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Z OLD ESA 1- Metabolism > Energy Production- Lipids > Flashcards

Energy Production- Lipids Flashcards

1
Q

Are lipids structurally similar or diverse?

A

Diverse

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2
Q

Are lipids generally hydrophilic or hydrophobic?

A

Hydrophobic

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3
Q

What is the result of lipids generally being hydrophobic?

A

They’re generally insoluble in water

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4
Q

What elements to most lipids contain?

A

C, H and O only

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5
Q

What elements do some lipids contain?

A

Phospholipids contain P and N

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6
Q

Are lipids more or less reduced than carbohydrates?

A

More

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7
Q

What is the result of lipids being more reduced than carbohydrates?

A

NAME?

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8
Q

What are the 3 classes of lipids?

A
  • Fatty acid derivatives
  • Hydroxy-methyl-glutaric acid derivates
  • Vitamins
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9
Q

What are the 4 types of fatty acid derivatives?

A

NAME?

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10
Q

What are fatty acids used for?

A

Fuel molecules

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11
Q

What are triglycerides used for?

A

NAME?

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12
Q

What are phospholipids used for?

A

Components of membranes and plasma lipoproteins

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13
Q

What are eicosanoids used for?

A

Local mediators

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14
Q

What do local mediators do?

A

Signal between cells

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15
Q

What is the advantage of having local mediators?

A

They produce a coordinated response

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16
Q

What are the 4 types of hydroxy-methyl-glutatic acid derivatives?

A

NAME?

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17
Q

What are ketone bodies?

A

Water soluble fuel molecules

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18
Q

What are ketone bodies derived from?

A

Fats

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19
Q

What is cholesterol used for?

A
  • Membranes

- Steroid hormone synthesis

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20
Q

What are cholesterol esters used for?

A

Cholesterol storage

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21
Q

What are bile acids and salts used for?

A

Lipid digestion

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22
Q

Can the body make vitamins?

A

No

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23
Q

What are triacylglycerols (TAGs) composed of?

A
  • Glycerol backbone

- Fatty acid side chain

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24
Q

What is the glycerol backbone in TAGs?

A

3C sugar derived from glycolysis

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25
Q

What does the fact that the glycerol backbone comes from glycolysis mean?

A

Fatty acid synthesis requires glycolysis

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26
Q

Why is it said that the fatty acid side chains are highly reduced?

A

There are 2 H’s on every atom

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27
Q

What is the process of producing TAGs from glycerol and fatty acids called?

A

Esterification

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28
Q

What is the process of producing glycerol and fatty acids from TAGs called?

A

Lipolysis

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29
Q

What must be done due to the fact that TAGs are hydrophobic?

A

They must be stored in anhydrous form

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30
Q

What tissues are TAGs stored in?

A

Specialised tissue- adipose

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31
Q

When are TAGs utilised?

A

NAME?

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32
Q

How is storage and mobilisation of TAGs controlled?

A

Hormones

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33
Q

What are triglycerides broken down to in the GI tract?

A

NAME?

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34
Q

Can glycerol and fatty acids be transported in the blood?

A
  • Glycerol can

- Fatty acids can’t

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35
Q

How are fatty acids transported in the blood?

A

On chylomicrons

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36
Q

Where does glycerol end up?

A

Liver

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37
Q

Where do chylomicrons take fatty acids?

A

Adipose tissue

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38
Q

What happens when the muscles demand fuel?

A

Adipose is broken down to release fatty acids, which are carried in the blood to muscles

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39
Q

Where does stage 1 of dietary triacylglycerol metabolism occur?

A

In the GI tract- extracellular

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40
Q

What does stage 1 of dietary TAG metabolism occur due to?

A

Lipases

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41
Q

What releases the lipases responsible for stage 1 of TAG metabolism?

A

Pancreas

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42
Q

What do the lipases do in stage 1 of TAG metabolism?

A

Hydrolyse lipids in the small intestine into fatty acids and glycerol

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43
Q

What happens once the lipids have been hydrolysed in the small intestine?

A

They are recombined in the small intestine and transported as TAG by lipoproteins (chylomicrons)

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44
Q

Where do chylomicrons transport TAG’s to?

A

Adipose tissue and consumer tissue

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45
Q

What happens to TAGs in adipose tissue?

A

It is stored as TAG until fat mobilisation

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46
Q

What stimulates fat mobilisation?

A

Glucagon / adrenaline

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47
Q

What inhibits fat mobilisation?

A

Insulin

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48
Q

What enzyme is responsible for fat mobilisation?

A

Hormone-sensitive lipase

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49
Q

What carries mobilised fat from adipose tissue to consumer tissues?

A

FA-albumin

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50
Q

Why is FA-albumin needed to carry mobilised fat?

A

Because fat is insoluble, therefore can’t go around on it’s own

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51
Q

What happens to fats at consumer tissues?

A

Fatty acids are oxidised to produce energy

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52
Q

Where can fatty acid oxidation not occur?

