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ESA2 > MEH Carb metabolism > Flashcards

MEH Carb metabolism Flashcards

1
Q

How much glucose is present in blood at any one time?

A

5mM

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2
Q

Name 4 types of sugar disorder/disease

A

Galactosaemia
Fructose intolerance
Lactose intolerance
Diabetes

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3
Q

What level of glucose in the blood is considered too high (e.g. in diabetes)

A

≥ 7mM

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4
Q

Why can sugars be metabolised using less energy than for fats?

A

As they are partially oxidised so require less O2 for complete oxidation

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5
Q

Where is glycogen synthesised in the body? What bonds does it contain?

A

Liver and skeletal muscle

alpha-1,4 and alpha 1,6 (branching) glycosidic bonds

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6
Q

Why do RBC have an absolute requirement for Glucose?

A

No mitochondria so need glucose to undergo anaerobic glycolysis for energy

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7
Q

Why do neutrophils have an absolute requirement for glucose?

A

Because they use their O2 for other processes - respiratory burst to kill pathogens

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8
Q

Why do the innermost cells of the kidney medulla have an absolute requirement for glucose?

A

Because they have a high demand for O2 but O2 in the blood is low when it gets here, so need anaerobic glycolysis

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9
Q

Why does the lens of the eye have an absolute requirement for glucose?

A

Poor blood supply of O2 as needs to be transparent so replies on anaerobic glycolysis

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10
Q

Does the CNS have an absolute requirement for glucose? What else can it use?

A

No but it prefers it

Can supplement with ketone in times of starvation but needs time to adapt.

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11
Q

What happens to GLUT4 and glucose uptake into tissues in the presence of insulin?

A

Insulin triggers uptake of glucose into adipose and skeletal muscle via GLUT4 - upregulation of receptors on membrane

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12
Q

Where in the body is the main site of fructose and galactose metabolism?

A

Liver

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13
Q

What is glycolysis driven by the need for? What is it driven by in the liver?

A

Driven by the need for energy. In the liver driven by glucose delivered

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14
Q

How many ATP produced in glycolysis? What size Carbon intermediates does it produce per glucose molecule?

A

2 (makes 4 but used 2 in the investment stage)

3C and 6C intermediates

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15
Q

Is glycolysis oxidation or reduction of glucose?

A

Oxidation

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16
Q

Is glycolysis in the cytosol or mito?

A

Cytosol

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17
Q

Does glycolysis occur in all tissues?

A

Yes

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18
Q

How can glycolysis be anaerobic?

A

With an enzyme pyruvate dehydrogenase

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19
Q

What is the difference between Hexo and Glucokinase?

A

Hexo - low affinity and inhibited by glucose-6P

Gluco - in liver - high affinity and not inhibited by product

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20
Q

What are 3 main enzymes of glycolysis and what products do they form? Are they reversible?

A

1) Hexokinase/Gluco Glucose –> Glucose 6P
2) PFK –> Fructose 6P to Fructose 1,6BisP
3) Pyruvate kinase –> phosphoenolpyruvate to pyruvate

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21
Q

Which enzyme in glycolysis is a key control enzyme?

A

PFK

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22
Q

Why so many stages of glycolysis?

A

1) Gives versatility
2) Some parts reversible
3) Allows fine control
4) Chemical reactions easier in smaller parts

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23
Q

Why are stages 1, 3, 10 of glycolysis irreversible?

A

As they have a large -ve gibbs free energy

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24
Q

Why is step 3 the committing step of glycolysis?

A

As step 2 fructose 6P can be reversibly changed to glucose6P that can go onto other pathways. But fructose 1,6bisP cannot be converted back - so the only way is glycolysis

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25
Q

Why can glucose 6P not cross the plasma membrane but glucose can?

A

As glucose has been phosphorylated it is now negatively charged so can’t cross membrane

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26
Q

What happens after fructose 1,6bisP in glycolysis?

A

the 6C is converted into 2 3C intermediates that are interchangeable

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27
Q

Is there loss of CO2 in glycolysis?

