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MEH > Session 2 > Flashcards

Session 2 Flashcards

1
Q

What is the main product of glycolysis?

A

Pyruvate

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2
Q

What happens to the pyruvate produced in glycolysis?

A

Enters the link reaction where it is converted to acetyl CoA and carbon dioxide is given off

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3
Q

How many carbons are in a molecule of pyruvate? How many carbons are in a molecule of acetyl CoA?

A

3

2

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4
Q

Where does the conversion of pyruvate to acetyl CoA take place in the cell? What enzyme catalyses this reaction?

A

Mitochondrial matrix

Pyruvate dehydrogenase

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5
Q

What is the structure of Pyruvate dehydrogenase?

A

Complex made up of 5 enzymes

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6
Q

Give examples of cofactors required for the different enzymes that make up pyruvate dehydrogenase. What are these derived from? What are the clinical implications of this?

A

FAD, lipolic acid

B vitamins

Reactions are sensitive to vitamin B1 deficiency

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7
Q

Is the link reaction reversible or irreversible? Why?

A

Irreversible

Involves the loss of carbon dioxide

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8
Q

What reaction takes place in the link reaction?

A

Pyruvate + CoA + NAD+ ——> Acetyl CoA + CO2 + NADH + H+

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9
Q

PDH deficiency can result in…

A

Lactic acidosis

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10
Q

High energy substrates will cause PDH to ___________ its activated

Low energy substrates will cause PDH to __________ its activity

A

Lower

Increase

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11
Q

Give examples of molecules that act as activators for PDH

How do these molecules have an effect on PDH

A

Pyruvate
NAD+
ADP
Insulin

Through dephosphorylation

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12
Q

Give examples of molecules that act as inhibitors for PDH

How do these molecules have an effect on the PDH

A

Acetyl CoA
NADH
ATP
Citrate

Through phosphorylation

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13
Q

Where does the TCA cycle (Krebs cycle) take place in a cell?

A

Mitochondrial matrix

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14
Q

How many molecules of carbon dioxide are released per acetyl CoA entering the TCA cycle?

A

2

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15
Q

Does the TCA cycle involve oxidative or reductive reactions?

A

Oxidative

Requires NAD+ and FAD

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16
Q

Is energy produced in the TCA cycle? If so, in which forms?

A

Yes

ATP & GTP

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17
Q

The TCA cycle is important for producing precursors for ____________

A

Biosynthesis

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18
Q

Can the TCA cycle function in the absence of oxygen?

A

No

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19
Q

Per glucose entering glycolysis TCA produces…

A

6 NADH
2 FADH2
2 GTP
4 CO2

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20
Q

Acetyl CoA joins with which 4 carbon compound to form which 6 carbon compound in the TCA cycle?

A

Oxaloacetate

Citrate

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21
Q

How is the TCA cycle regulated?

A

By energy availability (e.g. High energy switches TCA cycle down)

By enzymes acting on the irreversible steps that involve the release of carbon dioxide

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22
Q

Which enzyme regulates the first irreversible step of the TCA cycle? What reaction does it catalyse?

A

Isocitrate dehydrogenase

Iscocitrate —> a-ketoglutarate

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23
Q

Which enzyme catalyses the second irreversible reaction of the TCA cycle? What reaction does it catalyse?

A

A-ketoglutarate dehydrogenase

A-ketoglutarate —> succinyl-CoA

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24
Q

TCA supplies precursors for biosynthetic processes , give some examples.

A

Citrate can be used to form fatty acids

Malate can be used to form amino acids

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25
Q

At the end of the TCA cycle all C-C and C–H bonds have been broken. What has happened to all the C atoms and H atoms?

A

All the C atoms have been oxidised to CO2

All the H atoms have been transferred to NAD+ and FAD

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26
Q

The high energy electrons in NADH and FADH2 are transferred to __________ with the release of large amounts of __________ which is used to drive _________ _________

A

Oxygen

Energy

ATP synthesis

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27
Q

What is stage 4 of carbohydrate metabolism? Where does this take place in the cell?

