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Z OLD ESA 1- Metabolism > Energy storage > Flashcards

Energy storage Flashcards

1
Q

What is the bodies preferred fuel?

A

Glucose

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2
Q

What is the result of glucose being the bodies preferred food source?

A

The body requires a constant level of glucose as an energy source

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3
Q

Which tissues have an absolute requirement for glucose as energy source?

A
  • Erythrocytes (RBCs) and leukocytes
  • Testes
  • Kidney medulla
  • Lens and cornea of eye
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4
Q

Why is a stable glucose level required for normal brain function?

A

Because the brain prefers to use glucose as a fuel

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5
Q

Can the brain use any source other than glucose for fuel?

A

Yes, it can use ketone bodies, but not immediately

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6
Q

How long does it take for the brain to be able to utilise ketone bodies?

A

Oct-14

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7
Q

How much of the brains energy requirement can be obtained from ketone bodies?

A

~50%

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8
Q

What is required to enable blood glucose to be kept at required levels?

A

Store of glycogen

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9
Q

What form is glycogen stored in?

A

Granules

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10
Q

What cells have glycogen stores?

A

All of them to an extent

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11
Q

How is muscle glycogen present?

A

As both intra- and intermyofibrillar glycogen granules

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12
Q

How is liver glycogen stored?

A

As granules within hepatocytes

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13
Q

Describe the structure of glycogen

A
  • Polymer consisting of chains of glucose residues
  • Chains organised in branches
  • Residues linked by α-1,4- glycosidic bonds, with α-1,6-glycosidic bonds forming at branch points
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14
Q

Where to the branches in glycogen originate from?

A

A dimer of the protein glycogenin

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15
Q

What does the protein glycogenin act as in glycogen?

A

A primer at core of glycogen structure

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16
Q

How often are the branch points in glycogen?

A

Every 8-10 residues

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17
Q

What is the name given to glycogen synthesis?

A

Glycogenesis

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18
Q

Give the reactions that lead to the conversion of glucose to glycogen

A
  • Glucose + ATP → glucose 6-phosphate + ADP
  • Glucose 6-phosphate ↔ glucose 1-phosphate
  • Glucose 1-phosphate + UTP + H 2 O→ UDP-glucose + 2Pi
  • Glycogen (n resides) + UDP-glucose→ glycogen (n+1 residues) +UDP
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19
Q

What enzyme is required for conversion of glucose to G-6-P?

A

Hexokinase

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20
Q

What is hexokinase called in the liver?

A

Glucokinase

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21
Q

What is the enzyme for the conversion of G-6-P to G-1-P?

A

Phosphoglucomutase

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22
Q

What is the enzyme for the addition of glycogen residues (in reaction 4)?

A

NAME?

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23
Q

What does glycogen synthase do?

A

Adds α-1,4-glycosidic bonds

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24
Q

What does branching enzyme do?

A

Adds α-1,6-glycosidic bonds

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25
Q

What is the name given to glycogen degredation?

A

Glycogenolysis

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26
Q

Give the equations for glycogenolysis

A
  • Glycogen (n residues) + Pi → G-1-P + glycogen (n-1 residues)
  • G-1-P ↔ G-6-P
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27
Q

What is the enzyme used for removal of glycogen residues?

A
  • Glycogen phosphorylase

- or de-branching enzyme

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28
Q

What happens to G-6-P in muscle?

A

Glycolysis

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29
Q

What is happening when the muscle performs glycolysis on the G-6-P released from glycogen?

A

It is being used for local energy production

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30
Q

What happens to G-6-P in the liver?

A

Converted to glucose

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31
Q

What happens to the glucose produced from glycogen by the liver?

A

It is released into the blood for use by other body tissues

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32
Q

Is glycogenolysis just reversal of glycogenesis?

A

No

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33
Q

What is the result of glycogenolysis not being a simple reversal of glycogenesis?

A

Different enzymes allow for simultaneous inhibition of one pathway and stimulation of the other

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34
Q

Other than glycogenolysis, what other method does the liver have of producing G-6-P?

