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Membranes > Cholesterol > Flashcards

Cholesterol Flashcards

1
Q

What are the main functions of lipids?

A
  1. energy storage
  2. component of cell membranes
  3. required to solubilise fat-soluble vitamins
  4. biosynthetic precursors
  5. signalling molecules
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2
Q

How much cholesterol comes from the diet?

A

25% of the cholesterol in the body comes from the diet

The liver also synthesises cholesterol

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3
Q

How is cholesterol transported in the blood plasma?

A

It is insoluble in the liquid blood plasma

It is transported by a lipoprotein

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4
Q

What are lipoproteins?

A

They are particles found in the plasma that will transport ANY type of lipid

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5
Q

How are do lipoproteins differ from one another?

A

They all share a general structure

They have different ratios of proteins to lipids

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6
Q

How are lipoproteins classified?

A

According to their density and chemical properties

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7
Q

What is the largest and least dense lipoprotein?

What is its role and where is it synthesised?

A

The chylomicron

It is synthesised in the intestines

They carry dietary fats from the intestine to the tissue

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8
Q

What is VLDL?

Where is it synthesised?

A

Very low density lipoprotein

It is synthesised in the liver

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9
Q

What is the role of VLDL?

A

It transports lipids from the liver into the tissues

This includes the transport of cholesterol

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10
Q

What is LDL?

Where is it synthesised?

A

Low density lipoprotein

LDLs are derived from VLDLS

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11
Q

What is the role of LDL?

A

It is the main carrier of cholesterol around the body

It transports cholesterol to the peripheral tissues

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12
Q

What is HDL?

Where is it synthesised?

A

High density lipoprotein

Formed in the blood

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13
Q

What is the role of HDL?

A

It transports cholesterol from the peripheral tissues back to the liver for degradation

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14
Q

What is found in the external monolayer of lipoproteins?

A
  1. apolipoproteins
  2. free cholesterol
  3. phospholipids
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15
Q

What is found in the core of lipoproteins?

A
  1. esterified cholesterol

2. triacylglycerols

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16
Q

What is responsible for distinguishing the functions of each lipoprotein?

A

The apolipoproteins

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17
Q

Why is it important to distinguish the function of each lipoprotein?

A

It allows the determination of the start and end-points for cholesterol and lipid transport to particular tissues

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18
Q

What are the major classes of apolipoproteins?

A
  1. ApoA
  2. ApoB
  3. ApoC
  4. ApoE

There are subclasses of ApoA, B and C

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19
Q

What are the roles of ApoA?

A
  1. major component of HDL that allows HDL to be recognised

2. mediates efflux of cholesterol from peripheral cells and influx to the liver

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20
Q

What are the roles of ApoB?

A

It recognises apoB (LDL) and apoE receptors

It facilitates the uptake of LDL

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21
Q

What is the role of ApoC?

A

activator of lipoprotein lipase

This breaks down fats for energy or storage

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22
Q

What is the role of ApoE?

A

It stabilises VLDL for cellular uptake

It is a ligand for the apoB/E (LDL) receptor

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23
Q

What regulates apoplipoprotein synthesis?

Where are they synthesised?

A

Apolipoprotein synthesis is regulated by dietary fat intake

Ingesting fat stimulates their production

They are synthesised in the intestine

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24
Q

What stimulates synthesis of apolipoproteins in the liver?

A

The influence of hormones and drugs

e.g. insulin, glucagon, sex hormones

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25
Q

What apolipoproteins are involved in regulating key enzymes in lipoprotein metabolism?

A

apoC-II regulates lipoprotein lipase

apoA-1 regulates lecithin-cholesterol acyltransferase (LCAT)

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26
Q

How do apolipoproteins allow lipoproteins to be targeted to the correct tissues?

A

Apolipoproteins are ligands for interactions with lipoprotein receptors

apoB100 and apoE for LDL receptors

apoA-I for HDL receptors

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27
Q

What is the structure of LDL?

A

It has a single strand of ApoB running around the exterior

It has a hydrophobic core of triacylglycerols and cholesterol esters

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28
Q

What is the problem with LDL being susceptible to oxidation?

A

The oxidative form of LDL is responsible for forming atherosclerotic plaques

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29
Q

What is the structure of HDL?

A

It has 2 ApoA strands

ApoA I and ApoA II

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30
Q

What is the function of the ApoA strands in HDL?

A

They protect the HDL particle from undergoing oxidative modifications

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31
Q

Why does the blood appear milky after eating a meal high in fat?

