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Z OLD ESA 1- Metabolism > Lipid Transport > Flashcards

Lipid Transport Flashcards

1
Q

What is the problem for lipid transport in blood?

A

They are hydrophobic molecules that are insoluble in water

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2
Q

How are lipids transported in blood?

A

Bound to carriers

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3
Q

What percentage of lipids are carried in blood bound to albumin?

A

~2%

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4
Q

What type of lipids predominate in those carried by albumin?

A

Fatty acids

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5
Q

What is the problem with carrying lipids bound to albumin?

A

It has a limited capacity

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6
Q

What is the capacity of carrying lipids bound to albumin?

A

~3mmol/L

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7
Q

How are ~98% of lipids carried?

A

As lipoprotein particles

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8
Q

What do lipoprotein particles consist of?

A
  • Phospholipids
  • Cholesterol esters
  • Proteins
  • TAG
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9
Q

What do the phospholipids in lipoprotein particles act as?

A

A shell

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10
Q

What do phospholipids consist of?

A

NAME?

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11
Q

Is a phospholipid molecule hydrophilic or hydrophobic?

A

NAME?

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12
Q

How are phospholipids classified?

A

According to head group

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13
Q

What do phospholipids have between their head and tail?

A

Phosphate and glycerol

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14
Q

What structures do phospholipids form?

A
  • Liposomes
  • Micelle
  • Bilayer sheet
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15
Q

What is a liposome?

A

Sphere with bilayer

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16
Q

What is a micelle?

A

Sphere with single layer

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17
Q

Where does cholesterol in the body come from?

A

NAME?

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18
Q

What is cholesterol used for?

A
  • Essential component of membranes
  • Precursor of steroid hormones
  • Precursor of bile acids
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19
Q

Question…

A

Answer…

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20
Q

Why is cholesterol essential for membranes?

A

Moderates fluidity

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21
Q

Give 4 steroid hormones that cholesterol is a precursor for

A
  • Cortisol
  • Aldesterone
  • Testosterone
  • Oestrogen
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22
Q

How is cholesterol transported around the body?

A

As cholesterol esters

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23
Q

What is required to esterify cholesterol?

A

Enzymes that add a fatty acid

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24
Q

Give 2 enzymes that can produce cholesterol esters?

A

NAME?

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25
Q

What are lipoproteins?

A

Lipid carriers

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26
Q

Describe the structure of lipoproteins

A
  • Spheres with phospholipid monolayer
  • Have intergral apolipoproteins
  • Have peripheral apolipoproteins
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27
Q

What does the phospholipid monolayer of lipoproteins contain?

A

A small amount of cholesterol

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28
Q

What is meant by integral?

A

Pass through the membrane

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29
Q

Give 2 examples of integral apolipoproteins

A

NAME?

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30
Q

Give 2 examples of peripheral apolipoproteins

A

NAME?

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31
Q

What does the cargo of lipoproteins consist of?

A
  • Triacylglycerols
  • Cholesterol esters
  • Fat soluble vitamins
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32
Q

How many distinct classes of lipoproteins are there?

A

5

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33
Q

What are the classes of lipoproteins named according to?

A

Density

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34
Q

What are the 5 classes of lipoproteins?

A
  • Chylomicrons
  • VLDL (very low density lipoproteins)
  • IDL (intermediate density lipoproteins)
  • LDL (low density lipoproteins)
  • HDL (high density lipoproteins)
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35
Q

Which of the lipoprotein classes is very short lived?

A

IDL

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36
Q

What does each class of lipoprotein contain?

A

A variable content of apolipoprotein, triglyceride, cholesterol and cholesterol ester

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37
Q

What are the main carriers of fat?

A

Chylomicrons and VLDL

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38
Q

Why are levels of lipoproteins in blood important?

A

They are of significant clinical importance

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39
Q

How are levels of lipoproteins in the blood determined?

A

Density obtained by flotation ultracentrifugation

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40
Q

How is particle diameter related to density?

A

Inversely proportional

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41
Q

What does a higher % of protein in a lipoprotein mean?

A

More dense

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42
Q

When are chylomicrons normally present in the blood?

A

4-6 hours after a meal

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43
Q

What does each class of lipoprotein have?

A

A particular component of associated proteins- apolipoproteins

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44
Q

What are the 6 major classes of apolipoproteins?

A
  • A
  • B
  • C
  • D
  • E
  • H
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45
Q

What are the two most important apolipoproteins?

A

NAME?

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46
Q

Where is apoB found?

A

NAME?

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47
Q

Where is apoAI found?

A

HDL

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48
Q

Are apolipoproteins integral or peripheral?

A

Can be either

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49
Q

What are the roles of apolipoproteins?

A
  • Structural

- Functional

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50
Q

What is the structural role of apolipoproteins?

A

Help keep integrity of lipoproteins in tact

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51
Q

What are the functional roles of apolipoproteins?

A
  • Cofactors for enzymes

- Ligands for cell surface receptors

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52
Q

Where are chylomicrons loaded at the beginning of their metabolism?