A
  • Tissues without mitochondria, e.g. RBCs

- Brain

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53
Q

Why can’t fatty acids be oxidised to produce energy in tissues without mitochondria?

A

They are highly reduced, so produce lots of reducing equivalents, which needs mitochondria

54
Q

Why can’t fatty acids be oxidised to produce energy in the brain?

A

Fatty acids don’t easily pass through the blood-brain barrier

55
Q

What happens to fatty acids in the GI tract?

A

They are converted back to triglycerides

56
Q

How are fatty acids packaged?

A

Into lipoprotein particles- chylomicrons

57
Q

How are packaged fatty acids released into circulation?

A

Via lymphatics

58
Q

What does low extracellular [glucose] result in?

A

Fatty acid release as an alternative fuel

59
Q

Why does low extracellular [glucose] lead to fatty acid release as an alternative fuel?

A

If [glucose] falls, [glycerol-1-P] also falls, so substrate not available for resynthesis, leading to fatty acid build up

60
Q

What is the general formula of fatty acids?

A 
CH 3 (CH 2 ) n COOH
 where n=14-18
61
Q

Are fatty acids saturated or unsaturated?

A

Can be either

62
Q

What is meant by fatty acids being amphipathic?

A

They contain both hydrophilic and hydrophobic groups

63
Q

Why are certain polyunsaturated fatty acids essential?

A

Mammals cannot introduce a double bond beyond C9

64
Q

Where does stage 2 of FA metabolism occur?

A

Mitochondria

65
Q

Where is the FA activated?

A

Outside of mitochondrion, in the cytoplasm

66
Q

How is a FA activated?

A

By linking of CoA, via a high energy bond

67
Q

What enzyme is used to activate FA’s?

A

Fatty acid CoA synthase

68
Q

Give the equation for the activation of fatty acids

A

Fatty acid + ATP + CoA → fatty acid~CoA + AMP +2Pi

69
Q

What is 2Pi

A

Pyruphosphate- 2 phosphates together

70
Q

Is 2Pi stable or unstable?

A

Very unstable

71
Q

What is the result of 2Pi being very unstable?

A

It hydrolyses spontaneously, pushing the reaction in the forward direction

72
Q

How are activated fatty acids transported across inner mitochondrial membrane?

A

Using carnitine shuttle

73
Q

What happens to FA during stage 2 of FA metabolism?

A

They cycle through a sequence of oxidative reactions, with C 2 removed each cycle

74
Q

Give the equation for the reaction that occurs at each cycle of stage 2 of FA metabolism?

A

C n + FAD + H 2 O + NAD + → C n-2 + C 2 + FADH 2 + NADH + H +

75
Q

What does the carnitine shuttle do?

A

Transports fatty acyl~CoA across the mitochondrial membrane

76
Q

How does the carnitine shuttle work?

A
  • In the intermembrane space, carnitine is converted to acyl carnitine by action of the enzyme of CAT1. This reaction also converts acyl~CoA to CoA
  • The acyl carnitine can be transported through the inner mitochondrial membrane by the carnitine shuttle transporter
  • In the matrix, acyl carnitine is converted to carnitine by the action of CAT2. This reaction also converts CoA to acyl~CoA- there is now acyl~CoA inside the matrix .
  • The carnitine produced can be transported back out to the intermembrane space by the carnitine shuttle transporter
77
Q

What is the result of the carnitine shuttle be regulated?

A

It controls the rate of FA oxidation

78
Q

What inhibits the carnitine shuttle?

A

Malonyl~CoA

79
Q

What is malonyl~CoA?

A

Short, activated fatty acid that is a precursor to fat biosynthesis

80
Q

What can happen if there are defects in the transport system?

A

Won’t be able to switch to fatty acid metabolism, because can’t get across mitochondrial membrane

81
Q

What are the symptoms of defects in the carnitine transport system?

A

NAME?

82
Q

What is fatty acid catabolism also known as?

A

ß-oxidation

83
Q

Give the equation for ß-oxidation

A

C n + FAD + H 2 O + NAD + + CoA→ C n-2 + acetyl~CoA + FADH 2 + NADH + H +

84
Q

What are all intermediates linked to in ß-oxidation?

A

CoA

85
Q

Is more energy derived from glucose or FA metabolism?

A

FA

86
Q

Where is glycerol metabolised?

A

In the liver

87
Q

How does glycerol get to the liver?

A

It is transported in the blood

88
Q

Describe the metabolism of glycerol

A
  • Glycerol converted to glycerol phosphate by the action of glycerol kinase. This requires ATP
  • Glycerol phosphate can be used in triacylglycerol synthesis, or converted into DHAP (which also converts NAD + to NADH)
  • DHAP can then be used in glycolysis
89
Q

What is the main convergence point for catabolic pathways?

A

Acetyl-CoA

90
Q

What does acetyl-CoA consist of?

A

CH 3 CO group linked to CoA

91
Q

How is theCH 3 CO group linked to CoA?

A

Via a S atom

92
Q

What is the significance of acetyl-CoA being linked by a S atom?