A

This is due to the abundance of chylomicrons

These are made in the intestine and transport triglycerides and cholesterol in the blood

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32
Q

What is the action of lipoprotein lipase?

A

It hydrolyses triglycerides to fatty acids

They are taken up by target tissues and used for energy production or storage

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33
Q

What happens once the chylomicrons have released their triglycerides?

A

They shrink and the remnants are transported back to the liver

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34
Q

What happens to VLDLs once they have been made by the liver?

A

They transport lipids to their target tissues

They are acted on by lipoprotein lipase to release fatty acids

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35
Q

What happens to VLDL remnants once they have released their lipids?

A

They remain in the blood and become LDL

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36
Q

How does the liver primarily dispose of cholesterol?

A

In the form of bile salts

37
Q

How do lipoproteins enter cells?

A

They cannot enter cells without a receptor

Membrane-bound receptors allow allow cholesterol to enter hepatic and peripheral cells

38
Q

What will the LDL receptor bind to?

A

This is the ApoB/E receptor

It will bind to apoB100 or apoE

39
Q

What regulates LDL receptor gene expression?

A

Intracellular cholesterol concentration

If cells have a high level of cholesterol, they will stop making receptors

40
Q

What happens once LDL binds to the LDL receptor?

A

It stimulates receptor-mediated endocytosis

41
Q

What happens to LDL and its receptor in the endosome?

A

LDL is released from the receptor in the endosome

The receptor is recycled to the plasma membrane

The cholesterol is then released and used within the cell

42
Q

What happens to the LDL particle once the ApoB-100 protein has bound to the receptor?

A

The LDL particle is taken in via a clathrin coated pit

The clathrin-coated vesicle will then form

43
Q

What happens once the clathrin-coated vesicle forms?

A

The clathrin dissociates into clathrin triskelions

The LDL with the receptor is still in the vesicle

44
Q

What is the change in pH in the uncoated vesicle?

What happens when the pH changes?

A

It goes from pH 7 to pH 5

The receptor begins to be nipped off in a separate vesicle

45
Q

When will the recycled LDL receptors be re-expressed?

A

When the cell requires cholesterol

46
Q

What happens to LDL receptors when there is high intracellular cholesterol?

A

This suppresses LDL receptor synthesis

This prevents excessive uptake of cholesterol by cells

Excess cholesterol remains in the blood as LDL

47
Q

What does high blood levels of HDL correlate with?

A

Low incidence of atherosclerosis

48
Q

Why is HDL known as “good cholesterol”?

A

It scavenges cholesterol from cells and other lipoproteins

It returns it to the liver to be excreted in the bile

49
Q

Which process allows HDL to protect against atherosclerosis?

A

reverse cholesterol transport

50
Q

How does HDL become mature HDL?

A
  1. nascent HDL has a huge capacity to extract cholesterol from cells
  2. once it has extracted cholesterol, it becomes cholesterol-laden mature HDL
51
Q

What happens to the mature HDL after it has extracted cholesterol?

A

It returns to the liver and binds to a scavenger receptor

Cholesterol esters are converted back into free cholesterol which is secreted in bile

52
Q

What are dyslipidaemias?

A

Inherited diseases that are NOT related to lifestyle or diet

53
Q

What causes familial hypercholesterolaemia?

A

Mutations affecting the LDL receptor

This means that cells cannot take up LDL

54
Q

What happens if cells cannot take up LDL?

A

There is an increased amount of circulating LDL

Excess cholesterol is deposited in the arteries, increasing risk of atherosclerosis

55
Q

Why is cholesterol essential?

A
  1. it is a structural component of cell membranes

2. it is needed for synthesis of bile acids, steroid hormones and fat-soluble vitamins (A, D, E and K)

56
Q

What are high serum levels of cholesterol indicative of?

A

The risk for cardiovascular disease

57
Q

What are the cardiac manifestations of atherosclerosis?

A
  1. chest pain
  2. palpitations
  3. heart attack
58
Q

What happens if atherosclerosis occurs in cerebral arteries?

A

It can lead to stroke of cerebral haemorrhage

59
Q

What does peripheral atherosclerosis lead to?

A
  1. pain
  2. ischaemia
  3. ulceration and gangrene
60
Q

What is the first stage in the development of plaques?

A

A fatty streak develops around age 20

This is independent of lifestyle and develops in everyone

61
Q

What will the fatty streak progress to and what is this dependent on?

