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Fundamentals Of Living Cells > Lipid Transport > Flashcards

Lipid Transport Flashcards

1
Q

What are the three lipid transport systems?

A

Exogenous
Endogenous
??

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2
Q

What is the function of the exogenous lipid transport system?

A

Transport lipids from the gut to the liver

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3
Q

What is the function of the endogenous lipid transport system?

A

Lipids synthesised by the liver to non- hepatic tissues include including adipocytes

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4
Q

Give the makeup (inc percentage) of fatty acids in circulation

A

Triglycerides(45%)
Phospholipids (35%)
Cholesterol (15%)
Free fatty acids (5%)

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5
Q

What are free fatty acids formed from?

A

Triglycerides stored in adipose tissue

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6
Q

What do free fatty acids circulate with?

A

Bound to protein as an Na+ salt - particularly albumin

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7
Q

What would an unbound fatty acid act as in the fluid?

A

A detergent

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8
Q

What does saturation of FA molecules occur at?

A

2mM

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9
Q

How do fatty acids enter cells?

A

Simple diffusion

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10
Q

What are lipoproteins carried in the blood as?

A

Plasma lipoproteins

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11
Q

What are the 5 types of lipoprotein?

A 
Chylomicron
Very low density lipoprotein (VLDL)
Intermediate density lipoprotein (IDL)
Low density lipoprotein (LDL)
High density lipoprotein (HDL)
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12
Q

What does the hydrophobic core consist of?

A

Triglycerides and cholesterol esters

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13
Q

What does the hydrophilic surface consist of?

A

Phospholipids and cholesterol

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14
Q

What’s the difference between an apolipoprotein and a lipoprotein?

A 
Lipoprotein = particle
Apolipoprotein = associated with the lipoprotein
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15
Q

What apoproteins do chylomicrons have?

A

B48, APOCII, E

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16
Q

What apoproteins do VLDL have?

A

B100, APOCI, APOCII, APOCIII and E

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17
Q

What apoproteins do LDLs have?

A

B100

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18
Q

What apoproteins do IDLs have?

A

B100 and APOE

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19
Q

What apoproteins do HDLs have?

A

APOAII, APOAII, APOCII, APOCIII, APOD and APOE

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20
Q

Give functions of apoproteins

A

Structural
To solubilise lipids
Act as enzyme cofactors
Tissue targeting

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21
Q

What are the enzymes or enzyme cofactors for lipoprotein lipase?

A

APOCII

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22
Q

Which apoproteins bind to LDL receptors?

A

Apo B100 and APO E

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23
Q

Which apoproteins bind to HDL receptors?

A

APOE

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24
Q

How do dietary lipids enter the gut?

A

Triglycerides

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25
Q

What does lipase break down triglycerides into?

A

Fatty acids and monoacylglycerol

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26
Q

What do phospholipids and cholesterol esters form?

A

A chylomicron which only expresses APOB48

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27
Q

What do nascent chylomicrons interact with?

A

A HDL and picks up Apo CII and Apo E

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28
Q

Where is the B48 added to the chylomicron?

A

SER

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29
Q

How are chylomicrons secreted in the lymphatic system?

A

Reverse pinocytosis

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30
Q

Where do chylomicrons get their Apo C2, C3 and E from?

A

HDLs

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31
Q

How does the chylomicron undergo enzymatic degradation?

A

Interaction with lipoproteinlipase

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32
Q

Where is lipoproteinlipase b mainly expressed

A

Tissues which mainly metabolise lipids (like muscle, adipocytes and mammary glands)

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33
Q

How does the Km of LPL isoform in adipocytes compare to the Km in muscle?

A

Greater in adipocytes

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34
Q

What is LPL activated by?

A

APO CII

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35
Q

What is LPL on adipocytes stimulated by?

A

Insulin

36
Q

What is type 1 hyperlipidaemia?

A

Deficiency in lipoproteinlipase or apo C2

37
Q

What is type 1 hyperlipidaemia characterised by?

A

High plasma triglyceride

38
Q

What is type 2 hyperlipidaemia?

A

Caused by a genetic defect in the synthesis, processing or function of the LDL receptor v

39
Q

What is type 2 hyperlipidaemia characterised by?

A

High LDL levels

40
Q

What is type 4 hyperlipidaemia?

A

Raised VLDL concs often due to obesity or alcohol abuse

41
Q

Why do chylomicrons have a low density?

A

High TG levels

42
Q

What fat soluble vitamins do chylomicrons contain?

A

A and E

43
Q

What is a chylomicrons lifetime in circulation?

A

1 hour

44
Q

What is a triglycerides lifetime in circulation?

A

5 mins

45
Q

How are remnants of chylomicrons and VLDLs removed by the liver?

