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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
What do chylomicrons carry?
Mainly dietary fat
26
What do VLDL carry?
Mainly endogenous triacylglycerol
27
What do LDL carry?
Mainly cholesterol to tissues
28
What do HDL carry?
Mainly cholesterol from tissues to liver
29
What are nascent chylomicrons?
First-formed chylomicron from gut with apo B-48
30
What apoprotein do nascent chylomicrons have?
Apo B-48
31
How does a nascent chylomicron become a chylomicron?
In blood, picks up apo C-II and apo E from HDL
32
What part of triacylglycerols are taken up by adipose tissue?
Fatty acids
33
What enzyme hydrolyses triacylglycerol before fatty acid uptake? Where is it?
Lipoprotein lipase In capillaries
34
What activates lipoprotein lipase?
Insulin Apo C-II
35
Why is glycerol not used by adipose cells?
Do not have glycerol kinase to form glycerol phosphate
36
What apoproteins do chylomicron remnants have?
Apo E Apo B-48
37
Where does the chylomicron remnant go?
To liver via blood stream Taken up via apo E receptors on liver cells
38
What types of lipoprotein is synthesised by the liver?
VLDL HDL
39
What apoprotein is present on VLDL?
Apo B-100
40
What happens to VLDL when it enters the blood stream from the liver?
Picks up apo C-II and apo E from HDL
41
What is left after VLDL have passed the adipose tissue?
IDL - intermediate density lipoprotein
42
What do apoproteins do IDL have?
Apo E Apo C-II Apo B-100
43
What happens to IDL?
Half loses B-100 to become HDL Half loses apo C-II and apo E to become LDL
44
What apoproteins are found on HDL?
Apo E Apo C-II Apo A-I
45
Where are B-100 receptors found?
Liver cells Peripheral tissue
46
What do LDL receptors recognise?
Apo B-100
47
Where is HDL synthesised?
Liver Small intestine
48
What does newly synthesised HDL do?
Takes in cholesterol from periphery and esterifies it Stored inside (neutral) so gets rounder
49
How does HDL esterify cholesterol?
LCAT/PCAT transfers a fatty acid from lecithin/phosphatidyl choline to cholesterol To form a cholesterol ester and lysolecithin/lysophosphatidyl choline
50
What does LCAT/PCAT stand for?
Lecithin (phosphatidyl choline) cholesterol acyl transferase
51
Where is LCAT found?
In/on HDL
52
What does CETP stand for?
Cholesterol ester transfer protein
53
What is the function of CETP?
Passes some cholesterol ester from HDL to VLDL Prevents product inhibition of LCAT so cholesterol uptake can continue
54
What receptor on the liver recognises HDL?
SR-B1 (scavenger receptor B1)
55
What is cholesterol a precursor for?
Steroid hormones Bile acids
56
What can cholesterol control?
Its own synthesis The number of LDL/B-100 receptors on the cell surface
57
What happens when LDL is taken up?
Endocytosis of LDL AND B-100 receptors Cholesterol released and enters nucleus to inhibit production of enzymes involved in cholesterol synthesis Receptors recycled
58
What is the synthesis pathway of cholesterol?
``` Acetyl CoA + acetoacetyl CoA | HMG CoA | HMG CoA reductase Mevalonate I | Cholesterol ```
59
What is the rate-limiting step in cholesterol synthesis?
HMG CoA --> Mevalonate I by HMG CoA reductase
60
What do statins inhibit?
HMG CoA reductase
61
What do LDL receptors recognise?
Apo B-100
62
What condition is caused by defective/deficient LDL receptors?
Familial hypercholesterolaemia
63
How do people die from familial hypercholesterolaemia?
Atherosclerosis
64
How can you try to treat familial hypercholesterolaemia?
Liver transplants
65
What are some genetic factors that may cause hyperlipidaemia? (4)
Defective LDL receptor Lipoprotein lipase deficiency Apo C-II deficiency Deficiency in apoproteins involved in remnant uptake
66
What would defective LDL receptors cause?
Hypercholesterolaemia High LDL in blood
67
What would lipoprotein lipase deficiency cause?
High chylomicrons and VLDL in blood
68
What would apo C-II deficiency cause?
High chylomicrons and VLDL in blood
69
What would deficiency in apoproteins in remnant uptake cause?
High chylomicron and VLDL remnant in blood
70
What are some risk factors for secondary hyperlipidaemia?
Obesity Type II diabetes Alcoholism Dietary fatty acid Dietary cholesterol?
71
What is lipoprotein (a)?
LDL and apo a
72
What is high plasma Lp(a) concentration associated with?
Coronary heart disease
73
What can increase the plasma Lp(a) concentration?
Transfats
74
What can decrease the plasma Lp(a) concentration?
Oestrogen
75
What compound is Lp(a) related to and how may that be dangerous?
Plasminogen May slow down breakdown of blood clots by competing with plasminogen (atherogenic)
76
What is high blood cholesterol associated with?
Mortality from coronary heart disease
77
What is plaque?
Complex structure involving inflammation and proliferation of smooth muscle in artery wall Contains connective tissue and a pool of cholesterol-rich lipid
78
What is a foam cell?
Macrophage filled with lipid (mainly cholesterol)
79
What does a plaque begin as?
Fatty streak from an accumulation of foam cells
80
Why do foam cells develop?
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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