A

it progresses to a fibrous plaque

This is cholesterol-laden

It depends on age and lifestyle

62
Q

What happens once the fibrous plaque has formed?

A

The plaque is now depositing in the lumen of the artery

It will advance to an advanced plaque which shows complete occlusion

63
Q

How does the plaque cause heart attacks/stroke?

A

When the plaque ruptures, the blood will clot and cause thrombosis

64
Q

Why are statins taken at night?

A

Cholesterol is made in the liver

This process occurs overnight whilst we are sleeping

65
Q

What molecule is a precursor for the liver to make cholesterol?

How is this formed?

A

Mevalonate

This is formed from HMG-CoA by the action of HMG-CoA reductase

66
Q

What is the synthetic pathway involved with cholesterol formation?

A
  1. HMG-CoA
  2. Mevalonate
  3. IPP
  4. FPP
  5. Squalene
  6. Cholesterol
67
Q

What are the two organs that primarily control blood cholesterol levels?

A
  1. Liver produces cholesterol and bile acids

2. Intestine absorbs cholesterol from food and bile

68
Q

How do statins affect the liver?

A

they prevent cholesterol synthesis in the liver

69
Q

What is the role of cholesterol absorption inhibitors?

What is an example?

A

They prevent the uptake of cholesterol from the intestine

e.g. ezetimibe

70
Q

How do plant sterols act as a cholesterol absorption inhibitor?

A

The plant sterols are taken up preferentially

The cholesterol remains in the intestine and is excreted

71
Q

What is the role of fibrates?

What are examples?

A

They reduce triglycerides and increase HDL

e.g. gemfibrozil and fenofibrate

72
Q

How do statins work?

A

They inhibit HMG-CoA reductase

This means that HMG-CoA cannot be converted to mevalonate

They lower plasma cholesterol levels by decreasing cholesterol synthesis

73
Q

When statins are used, what is the result of lowering intracellular cholesterol levels?

A

There is increased expression of the LDL receptor

More LDL receptors increase the uptake of cholesterol from the blood

74
Q

What is a pleiotropic effect?

A

It is an action of a drug, other than those for which the agent was specifically developed

This may be an undesirable side effect or a beneficial effect

75
Q

What is the pleiotropic effect of statins?

A

FPP is converted to GGPP

This cannot occur if statins are being taken

76
Q

What type of molecules are FPP and GGPP?

What is their role?

A

They are isoprenoids

They make a tail for small G-proteins, such as Ras and Rho

77
Q

What are Ras and Rho?

A

Signalling molecules that control gene expression

78
Q

What must happen to small G-proteins before they can perform any cell signalling activity?

A

They must be prenylated through the attachment of FPP or GGPP

The isoprenoid lipid tail attaches the small G protein to the membrane

79
Q

What is the difference in the way Ras and Rho are prenylated?

A

Ras is farnesylated (attached to FPP)

Rho is geranylgeranylated (attached to GGPP)

80
Q

What is the problem with some of the signalling pathways activated by Ras and Rho?

A

They can lead to actions in the cell that may be supportive of cardiovascular disease

e.g. thrombosis, production of inflammatory molecules

81
Q

How may statins work to decrease the risk of cardiovascular disease?

A

They inhibit synthesis of cholesterol and isoprenoids

82
Q

What is the enzyme that converts FPP to squalene in the liver?

A

Squalene synthase

83
Q

What are the 4 pleiotropic effects of statins?

A
  1. improved endothelial dysfunctin
  2. antioxidant properties
  3. inhibition of inflammatory responses
  4. stabilising atherosclerotic plaques
84
Q

What is PCSK9?

A

Proprotein convertase stubtilisin/kexin type 9

It is a protease enzyme expressed by the liver and intestine

85
Q

What is the role of PCSK9?

A

It promotes degradation of the LDL receptor inside the cell

This prevents recycling of the LDL receptor to the cell surface

86
Q

How does PCSK9 enter the cell?

A
  1. it binds to the receptor that has bound LDL carrying cholesterol
  2. it is taken up with the receptor
87
Q

What is the action of PCSK9 once it is inside the cell?

A

It degrades the LDL receptor so it cannot be recycled to the membrane

This decreases LDL uptake

88
Q

What are PCSK9 inhibitors?

A

Antibodies that will mop up any PCSK9 in the blood

This allows the LDL receptor to be internalised and recycled

89
Q

What is increased PCSK9 concentration associated with?

A

Increased risk of cardiovascular disease and hypercholesterolaemia

Membranes (5 decks)

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