A

Gluconeogenesis

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35
Q

What is liver glycogen a buffer for?

A

Blood glucose concentration

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36
Q

How much of the liver mass is glycogen?

A

10%

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37
Q

What happens to the glucose in muscle?

A

It enters glycolysis, either being oxidised to CO 2 + ATP, or converted into lactate

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38
Q

What enzyme does the muscle lack?

A

G-6-Pase

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39
Q

What is the rate limiting enzyme in glycogen synthesis in the liver?

A

Glycogen synthase

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40
Q

What is the rate limiting enzyme in glycogen degradation?

A

Glycogen phosphorylase

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41
Q

In what fashion does glycogen metabolism regulation occur?

A

Reciprocal

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42
Q

What hormones regulate liver glycogen metabolism?

A
  • Glucagon
  • Adrenaline
  • Insulin
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43
Q

What effect does glucagon and adrenaline have on glycogen synthase?

A

Decreases enzyme activity

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44
Q

What effect does glucagon and adrenaline have on glycogen phosphorylase?

A

Increases enzyme activity

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45
Q

By what mechanism do adrenaline and glucagon affect the activity of enzymes?

A

Phosphorylation

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46
Q

What effect does insulin have on glycogen synthase?

A

Increases enzyme activity

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47
Q

What effect does insulin have on glycogen phosphorylase?

A

Decreases enzyme activity

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48
Q

By what mechanism does insulin affect the activity of enzymes?

A

De-phosphorylation

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49
Q

In what way does regulation of muscle glycogen differ from liver glycogen?

A
  • Glucagon has no effect

- AMP acts as an allosteric activator of muscle glycogen phosphorylase, but not liver form of enzyme

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50
Q

What are glycogen storage diseases?

A

Inborn errors in metabolism

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51
Q

What do glycogen storage diseases arise from?

A

Deficiency or dysfunction of enzymes of glycogen metabolism

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52
Q

How many distinct glycogen storage diseases are there?

A

11

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53
Q

What does the severity of a glycogen storage disease depend on?

A

The enzyme/tissue affected

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54
Q

What tissues can be affected by glycogen storage diseases?

A

Liver and/or muscle

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55
Q

How can someone have a disease in the liver or the muscle, but not both?

A

Glycogen phosphorylase is coded for by a different gene in liver than in the muscle, so it can be mutated in one but not the other

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56
Q

What can excess glycogen storage lead too?

A

Tissue damage

57
Q

What can diminished glycogen stores lead to?

A

Hypoglycaemia and poor exercise tolerance

58
Q

Give two examples of glycogen storage diseases

A
  • von Gierkes disease

- McArdles disease

59
Q

What causes von Gierkes disease?

A

Glucose-6-phosphate deficiency

60
Q

What causes McArdles disease?

A

Muscle glycogen phosphate deficiency

61
Q

What is gluconeogenesis?

A

The production of new glucose not pre-exisiting stores in glycogen

62
Q

When do we need to be able to synthesise new glucose?

A

When glycogen stores are low

63
Q

What happens beyond ~8 hours fasting?

A

Liver glycogen stores start to deplete

64
Q

Where does gluconeogenesis occur?

A

In liver, and to a lesser extent kidney cortex

65
Q

How many major precursors for gluconeogenesis are there?

A

3

66
Q

What are the 3 major precursors for gluconeogenesis?

A
  • Lactate
  • Glycerol
  • Amino acids
67
Q

When is lactate produced?

A

In anaerobic glycolysis in exercising muscles and RBC’s

68
Q

How does the process of gluconeogenesis using lactate occur?

A

Using the Cori Cycle

69
Q

What happens in the Cori cycle?

A
  • In the liver, 2 lactate molecules are converted to glucose
  • Glucose is transported from liver to muscle in the blood
  • In the muscle, glucose is converted into two lactate
  • The lactate produced in the muscle is transported in the blood to the liver
70
Q

When is glycerol released?

A

From adipose tissue when triglycerides are broken down

71
Q

What amino acids are used for gluconeogenesis?

