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BMS07 > Fat Storage & Transport > Flashcards

Fat Storage & Transport Flashcards

1
Q

When is fuel stored?

A

When energy-providing foods are consumed in quantities greater than needed at the time

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2
Q

What are lipids stored as?

A

Triacylglycerol

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3
Q

What stimulates fatty acid synthesis?

A

Insulin (fed state)

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4
Q

What are fatty acids synthesised from?

A

Acetyl CoA

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5
Q

Why does the liver carry out glycolysis in the fed state?

A

To produce acetyl CoA for fatty acid synthesis (and fat storage)

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6
Q

Where does fatty acid synthesis occur?

A

Cytosol of hepatocytes

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7
Q

How is acetyl CoA transported out of the mitochondria?

A

Combines with oxaloacetate to form citrate

Citrate leaves mitochondria in high glucose concentrations

Citrate –> acetyl CoA + oxaloacetate in cytosol

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8
Q

What is the first step in fatty acid synthesis?

A

Acetyl CoA + bicarbonate –> malonyl CoA

Acetyl CoA carboxylase

ATP –> ADP + Pi

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9
Q

What is the rate-limiting step of fatty acid synthesis?

A

Acetyl CoA + bicarbonate –> malonyl CoA

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10
Q

Why don’t newly synthesised fatty acids enter mitochondria for beta oxidation?

A

Malonyl CoA inhibits carnitine palmitoyl transferase

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11
Q

Describe the process of fatty acid formation

A

Malonyl CoA + acetyl CoA then remove carbon dioxide

Repeatedly add malonyl CoA and remove carbon dioxide

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12
Q

What cofactor is required for fatty acid synthesis? Where does it come from?

A

NADPH

Hexose monophosphate shunt

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13
Q

What enzyme catalyses the formation of fatty acids?

A

Fatty acid synthetase/synthase

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14
Q

What is special about fatty acid synthetase?

A

Large enzyme with many active sites

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15
Q

What is triacylglycerol formed from?

A

Glycerol phosphate

3 fatty acids

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16
Q

Where is glycerol phosphate sourced from?

A

Glycolysis

If there is excess glycerol, the liver can use glycerol kinase

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17
Q

What happens when glycerol phosphate and the fatty acids are joined together?

A

Phosphate is lost

To give a neutral/non-polar/uncharged molecule

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18
Q

Why are triacylglycerols modified before leaving the cell?

A

Water-insoluble

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19
Q

What is added to triacylglycerol during modification?

A

Apoproteins

Lipids with polar areas (phospholipids and cholesterol)

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20
Q

What is the general structure of a lipoprotein?

A

Inner core of triglycerides and cholesterol esters

Outer shell is made up of a single layer of phospholipids, cholesterol and apoproteins

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21
Q

What is the role of apoproteins?

A

Structure

Recognition by receptors

Activation of enzymes in lipid metabolism

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22
Q

What are the four classes of lipoproteins?

A

Chylomicrons

VLDL - very low density lipoproteins

LDL - low density lipoproteins

HDL - high density lipoproteins

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23
Q

What type of lipoprotein is the largest?

A

Chylomicrons

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24
Q

What type of lipoprotein is the least dense?

A

Chylomicrons

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25
Q

What do chylomicrons carry?

A

Mainly dietary fat

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26
Q

What do VLDL carry?

A

Mainly endogenous triacylglycerol

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27
Q

What do LDL carry?

A

Mainly cholesterol to tissues

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28
Q

What do HDL carry?

A

Mainly cholesterol from tissues to liver

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29
Q

What are nascent chylomicrons?

A

First-formed chylomicron from gut with apo B-48

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30
Q

What apoprotein do nascent chylomicrons have?

A

Apo B-48

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31
Q

How does a nascent chylomicron become a chylomicron?

A

In blood, picks up apo C-II and apo E from HDL

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32
Q

What part of triacylglycerols are taken up by adipose tissue?

A

Fatty acids

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33
Q

What enzyme hydrolyses triacylglycerol before fatty acid uptake? Where is it?

A

Lipoprotein lipase

In capillaries

34
Q

What activates lipoprotein lipase?

A

Insulin

Apo C-II

35
Q

Why is glycerol not used by adipose cells?

A

Do not have glycerol kinase to form glycerol phosphate

36
Q

What apoproteins do chylomicron remnants have?

A

Apo E

Apo B-48

37
Q

Where does the chylomicron remnant go?

A

To liver via blood stream

Taken up via apo E receptors on liver cells

38
Q

What types of lipoprotein is synthesised by the liver?

A

VLDL

HDL

39
Q

What apoprotein is present on VLDL?

A

Apo B-100

40
Q

What happens to VLDL when it enters the blood stream from the liver?

A

Picks up apo C-II and apo E from HDL

41
Q

What is left after VLDL have passed the adipose tissue?