A

Electron transport and ATP synthesis

Inner mitochondrial membrane

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28
Q

What happens to the NADH/FADH2 in stage 4 of carbohydrate metabolism?

A

They are re-oxidised back to NAD+ and FAD

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29
Q

What happens to oxygen in stage 4 of carbohydrate metabolism?

A

Gains electrons and is reduced to water

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30
Q

A concentration gradient of which ions is set up across the inner mitochondrial membrane during stage 4 of carbohydrate metabolism? What is another term for this concentration/electrical gradient created?

A

H+ ions

Proton motive force

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31
Q

Describe the permeabilities of the inner and outer mitochondrial membranes

A

Outer - relatively permeable

Inner - highly impermeable

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32
Q

How are hydrogen ions pumped into the intermembrane space?

A

Electrons are released in the oxidation of NADH (and FADH2)

Electrons are passes on to proton translocation complexes in the inner mitochondrial membrane

Electrons lose energy as they pass through the PTC, energy used to drive H+ ions through the PTC into the inter-membrane space

H+ ion gradient created

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33
Q

How many PTCs do the electrons released in the oxidation of NADH pass through?

A

3

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34
Q

How many PTCs do the electrons produced in the oxidation of FADH2 pass through? Why is this number different than for NADH?

A

2

Electrons are already at lower energy in FADH2

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35
Q

How many H+ ions are pumped through in the oxidation of one molecule of NADH? How many H+ ions are pumped through in the oxidation of one molecule of FADH2?

A

6

4

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36
Q

What happens at the end of the electron transport chain to produce water?

A

2 electrons are picked up by atomic oxygen and 2 hydrogen ions to produce water (reduction reaction)

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37
Q

What happens to the hydrogen ions in the intermembrane space to produce ATP?

A

Pass through ATP synthase in the inner mitochondrial membrane back through to the matrix driving ATP synthesis

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38
Q

Can ATP synthase also work in the reverse direction?

A

Yes as ATPase

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39
Q

Which is the only route by which hydrogen ions can pass back through the inner mitochondrial membrane? Why is this?

A

via ATP synthase

Inner mitochondrial membrane is impermeable

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40
Q

How many moles of ATP are produced in the oxidation of 2 moles of NADH? How many moles of ATP are produced in the oxidation of 2 moles of FADH2?

A

5

3

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41
Q

Both oxidative phosphorylation and the electron transport chain are regulated by…

Give an example of how this works

A

Mitochondrial [ATP]

High ATP = Low ADP 
No substrate for ATP synthesis 
Inward flow of H+ stops 
Increased H+ ion concentration in intermembrane space 
Less H+ ions pumped 
Electron transport chain stopped
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42
Q

Give an example of an inhibitor that blocks electron transport. What consequence will this have on oxidative phosphorylation?

A

CO, CN-

No PMF, no oxidative phosphorylation

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43
Q

How does cyanide (CN-) specifically work as an inhibitor of the electron transport chain?

A

Prevents acceptance of electrons by oxygen

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44
Q

Give an example of an uncoupler of oxidative phosphorylation

A

Dinitrophenol
Dinitrocresol
Fatty acids

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45
Q

How do uncouplers of oxidative phosphorylation work?

A

Increase the permeability of the inner mitochondrial membrane to H+ ions
Protein gradient dissipated through uncoupling molecule rather than ATP synthase
Reduced proton motive force
Less ATP synthesis

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46
Q

What are ox/phos disease caused by? What effect can they have on carbohydrate metabolism?

A

Genetic defects in proteins encoded by mtDNA (e.g. Subunits of PTCs and ATP synthase)

Reduction in electron transport and ATP synthesis

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47
Q

Efficiency of the electron transport chain/oxidative phosphorylation depends on tightness of coupling.

In which form is energy commonly lost in these processes?

In brown adipose tissue, how is this coupling controlled?

What does this allow?