A

Mainly alanine

72
Q

Can acetyl~CoA be converted into pyruvate?

A

No

73
Q

Why can’t acetyl~CoA be converted into pyruvate?

A

Because the pyruvate dehydrogenase reaction is irreversible

74
Q

What is the result of the inability of acetyl~CoA to be converted into pyruvate?

A

There is no net synthesis of glucose from acetyl~CoA

75
Q

How many reactions in gluconeogenesis are not simple reversions of corresponding steps in glycolysis?

A

3

76
Q

What are the key enzymes in gluconeogenesis?

A
  • Phosphoenolpyruvate carboxykinase (PEPCK)
  • Fructose 1,6-bisphosphatease
  • Glucose 6-phosphatease
77
Q

Which of the key enzymes in gluconeogenesis are key sites of control for the pathway?

A
  • Phosphoenolpyruvate carboxykinase (PEPCK)

- Fructose 1,6-bisphosphatease

78
Q

What does PEPCK do?

A

Catalyses conversion of oxaloacetate to phosphoenolpyruvate

79
Q

What does fructose 1,6-bisphosphatease do?

A

Catalyses conversion of fructose 1,6-bisphosphate to fructose 6-phosphate

80
Q

What are the 2 key control enzymes in gluconeogenesis controlled by?

A

Hormones

81
Q

What are the 2 key control enzymes in gluconeogenesis controlled in response to?

A
  • Starvation
  • Prolonged exercise
  • Stress
82
Q

What hormones affect the action of the key control enzymes in gluconeogenesis?

A
  • Glucagon
  • Cortisol
  • Insulin
83
Q

What affect does glucagon and cortisol have on PEPCK?

A

Increases the amount

84
Q

What effect does glucagon and cortisol have on fructose 1,6-bisphosphate?

A

Increased amount and activity

85
Q

What is the overall effect of glucagon and cortisol on gluconeogenesis?

A

Stimulates

86
Q

What effect does insulin have on PEPCK?

A

Decreases amount

87
Q

What effect does insulin have on fructose 1,6-bisphosphate?

A

It decreases the amount and activity

88
Q

What is the overall effect of insulin on gluconeogenesis?

A

Inhibits

89
Q

How are lipids stored?

A

As triacylglycerols (TAGs)

90
Q

What happens when energy intake is in excess of requirements?

A

It’s converted to triacylglycerol for storage

91
Q

Are TAGs hydrophilic or hydrophobic?

A

Hydrophobic

92
Q

How must TAGs be stored due to them being hydrophobic?

A

In anhydrous form in specialised tissue

93
Q

What is the specialised storage tissue for TAGs?

A

Adipose tissue

94
Q

Is TAG an efficient energy store?

A

Yes, highly

95
Q

How does the energy content per gram differ in TAGs and carbohydrate/protein?

A

x2 more in TAG than in carbohydrate or protein

96
Q

Under what conditions are TAG’s utilised?

A

NAME?

97
Q

How is storage and metabolism of TAGs controlled?

A

Hormones

98
Q

Describe the structure of adipocytes

A

A large lipid droplet with cytoplasm and organelles pushed to edge

99
Q

What does the lipid droplet in adipocytes consist of?

A

Mainly TAG and cholesterol ester

100
Q

How big are adipocytes?

A

~0.1mm in diameter, but expand as more fat is added

101
Q

How much can adipocytes increase in size on weight gain?

A

About fourfold

102
Q

What happens once adipocytes can’t expand anymore on weight gain?

A

They divide, increasing the total no. of fat cells

103
Q

What is fatty acid synthesis called?

A

Lipogenesis

104
Q

Where does lipogenesis occur?

A

Mainly in liver

105
Q

What is the major source of carbon for lipogenesis?

A

Dietary glucose

106
Q

How are fatty acids produced from glucose?