A

IDL - intermediate density lipoprotein

42
Q

What do apoproteins do IDL have?

A

Apo E

Apo C-II

Apo B-100

43
Q

What happens to IDL?

A

Half loses B-100 to become HDL

Half loses apo C-II and apo E to become LDL

44
Q

What apoproteins are found on HDL?

A

Apo E

Apo C-II

Apo A-I

45
Q

Where are B-100 receptors found?

A

Liver cells

Peripheral tissue

46
Q

What do LDL receptors recognise?

A

Apo B-100

47
Q

Where is HDL synthesised?

A

Liver

Small intestine

48
Q

What does newly synthesised HDL do?

A

Takes in cholesterol from periphery and esterifies it

Stored inside (neutral) so gets rounder

49
Q

How does HDL esterify cholesterol?

A

LCAT/PCAT transfers a fatty acid from lecithin/phosphatidyl choline to cholesterol

To form a cholesterol ester and lysolecithin/lysophosphatidyl choline

50
Q

What does LCAT/PCAT stand for?

A

Lecithin (phosphatidyl choline) cholesterol acyl transferase

51
Q

Where is LCAT found?

A

In/on HDL

52
Q

What does CETP stand for?

A

Cholesterol ester transfer protein

53
Q

What is the function of CETP?

A

Passes some cholesterol ester from HDL to VLDL

Prevents product inhibition of LCAT so cholesterol uptake can continue

54
Q

What receptor on the liver recognises HDL?

A

SR-B1 (scavenger receptor B1)

55
Q

What is cholesterol a precursor for?

A

Steroid hormones

Bile acids

56
Q

What can cholesterol control?

A

Its own synthesis

The number of LDL/B-100 receptors on the cell surface

57
Q

What happens when LDL is taken up?

A

Endocytosis of LDL AND B-100 receptors

Cholesterol released and enters nucleus to inhibit production of enzymes involved in cholesterol synthesis

Receptors recycled

58
Q

What is the synthesis pathway of cholesterol?

A 
Acetyl CoA + acetoacetyl CoA
|
HMG CoA
| HMG CoA reductase
Mevalonate I
|
Cholesterol
59
Q

What is the rate-limiting step in cholesterol synthesis?

A

HMG CoA –> Mevalonate I by HMG CoA reductase

60
Q

What do statins inhibit?

A

HMG CoA reductase

61
Q

What do LDL receptors recognise?

A

Apo B-100

62
Q

What condition is caused by defective/deficient LDL receptors?

A

Familial hypercholesterolaemia

63
Q

How do people die from familial hypercholesterolaemia?

A

Atherosclerosis

64
Q

How can you try to treat familial hypercholesterolaemia?

A

Liver transplants

65
Q

What are some genetic factors that may cause hyperlipidaemia? (4)

A

Defective LDL receptor

Lipoprotein lipase deficiency

Apo C-II deficiency

Deficiency in apoproteins involved in remnant uptake

66
Q

What would defective LDL receptors cause?

A

Hypercholesterolaemia

High LDL in blood

67
Q

What would lipoprotein lipase deficiency cause?

A

High chylomicrons and VLDL in blood

68
Q

What would apo C-II deficiency cause?

A

High chylomicrons and VLDL in blood

69
Q

What would deficiency in apoproteins in remnant uptake cause?

A

High chylomicron and VLDL remnant in blood

70
Q

What are some risk factors for secondary hyperlipidaemia?

A

Obesity

Type II diabetes

Alcoholism

Dietary fatty acid

Dietary cholesterol?

71
Q

What is lipoprotein (a)?

A

LDL and apo a

72
Q

What is high plasma Lp(a) concentration associated with?

A

Coronary heart disease

73
Q

What can increase the plasma Lp(a) concentration?

A

Transfats

74
Q

What can decrease the plasma Lp(a) concentration?

A

Oestrogen

75
Q

What compound is Lp(a) related to and how may that be dangerous?

A

Plasminogen

May slow down breakdown of blood clots by competing with plasminogen (atherogenic)

76
Q

What is high blood cholesterol associated with?

A

Mortality from coronary heart disease

77
Q

What is plaque?

A

Complex structure involving inflammation and proliferation of smooth muscle in artery wall

Contains connective tissue and a pool of cholesterol-rich lipid

78
Q

What is a foam cell?

A

Macrophage filled with lipid (mainly cholesterol)

79
Q

What does a plaque begin as?

A

Fatty streak from an accumulation of foam cells

80
Q

Why do foam cells develop?

A

High LDL in blood so some is oxidised/modified (apo B-100 damaged)

Oxidised LDL not recognised by LDL receptors

Scavenger receptors on macrophages take up LDL

Macrophage receptors are not down-regulated so LDL uptake continues and cholesterol accumulates

BMS07 (7 decks)

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