

104
Q

Where are ApoEs found? Ultimate source?

A

VLDL, IDL, chylomicrons

liver

105
Q

How is energy released from adipose tissue for use by other tissues?

A

The TAGs are broken down in the adipose tissue to fatty acids.
The fatty acids are released into the bloodstream.
The fatty acids go to muscle or whatever to provide it energy.
TAG are resynthesized in the liver when fatty acids are taken up…

106
Q

The enzymes for glycerolneogenesis are similar to those for ______.
What are the 4 enzymes involved?

A 
Gluconeogenesis
Pyruvate carboxylase
malate dehydrogenase
PEPCK
Glycerol 3-phosphate dehydrogenase
107
Q

PEP Carboxykinase activity is stimulated by what type of drugs?

A 
thiazolidinediones
a class of diabetic drugs
108
Q

We know that HSL is essential for TAG breakdown…what does phosphorylating/activating HSL do?

A

It promotes the translocation of HSL from the cytosol to the surface of the lipid droplet.

109
Q

T/F PKA & PKG are involved in TAG mobilization via phosphorylation or not of HSL.

A

Very true.

110
Q

What does perilipin do for TAG mobilization?

A

the phosphorylation of perilipin induces a physical alteration to the droplet surface that initiates lypolysis

111
Q

What is the role of FABP4 in TAG mobilization?

A

It docks to HSL & favors the outflow of fatty acids from the lipid droplet.

112
Q

Atrial natriuretic peptides can bind to receptors on adipose tissue & stimulate via cGMP pathways the activation of PKG. PKG can phosphorylate HSL. This promotes its translocation & TAG mobilization.
When ANP isn’t doin’ its thang…insulin has a window of opportunity to stop the nonsense of TAG mobilization. How does it try to do this?

A

Insulin binds to the receptors on the adipose tissue. It stimulates phosphodiesterase 3B to degrade cAMP. Thus, PKA can’t be activated via the cAMP pathway…& HSL isn’t phosphorylated. NO TAG mobilization. What a downer.

113
Q

What would catecholamines promote in terms of TAG mobilization?

A

They would bind to adrenergic receptors & via the cAMP pathway activate PKA & HSL. TAG mobilization.

114
Q

What receptor does ANP bind @ adipose tissue?

A

NPR-A

115
Q

So…we have only been talking about HSL…what is the full process of TAG mobilization?

A

Triglyceride–>DAG via ATGL
DAG–>MAG via HSL
fatty acids freed from adipocytes

116
Q

What is the rate limiting step of the TAG mobilization process?

A

the one involving HSL

117
Q

What does ATGL stand for?

A

adipose triglyceride lipase

Block 3; Week 4 Michelle (9 decks)

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