A

No

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28
Q

When Glucose is oxidised - where do the electrons go?

A

to carrier molecule NAD+ that is reduced to NADH - then contains reducing power.

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29
Q

Is glycolysis exergonic or endergonic overall?

A

Exergonic

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30
Q

What is substrate level phosphorylation? What are the 2 net ATP a result of?

A

It is phosphorylation that is not couple to oxidation - is quicker. 2 net ATP in glycolysis are produced in this way by adding Pi to ADP

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31
Q

To convert pyruvate to glucose, which steps need to be bypassed? What is this called?

A

3 steps
10, 3, 1 (pyruvate kinase, PFK, hexo/glucokinase)

Called gluconeogenesis

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32
Q

What is FDG and what can it be used for clinically?

A

Radioactive hexokinase, can be used to scan for cancers as they have increased rates of glycolysis

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33
Q

How is PFK a key regulator of glycolysis? Which two ways?

A

1) Allosteric - inhibited by increased ATP, stimulated by high AMP
2) Hormonal - inhibited by glucagon, stimulated by insulin

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34
Q

Which hormone stimulates gluconeogenesis?

A

Glucagon

35
Q

4 ways that glycolysis is regulated via the 3 main enzymes? How is glycolysis regulated by high/low energy signals?

A

PFK - 3 ways explained in another Q
Hexokinase - product inhibition by glucose 6P
Pyruvate Kinase - stimulated by high insulin
Metabolic regulation - High NADH or low NAD+ is a high energy signal that inhibits glycolysis

36
Q

Name 2 important intermediates in glycolysis - what enzymes are used?

A

1) Glycerol phosphate - glycerol-3 phosphate dehydrogenase

2) 2,3 BPG - bisphosphoglycerate mutase

37
Q

What are these to glycolysis intermediates important for?

  • Glucose phosphate
  • 2,3 BPG
A

Glucose phosphate - important for lipid biosynthesis in adipose and liver

2,3 BPG - promotes release of O2 at tissues in RBCs

38
Q

Does lipid synthesis in adipose and liver require glycolysis?

A

Yes adipose

No liver - can also phosphorylate directly from glycerol

39
Q

Once NAD+ is reduced to NADH what is needed to regenerate it? Why is this relevant in RBCs for example?

A

Needs O2 to regenerate back to NADH

RBC don’t have mito so can regenerate NAD+ back to NADH so need lactate dehydrogenase to complete glycolysis

40
Q

What would happen if all NAD+ was reduced to NADH hypothetically?

A

Glycolysis would stop when all NAD+ is converted to NADH in step 6 of glycolysis.

41
Q

What reaction does lactate dehydrogenase catalyse? IS this reversible? Where in the body can use lactate as a direct fuel? Where else can lactate be used and how?

A

Pyruvate + NADH to Lactate + NAD+

Yes reversible using same enzyme e.g. in heart

In liver and kidney for gluconeogenesis that can then be used in glycolysis

42
Q

In low O2 conditions what happens to pyruvate in glycolysis?

A

Converted to lactate instead of stage 4 of metabolism that requires O2

43
Q

When would gluconeogenesis in the liver and kidney be impaired (3)

A

Liver disease
Vitamin deficiency
Enzyme deficiency

44
Q

What is normal, hyperlactaemia and lactic acidosis levels in the blood?

A

Normal below 1mM
Hyper - 2-5
Lactic acidosis about 5mM and reduction in pH

45
Q

Which 3 enzymes are involved in galactose metabolism so it can either enter glycolysis or be stored as glycogen? Can any or all result in galactosaemia if deficient?

A

1) Galactokinase (Galactose –> galactose 1P)
2) Uridyl transferase (Galactose 1P to glucose 1P)
3) UDP - galactose epimerase (Galactose 1P to UDP galactose)

Any of these can result in galactosaemia - uridyl transferase is the worst one

46
Q

What happens if fructokinase or aldolase are missing in humans? What is the treatment?