A

Heat

By fatty acids acting as uncouplers

Allowing extra heat generation

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48
Q

Where is brown adipose tissue commonly found? What is its function?

A

In newborn infants

To maintain heat, particularly around vital organs

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49
Q

What uncoupling protein is found in brown adipose tissue?

A

Thermogenin (UCP1)

50
Q

How does thermogenin (UCP1) work to produce extra heat in response to the cold?

A

Noradrenaline activates lipase which releases fatty acids from TAGs

Fatty acid oxidation produces NADH/FADH2 and begins electron transport

Fatty acids activate UCP1

UCP1 (rather than ATP synthase) transports H+ back into the mitochondria

Energy of PMF released as extra heat

51
Q

How many moles of ATP are produced per mole of glucose that enters glycolysis (in all stages of carbohydrate metabolism)?

A

32

52
Q

Does oxidative phosphorylation or substrate level phosphorylation provide most of the ATP required in cells?

A

Oxidative phosphorylation

53
Q

Can oxidative phosphorylation or substrate level phosphorylation occur in the absence of oxygen?

A

Oxidative - no

Substrate level - to a limited extent

54
Q

Are lipids generally soluble or insoluble?

A

Insoluble

55
Q

Lipids consist of which 3 elements only?

Phospholipids contain which 2 additional elements?

A

C, H and O

P and N

56
Q

Do lipids release more or less energy than carbohydrates when oxidised? Why?

A

More

More reduced than carbohydrates, so require more oxygen for complete oxidation

57
Q

What are the three classes of lipids?

A

Fatty acid derivatives
Hydroxy-methyl-glutaric acid derivatives
Vitamins

58
Q

Name some molecules that fit into the fatty acid derivative class of lipids (4)

A

Fatty acids
Triacylgylcerols
Phospholipids
Eicosanoids

59
Q

What is the function of fatty acids and triacylgylcerols?

A

Fuel molecule

Fuel storage and insulation

60
Q

What are eicosanoids?

A

Local mediators

61
Q

Name some molecules that fit into the hydroxy-methyl-glutamic acid derivative class of lipids (4)

A

Kentone bodies
Cholesterol
Cholesterol esters
Bile acids and salts

62
Q

What are ketone bodies? How many carbon atoms do they contain?

A

Water soluble fuel molecules

4

63
Q

What can cholesterol be used for? How many carbon atoms does cholesterol contain?

A

Membranes and steroid hormone synthesis

27

64
Q

What are the functions of cholesterol esters and bile acids/salts? How many carbon atoms do bile acids/salts contain?

A

Cholesterol storage

Lipid digestion
24

65
Q

Name the lipid soluble vitamins?

A

A, D, E and K

66
Q

The difference in energy storage between a healthy and obese person will be shown in their increased levels of…

How are the levels of glycogen stores and muscle protein affected?

A

Triacylglycerols

Remain the same

67
Q

What is the composition of a triacylglycerol? In which reaction type are they produced?

A

Glycerol backbone + 3 fatty acids

Esterification

68
Q

Triglycerides are hydrophobic and therefore stored in _____________ form

A

Anhydrous

69
Q

TAGs are stored in which tissues? In what circumstances are they utilised?

A

Adipose tissue

Prolonged exercise
Starvation
Pregnancy

70
Q

Where are dietary TAGs initially broken down in the body? (stage 1 of metabolism) What happens here? What are the TAGs broken down to?

A

In the GI tract, extracellularly

Hydrolysed in small intestine by pancreatic lipases

Fatty acids and glycerol

71
Q

Which enzymes hydrolyse TAGs in the small intestine?

A

Pancreatic lipases

72
Q

How many carbons are there in a glycerol molecule?

A

3

73
Q

What happens to the fatty acids and glycerol produced in the hydrolysis of dietary TAGs in the GI tract?

A

They are recombined in the small intestine and transported as TAG by chylomicrons. Then released into the circulation via lymphatics to adipose tissue.