A

Small intestine

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53
Q

What happens to chylomicrons in the small intestine?

A

ApoB-48 added

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54
Q

What happens to chylomicrons once apoB-48 has been added?

A

They enter the lymphatic system

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55
Q

Where do chylomicrons go once in the lymphatic system?

A

They travel to the thoracic duct, into the left subclavian vein

56
Q

Why do chylomicrons empty into the left subclavian vein?

A

It means by avoid the liver the first time round

57
Q

What happens to the chylomicrons once they’ve been emptied into the left subclavian vein?

A

ApoC and apoE are added once they’re in the blood

58
Q

What does apoC on chylomicrons do?

A

Binds lipoprotein lipase (LPL) on adipocytes and muscle

59
Q

What is the result of the binding of apoC and LPL?

A

Released fatty acids enter the cells, depleting the chylomicron of its fat content

60
Q

To what level is the chylomicrons triglyceride level depleted before the next stage?

A

~20%

61
Q

What happens once the chylomicron triglyceride content has depleted to ~20%?

A

The apoC dissociates and the chylomicron becomes a chylomicron remnant

62
Q

What happens to chylomicron remnants?

A

They return to the liver, where the LDL receptor on hepatocytes binds apoE and the chylomicron remnant is taken up by receptor mediated endocytosis. The lysosomes release remaining contents for use in metabolism

63
Q

What is released from the chylomicron remnants by lysosomes?

A

NAME?

64
Q

What is lipoprotein lipase?

A

An enzyme that hydrolyses triacylglycerols in lipoproteins

65
Q

What does LDL require to function?

A

ApoC-11 as a cofactor

66
Q

Where is LDL found?

A

Attached to surface of endothelial cells in capillaries

67
Q

What do chylomicrons carry?

A
  • Fat
  • Cholesterol
  • Vitamins
68
Q

Where are VLDLs made?

A

In the liver

69
Q

What is the purpose of VLDLs?

A

Transporting triacylglycerols (TAGs) to other tissues

70
Q

When are apolipoproteins added to VLDLs?

A

NAME?

71
Q

Where do VLDLs bind to LDL?

A

On endothelial cells in muscle and adipose tissue

72
Q

What happens when VLDL binds to LDL?

A

It starts to become depleted of triacylglycerol

73
Q

What happens to the fatty acids released from VLDLs in muscle?

A

They are taken up and used for energy production

74
Q

What happens to the fatty acids released from VLDLs in adipose tissue?

A

The fatty acids are used for re-synthesis of triacylglycerol and stored as fat

75
Q

What happens as triacylglycerol content of VLDL particles drops some?

A

VLDL particles dissociate from the LDL enzyme complex and return to the liver

76
Q

What happens when VLDL content depletes to ~30%?

A

Particle becomes short-lived IDL particle

77
Q

What happens to IDL particles?

A

They can be taken up by the liver or rebind to LPL enzyme for further depletion of TAG content

78
Q

What happens to IDL on depletion to ~10%?

A

IDL loses apoC and apoE, and so becomes a LDL particle

79
Q

Is the cholesterol content of a LDL particle high or low?

A

High

80
Q

What is the primary function of LDLs?

A

To provide cholesterol from liver to peripheral tissues

81
Q

What do peripheral tissues express?

A

LDL receptor

82
Q

How do peripheral cells take up LDL?

A

Receptor mediated endocytosis

83
Q

Do LDL particles have apoC or apoE?

A

No

84
Q

What does the lack of apoC and apoE on LDLs mean?

A

They cannot be effectively cleaved by the liver

85
Q

Why can LDLs not be effectively cleaved by the liver?

A

Liver LDL-receptor has a high affinity for apoE

86
Q

How does the half life of LDL in the blood differ from that of VLDL or LDL?

A

It is much longer

87
Q

What is the result of LDLs having a longer half life in the blood?

A

They are more susceptible to oxidative damage

88
Q

What happens to oxidised LDL?

A

It is taken up my macrophages, which can transform to foam cells

89
Q

What do foam cells contribute too?

A

The formation of atherosclerotic plaques

90
Q

What do cells requiring cholesterol express?

A

LDL receptors on the plasma membrane

91
Q

What acts as a ligand for the LDL receptors?

A

ApoB-100 on LDL

92
Q

How is the receptor/LDL complex taken into cells?

A

By endocytes, into endosomes

93
Q

What happens to the endosomes containing receptor/LDL complexes?

A

They fuse with the lysosome

94
Q

What is the purpose of the fusing of the endosomes containing the receptor/LDL complex with lysosomes?

A

Digestion to release cholesterol and fatty acids

95
Q

How can LDL-R expression be controlled?

A

Cholesterol concentration in the cell

96
Q

How can HDL be synthesised?

A
  • Nascent HDL can be synthesised by liver and intestine
  • HDL particles can ‘bud off’ from chylomicrons and VLDL as they are digested by LPL
  • Free apoA-1 can also acquire cholesterol and phospholipid from other lipoproteins and cell membranes to form nascent-like HDL
97
Q

How do HDL particles mature?