A
  • Glucose is converted to pyruvate in the cytoplasm
  • Pyruvate enters mitochondria, forms acetyl~CoA and OAA
  • Acetyl~CoA and OAA condenses to form citrate
  • Citrate goes back to cytoplasm, and is cleaved back to acetyl~CoA and OAA
  • Acetyl~CoA carboxylase produces malonyl~CoA from acetyl~CoA
  • Fatty acid synthase complex builds up fatty acids by sequential addition of 2 carbon units provided by malonyl~CoA
107
Q

What is the key regulator in fatty acid synthesis?

A

Acetyl~CoA carboxylase

108
Q

What does the fatty acid synthesis process require?

A

Both ATP and NADPH

109
Q

What increases fatty acid synthesis?

A
  • Insulin

- Citrate

110
Q

By what mechanism does insulin increase fatty acid synthesis?

A

Covalent de-phosphorylation

111
Q

By what mechanism does citrate increase fatty acid synthesis?

A

Allosteric activation

112
Q

What decreases fatty acid synthesis?

A

Glucagon/adrenaline and AMP

113
Q

By what mechanism do glucagon and adrenaline decrease fatty acid synthesis?

A

Covalent phosphorylation

114
Q

By what mechanism does AMP decrease fatty acid synthesis?

A

Allosteric inhibition

115
Q

What is the difference in the purpose cycle of reactions between FA oxidation and FA synthesis

A
  • In FA oxidation, the cycle of reactions remove C 2

- In FA synthesis, the cycle of reactions add C 2

116
Q

What is the difference in how is the C 2 is transferred in FA oxidation and FA synthesis?

A
  • In FA oxidation, C 2 removed as acetyl~CoA

- In FA synthesis, C 2 added as acetyl~CoA

117
Q

Which of FA oxidation or FA synthesis produced acetyl~CoA, and which consumes it?

A

NAME?

118
Q

What is the difference in the site of FA oxidation and FA synthesis?

A
  • Oxidation occurs in mitochondria

- Synthesis occurs in cytoplasm

119
Q

What is the difference in the enzymes used in FA oxidation and synthesis?

A

NAME?

120
Q

Is FA synthesis oxidative or reductive?

A

Reductive

121
Q

What is the result of FA synthesis being reductive?

A

It requires NADPH

122
Q

What is the difference in ATP requirement between FA oxidation and synthesis?

A

NAME?

123
Q

What is the difference in what the intermediates are linked to in FA oxidation and synthesis?

A

NAME?

124
Q

What is the difference in regulation between FA oxidation and synthesis?

A
  • Oxidation is regulated indirectly by availability of fatty acids in mitochondria
  • Synthesis is regulated directly by activity of acetyl~CoA carboxylase
125
Q

What is the difference in reaction to glucagon and adrenaline between FA oxidation and synthesis?

A

NAME?

126
Q

What is the difference in reaction to insulin between FA oxidation and synthesis?

A

NAME?

127
Q

What is the process of fat mobilisation called?

A

Lipolysis

128
Q

Give the equation for lipolysis

A

Triacylglycerol (in adipose tissue) → glycerol (in blood) + free fatty acids

129
Q

What enzyme catalyses lipolysis?

A

Hormone sensitive lipase

130
Q

What hormones is hormone sensitive lipase regulated by?

A

NAME?

131
Q

What is the effect of glucagon and adrenaline on hormone sensitive lipase?

A

Stimulates

132
Q

By what mechanism does glucagon and adrenaline stimulate hormone sensitive lipase?

A

Phosphorylation

133
Q

What is the effect of insulin on hormone sensitive lipase?

A

Inhibited

134
Q

By what mechanism does insulin inhibit hormone sensitive lipase?

A

Dephosphorylation

135
Q

Where does the glycerol in the blood produced by lipolysis go?

A

To liver

136
Q

What happens to glycerol in the liver?

A

It’s utilised as a carbon source for gluconeogenesis

137
Q

How do free fatty acids travel in the blood?

A

Complexed with albumin

138
Q

Where do free fatty acids in the blood go?

A

Muscle and other tissues

139
Q

What happens to free fatty acids in the muscle and other tissues?

A

ß-oxidation

Z OLD ESA 1- Metabolism (17 decks)

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