74
Q

TAGs can either be transported to ______________ tissues for…

OR

__________ tissue for…

A

Consumer
Fatty acid oxidation and energy production

Adipose tissue
Storage

75
Q

Where in a cell does fatty acid oxidation take place? Where will fatty acids not be transported to in the body? (2)

A

Mitochondria

To cells without mitochondria (e.g. RBCs)
The brain - don’t easily pass through the blood-brain barrier

76
Q

TAGs in adipose tissue can be mobilised under ___________ control

A

Hormonal

77
Q

How are fatty acids transported to consumer tissues once mobilised in adipose tissue?

A

Bound to albumin forming an FA-albumin complex

78
Q

What hormones result in increased/decreased fat mobilisation?

A

Insulin - decreased

Glucagon/Adrenaline - increased

79
Q

What happens to TAGs in adipose tissue?

A

Undergo a constant cycle of breakdown and resynthesis

80
Q

What does the resynthesis of TAGs in adipose tissue require? What will happen if there is not enough of this substance?

A

Constant supply of glucose

Results in fatty acids being released into the circulation as an alternative fuel (not resynthesised into TAG)

81
Q

Fatty acids can be either saturated, unsaturated or amphipathic. What is meant by this?

A

Containing only single C-C bonds
Containing one or more C=C bonds
Containing hydrophilic and hydrophobic groups

82
Q

Give an example of a polyunsaturated fatty acid that is essential and required in the diet? Why is it required from the diet?

A

Linolenic acid

Mammals cant introduce a double bond in fatty acids beyond C9

83
Q

Where does stage 2 of fatty acid metabolism take place in target tissues?

A

Mitochondria

84
Q

What happens to the fatty acids once they have been transported to consumer tissues?

A

Fatty acid is activated by linking to coenzyme A in the cytoplasm

85
Q

How are activated fatty acids transporter across the inner mitochondrial membrane into the mitochondria?

A

Using a carnitine shuttle

86
Q

What happens to the fatty acid once it has been transported into the mitochondria?

A

It cycles through a sequence of oxidative reactions with 2 carbons removed each cycle

87
Q

Where does fatty acid activation take place? Which enzyme catalyses the activation of fatty acids?

A

Cytoplasm

Fatty acyl CoA synthase

88
Q

What is the function of carnitine shuttles?

A

Transport activated fatty acids across the mitochondrial membrane

89
Q

How are acyl-CoA (activated fatty acids) transported in carnitine shuttles?

A

There is an exchange of CoA for carnitine producing acyl carnitine

Acyl carnitine can be recognised and transported by the carnitine shuttle

Reverse reaction occurs in the matrix, reproducing acyl-CoA and the carnitine is recycled

90
Q

Which enzymes catalyse the exchange of CoA for carnitine and then the reverse reaction?

A

CAT1

CAT2

91
Q

The carnitine shuttle process is regulated therefore controlling the rate of…

This process is inhibited by…

A

Fatty acid oxidation

High energy levels - e.g. Levels of malonyl-CoA (biosynthetic intermediate)

92
Q

Where does beta oxidation of fatty acids take place? Can it take place in the absence of oxygen?

A

Mitochondrial matrix

No

93
Q

What happens in the beta oxidation of fatty acids? What molecules are produced/used - how does this result in the production of ATP?

A

A series of oxidative reactions where 2C are removed from the fatty acid each cycle

FADH2 and NADH are produced to be used in the electron transport chain
Acetyl CoA (2C) produced for use in the TCA cycle

Water and CoA are required

94
Q

Are carbohydrates or fats a more high energy fuel?

A

Fats - fatty acid oxidation derives more energy

95
Q

How is glycerol transported in the body and where is it metabolised?

A

Blood

Liver

96
Q

Glycerol is converted during its metabolism into glycerol phosphate through the action of which enzyme?

A

Glycerol kinase

97
Q

Glycerol is metabolised in the liver and is used for either…

A

Glycolysis

Synthesis of TAGs

98
Q

Acetyl-CoA is derived from which vitamins?