A
  • Nascent HDL accumulate phospholipid and cholesterol from cells lining blood vessels
  • Hollow core of HDL progressively fills, and particle takes on more globular shape
98
Q

Does transfer of lipids to HDL require enzymes?

A

No

99
Q

What do HDL particles have the ability to do?

A

Remove cholesterol from cholesterol-laden cells, and return it to the liver

100
Q

What is the ability of HDL’s to remove cholesterol important for?

A

Blood vessels

101
Q

Why is the ability of HDL’s to remove cholesterol important for blood vessels?

A

Reduces the likelihood of foam cell and atherosclerotic plaque formation

102
Q

What facilitates the transfer of cholesterol to HDL?

A

ABCA1 protein within the cell

103
Q

What happens once HDL has taken up cholesterol?

A

The cholesterol is then converted to cholesterol ester by LCAT

104
Q

What happens to mature HDL?

A

It is taken up by the liver by specific receptors

105
Q

What happens when cells require additional cholesterol?

A

They can utilise the scavenger receptor to obtain cholesterol from HDL

106
Q

What is the scavenger receptor?

A

SR-B1

107
Q

Why might cells require additional cholesterol?

A

Steroid hormone synthesis

108
Q

What can HDL exchange cholesterol ester for?

A

TAG with VLDL

109
Q

How can HDL exchange cholesterol ester for TAG with VLDL?

A

By action of cholesterol exchange transfer protein (CETP)

110
Q

What is hyperlipoproteinemia?

A

Raised plasma levels of one of more lipoprotein classes

111
Q

What causeshyperlipoproteinemia?

A

Either over-production or under-removal

112
Q

What are the 6 main classes ofhyperlipoproteinemia?

A
  • I - Chylomicrons in fasting plasma
  • IIa
  • IIb
  • III - Raised IDL and chylomicron remnants
  • IV
  • V - Raised chylomicrons and VLDL in fasting plasma
113
Q

Which classes ofhyperlipoproteinemia are associated with coronary artery disease?

A

IIa (may be severe), IIb, III, IV, V

114
Q

What causes class I of hyperlipoproteinemia?

A

Defective lipoprotein lipase

115
Q

What causes class IIa ofhyperlipoproteinemia?

A

Defective LDL receptor

116
Q

What causes class III ofhyperlipoproteinemia?

A

Defective apoprotein (apoE)

117
Q

What are the clinical signs ofhyperlipoproteinemia?

A
  • High level of cholesterol in blood

- Cholesterol deposition in various areas of the body

118
Q

What conditions are caused by cholesterol deposition?

A
  • Xanthelasma
  • Tendon Xanthoma
  • Corneal arcus
119
Q

What is xanthelasma?

A

Yellow patches on eyelids

120
Q

What is tendon xanthoma?

A

Nodules on tendons

121
Q

What is corneal arcus?

A

An obvious white circle around the eye

122
Q

What is a raised serum LDL associated with?

A

Atherosclerosis

123
Q

Why is raised serum LDL associated with atherosclerosis?

A

Oxidised LDL is recognised and engulfed by macrophages. Lipid laden macrophages called foam cells accumulate in intima of blood vessel walls to form fatty streak. Fatty streaks can evolve into atherosclerotic plaque, which grows and encroaches on the lumen of artery.

124
Q

What can atherosclerotic plaques cause?

A

Angina

125
Q

What happens if an atherosclerotic plaque ruptures?

A

It triggers an acute thrombosis (clot)

126
Q

How does an atherosclerotic plaque rupture trigger a clot?

A

By activating platelets and clotting cascade

127
Q

What can a thrombosis cause?

A

NAME?

128
Q

What is the first approach to treatment of hyperlipoproteinemia?

A

Changing diet and lifestyle

129
Q

How is diet altered to treathyperlipoproteinemia?

A

NAME?

130
Q

How is lifestyle altered to treathyperlipoproteinemia?

A

NAME?

131
Q

What happens if someoneshyperlipoproteinemia doesn’t respond to diet and lifestyle changes?

A

Drug therapies

132
Q

What drug therapies are used to treathyperlipoproteinemia?

A
  • Statins

- Bile salt sequestrants

133
Q

What do statins do?

A

Reduce cholesterol synthesis by inhibiting HMG-CoA reductase

134
Q

How does the inhibition of HMG-CoA reductase reduce cholesterol levels?

A

By inhibiting HMG-CoA reductase, HMG-CoA not converted to mevalonate, so melavonate not converted to squalene (in several reactions), so squalene not converted to cholesterol (in many reactions)

135
Q

What do bile salts sequestrants do?

A

Bind bile salts in GI tract

136
Q

What is the result of bile salts being binded in the GI tract?

A

It forces the liver to produce more bile acids using more cholesterol

Z OLD ESA 1- Metabolism (17 decks)

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