A

With the involvement of APO E

46
Q

When are VLDLs synthesised?

A

When the dietary intake of carbs exceeds immediate needs

47
Q

What are the components of nascent VLDLs?

A

TG, fatty acids, phospholipids, cholesterol esters and APO B100

48
Q

What is the formation of VLDLs stimulated/ inhibited by?

A

Stimulated by insulin and inhibited by glucagon

49
Q

What molecules interfaces with and activates LDLs?

A

Apo CII

50
Q

What are foam cells?

A

Part of the initiating process of atherosclerotic cells within the blood vessel

51
Q

What happens when the products of a TG travel into an adipocyte cell?

A

They will be converted back into TGs and stored

52
Q

What happens when the products of a TG travel into an muscle cell?

A

Converted into ATP, o2 and water

53
Q

What happens when the TGs are removed from an LPL?

A

Becomes an IDL

54
Q

How much IDL will be transported into the liver?

A

60%

55
Q

What happens when IDLs interact with HDLs?

A

The HDLs take back the apo E and apo CII for future donations

56
Q

How much of the LDL is returned to the liver?

A

60-70%

57
Q

What happens when Apo B100 attaches to the peripheral tissue

A

Fatty acids, cholesterol, glycerol and amino acids are broken down and used in metabolism

58
Q

What happens if the LDL circulates for long enough?

A

It undergoes oxidation

59
Q

What happens if the macrophage accumulates too much oxidised LDL?

A

Forms a foam cell

60
Q

How long does it take for LDLs to be metabolised?

A

3 days

61
Q

What do HDLs do?

A

Takes cholesterol laden cells back to the liver

62
Q

What are the three ways in which HDLs can be made?

A

As nascent particles by the liver and intestine
Budding or apoproteins from chylomicrons
Free from apoA1

63
Q

What do nascent HDLs do?

A

Acquires cholesterol and phospholipids from endothelial cells

64
Q

What does the transfer of cholesterol and phospholipids from nascent HDLs require

A

ATP binding cassette protein 1 (ABC1)

65
Q

What does HDL possess that catalyses cholesterol esterification and what does it prevent?

A

Lecithin cholesterol acyltransferase (LCAT) prevents it returning to the cell

66
Q

What do Cholesterol rich HDLs do?

A

Delivers it to the liver or exchange it with other particles including VLDL and VLDL remnants

67
Q

What is the healthy HDL:LDL ratio

A

3:5

68
Q

Give the steps of receptor mediated endocytosis

A

LDL binds to the LDL receptor on the plasma membrane
The membrane invaginate and forms an endosome
Inside the endosome the LDL and receptor dissociates
Receptors is then broken down after fusion with a lysosome

69
Q

What is an LDL broken down into?

A

Amino acids
Fatty acids
Cholesterol ester droplets

70
Q

What happens to the cholesterol ester droplets after they’ve been broken down from LDLs

A

Reforms cholesterol which is incorporated into the ER or can be used to synthesise steroid hormones

71
Q

What regulates cholesterol uptake and synthesis?

A

Cholesterol regulates itself

72
Q

What happens if there’s an increase in cholesterol?

A

Inhibits HMG-CoA reductase activity

73
Q

What happens if there’s a decrease in cholesterol?

A

Increases LDL receptor synthesis and expression

74
Q

Where do you find SR-81?

A

Endothelial cells, intestine, macrophages, smooth muscle cells, keratinocytes etc etc

75
Q

What does SR-81 bind to?

A

HDL

76
Q

What does SR-A1 and SR-A2 bind to?

A

LDL

77
Q

Where do you find SR-A1 and SR-A2?

A

Macrophages

78
Q

What is the cause of familial hypercholesterolemia?

A

Single amino acid substitution that prevents localisation of the LDL receptor to the coated pits

79
Q

What happens in familial hypercholesterolemia?

A

LDL receptors don’t bind to LDL enough
Too much LDL in blood
Build up in cholesterol leads to the formation of a foam cell
Foam cells are the precursors for atherosclerosis

80
Q

What is high serum cholesterol?

A

800mg/ml

81
Q

What is a normal cholesterol level?

A

200mg/ml

82
Q

What happens to homozygous people with familial hypercholesterolemia?

A

Develop blocked arteries- die young from heart attacks

De novo synthesis is not regulated by LDL

83
Q

What is diabetes mellitus?

A

Increased FFA mobilisation

Decreased chylomicron and VLDL utilisation

84
Q

What does obesity cause?

A

Hypertension
NIDDM
Hyperlipademia
Hyperglycaemia

85
Q

What gene defects in receptors lead to?

A

Hypercholesterolemia

Atherosclerosis

Fundamentals Of Living Cells (41 decks)

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