It is an important intermediate in both _________ and __________ pathways

What is the structure of acetyl-CoA

A

B vitamins

Anabolic and catabolic

CH3CO group linked to coenzyme A

99
Q

Where are ketone bodies specifically synthesised? What are they?

A

Liver mitochondria

Water soluble fuel molecules

100
Q

What are the 3 ketone bodies produced in the body?

A

Acetoacetate
Acetone
B-hydroxybutyrate

101
Q

How is acetone produced?

A

Through the spontaneous breakdown of acetoacetate

102
Q

Are ketone bodies hydrophobic or hydrophilic? How are they transported in the plasma?

A

Hydrophilic

Freely, without carrier molecules

103
Q

What is the normal plasma ketone body concentration?

A

Less than 1 mM

104
Q

What is the plasma ketone body range seen in starvation (physiological ketosis)?

A

2-10 mM

105
Q

Ketone bodies are produced from…

How will the levels of ketone bodies in the plasma be affected in the case of reduced glucose levels?

A

Fatty acids —> Acetyl CoA —> Ketone bodies

Reduced glucose, will release fatty acids which and produce ketone bodies resulting in an increased concentration

106
Q

What plasma concentration of ketone bodies can be seen in untreated type 1 diabetes (pathological ketosis)?

A

> 10 mM

107
Q

Which enzyme is inhibited by statins?

A

HMG-CoA reductase

108
Q

Acetoacetate is produced from which molecule? Through the action of which enzyme?

A

HMG-CoA (from acetyl CoA)

HMG CoA lyase

109
Q

Which enzyme catalyses the production of HMG-CoA from Acetyl CoA?

A

HMG-CoA synthase

110
Q

How does a low glucose concentration resulting in increased production of ketone bodies?

A

Increased mobilisation of fatty acids
Oxidation of fatty acids producing NADH and acetyl CoA
Acetyl CoA can be used for the synthesis of ketone bodies

111
Q

In states of starvation (low glucose), how is acetyl CoA used for the production of ketone bodies rather than in the TCA cycle?

A

Oxidation of fatty acids produces NADH - a high energy signal that inhibits the regulatory enzymes of the TCA cycle

112
Q

What are the regulatory enzymes of the TCA cycle?

A

Isocitrate dehydrogenase

A-ketoglutarate dehydrogenase

113
Q

How are ketone bodies metabolised?

A

Transported in the blood from the liver to the muscles where they are converted to acetoacetate and fed into the TCA cycle for the resynthesis of acetyl CoA

114
Q

Ketone body synthesis is regulated by…

A

The insulin/glucagon ration

115
Q

Describe the regulation of ketone body synthesis in the fed state.

A

In the fed state, there is a high level of insulin - resulting in the inhibition of HMG-CoA lyase and the activation of HMG-CoA reductase resulting in cholesterol synthesis and less ketone body production

116
Q

Describe the regulation of ketone body synthesis in starvation?

A

High levels of glucagon
HMG CoA lyase activated, HMG CoA reductase inhibited
Increased ketone body synthesis, rather than cholesterol synthesis

117
Q

What happens in early starvation with regards to any remaining circulating glucose and ketone body production?

A

Ketone bodies begin to be produced

Any remaining circulating glucose conserved for use by the brain

118
Q

How is the brain fuelled in late starvation when glucose levels are very low?

A

Protein in muscle begins to break down to amino acids

Amino acids used for gluconeogenesis

Glycogenolysis: glycogen —> glucose

Glucose used in brain (rarely ketone bodies also used)

119
Q

Ketonuria is a common indicator of…

A

Diabetes

120
Q

What type of molecules are acetoacetate and b-hydroxybutyrate? What can this result in?

A

Strong organic acids

Ketoacidosis

121
Q

How can acetone be excreted via the lungs? What is the clinical significance of this?

A

It is volatile

Characteristic smell of nail polish remover on breath

MEH (9 decks)

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