A

High energy of hydrolysis, therefore is an energy storing bond

93
Q

What vitamin does CoA contain?

A

B

94
Q

What is the significance of CoA containing vit B?

A

The body can’t produce it

95
Q

What is the function of acetyl~CoA?

A

It’s an important intermediate in both catabolic and anabolic pathways

96
Q

What can acetyl~CoA be converted into?

A
  • Fatty acids
  • CO 2
  • Hydroxymethylglutaric acid (HMG)
97
Q

What can fatty acids be converted into?

A

NAME?

98
Q

What can HMG be converted into?

A

NAME?

99
Q

How many ketone bodies are produced in the body?

A

3

100
Q

What are the 3 ketone bodies produced in the body?

A

NAME?

101
Q

Effectively, what is acetoacetate?

A

2 acetate molecules linked together

102
Q

Where is acetoacetate found?

A

Liver

103
Q

What produces acetone?

A

Spontaneous (non-enzymatic) decarboxylation of acetoacetate

104
Q

Where is ß-hydroxybutayrate found?

A

In the liver

105
Q

What is the normal plasma ketone body concentration?

A
106
Q

What is it called when a patient has a plasma ketone concentration of 2-10mM?

A

Physiological ketosis

107
Q

When may physiological ketosis occur?

A

Starvation conditions

108
Q

What is it called when a patient has a plasma ketone concentration of >10mM?

A

Pathological ketosis

109
Q

When may pathological ketosis occur?

A

Untreated type 2 diabetes

110
Q

What synthesises ketone bodies?

A

Liver mitochondria

111
Q

Describe the synthesis of ketone bodies

A
  • Acetyl~CoA converted into HMG~CoA by action of synthase
  • HMG~CoA can be converted into mevalonate by action of HMG-CoA reducatase (which is consequently converted into cholesterol), or acetoacetate by action of lyase.
  • Acetoacetate converted to acetone by spontaneous breakdown, or ß-hydroxybutyrate
112
Q

How can HMG-CoA be used as a site of action clinically?

A

For statin drugs- if inhibited, it can reduced cholesterol levels in patients

113
Q

How is ketone body production controlled in the liver?

A

The acetyl-CoA can be diverted into the TCA cycle, which reduces substrate availability for ketone body production

114
Q

What enzymes are involved in the regulation of ketone body production in the liver?

A
  • Isocitrate dehydrogenase

- α-ketoglutarate dehydrogenase

115
Q

How does isocitrate dehydrogenase and α-ketoglutarate dehydrogenase regulate ketone body production in the liver?

A
  • These enzymes are inhibited by low NAD + substrate availability and NADH product inhibition.
  • If they are inhibited, build up of product, meaning less acetyl-CoA diverted into TCA cycle, so more ketone body production
116
Q

Describe the metabolism of ketone bodies

A
  • Acetoacetate and ß-hydroxybutyrate in the liver can be transported in the blood to the muscle
  • In the muscle,ß-hydroxybutyrate is converted into acetoacetate (which also causes conversion of NAD + to NADH)
  • Acetoacetate + succinyl CoA (in the TCA) → acetoacetate~CoA+ succinate (in the TCA) - this reaction keeps the TCA cycle going, which produces ATP
  • The acetoacetate~CoA is converted into acetyl~CoA, which feeds into the TCA cycle at citrate
117
Q

What happens when acetoacetate is carried in the blood?

A

Some is lost as acetate in the bloodstream

118
Q

What happens when ß-hydroxybutyrateis carried in the blood?

A

Italso carries hydrogen

119
Q

What hormone ratio regulates ketone body synthesis?

A

Insulin:glucagon

120
Q

In what insulin:glucagon ratio are ketone bodies synthesised?

A

When insulin is low, therefore glucagon is high

121
Q

In what conditions would insulin be low and glucagon high?

A

NAME?

122
Q

What happens when insulin is high and glucagon is low?

A

Lyase (the enzyme that produces ketone bodies is inhibited), and reductase is activated, leading to cholesterol synthesis

123
Q

What is the advantage of ketone bodies in starvation conditions?

A

They spare glucose

124
Q

Why is advantageous for ketone bodies to spare glucose?

A

The body needs to maintain circulating glucose to supply the brain, RBC etc

125
Q

Are ketone bodies hydrophilic or hydrophobic?

A

Hydrophilic

126
Q

What happens when ketone bodies rise above the renal threshold?

A

They are excreted in urine

127
Q

What is it called when ketone bodies are excreted in urine?

A

Ketouria

128
Q

What condition occurs when ketone body concentrations get to high?

A

Ketoacidosis

129
Q

What is ketoacidosis?

A

Acidification of the circulation

130
Q

Why does ketoacidosis occur?

A

Because acetoacetate and ß-hydroxybutyrate are relatively strong organic acids

131
Q

Why can ketoacidosis sometimes be detected on the breath?

A

Because the volatile acetone may be excreted via the lungs

Z OLD ESA 1- Metabolism (17 decks)

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