A

1) Fructo - essential fructosuria - no clinical signs - fructose in urine
2) Aldolase - fructose intolerance - Fructose 1P accumulates in liver and leads to liver damage.

Remove fructose from diet

47
Q

Where does the pentose phosphate pathway come off from glycolysis? What is it used for? What is the rate limiting enzyme?

A

From Glucose 6P
Essential for biosynthesis as creates NADPH, also for GSH maintenance and detoxification reactions
Rate limiting enzyme is G6PDH

48
Q

What else is made from the pentose phosphate pathway and what is it’s use? What can the 5C sugars in pentose phosphate pathway be used for?

A

Also creates Ribose - 5-P used to make DNA and RNA, nucleotides and coenzymes.

5C sugars can be converted to 6C and 3C sugars that are then fed back into glycolysis.

49
Q

Is ATP synthesised in the pentose phosphate pathway? is CO2 produces?

A

No ATP is not

Yes CO2 is produced unlike glycolysis

50
Q

What is the role of glutathione (GSH)?

A

Protective role against oxidative damage in cells.

51
Q

What happens in G6PDH deficiency?

A

Get low NADPH, low glutathione, cells prone to oxidative stress, particularly RBCs, become aggregated - Heinz bodies - results in haemolytic anaemia

52
Q

How does pyruvate enter stage 3 metabolism (TCA cycle)? What enzyme is used? Is this reversible and what are the implications of this? Where in the cell is this?

A

It does not enter directly - is metabolised first by pyruvate dehydrogenase. Is irreversible (irreversible loss of CO2) so you cannot convert Acetyl Co A to pyruvate to glucose. In mito matrix.

53
Q

What happens in pyruvate dehydrogenase deficiency?

A

Lactic acidosis - pyruvate gets converted to lactic acid instead

54
Q

How is PDH regulated?

A

Allosterically by acetyl co A
Stimulated by insulin (fed state)
Stimulated by ADP and inhibited by ATP and NADH

55
Q

Why are there no known genetic defects in the TCA cycle?

A

As they would be lethal

56
Q

Does the TCA cycle require oxygen?

A

Yes

57
Q

What is the main aim of TCA cycle in terms of breaking Acetyl Co A

A

To break the C-C bond in acetyl co A, and oxidise the C atoms to CO2. The H+ and e- released from acetate are transferred to NAD+ and FAD

58
Q

What does TCA cycle produce?

A

2 ATP (GTP)
2CO2
Precursors for biosynthesis - amino acids, haem, glucose, fatty acids
Is oxidative - produces NADH and FADH2

59
Q

What are two important irreversible(rate limiting) steps of the TCA cycle and why are they irreversible? What enzymes catalyse these steps? Are they oxidative? Where are the reducing equivalents?

A

Isocitrate (C6) to C5 - by isocitrate dehydrogenase
C5 to C4 - alpha-ketoglutarate dehydrogenase

Both irreversible as release CO2
Both oxidative as produce reducing equivalents in the form of NADH

60
Q

Are the rate limiting steps in the TCA cycle activated by high or low energy substrates.

A

Activated by low energy substrates - ADP and inhibited by low energy substrates ATP and NADH

61
Q

How can the TCA cycle produce precursors for many different things?

A

Because it produces carbon skeletons that can then go onto be synthesised into different things:

Amino acids, fatty acids, haem, glucose

62
Q

Is TCA cycle catabolic anabolic or both? Explain why

A

Both as breaks acetyl co A to release energy but also the carbon intermediates are used in biosynthesis of other molecules

63
Q

Where is the energy stored ready for ATP synthesis in the electron transport chain?

A

In high energy bonds of carrier molecules NADH and FADH2

64
Q

What are the two processes of the electron transport chain?

A

1) Electrons on NADH and FADH2 transferred through a series of carrier molecules to oxygen releasing energy in steps
2) Oxidative phosphorylation used to drive ATP synthesis

65
Q

Where in the mitochondria does the ETC occur?

A

Inner mitochondrial membrane

66
Q

What happens in the ETC?

A

Electrons are transferred from NADH and FADH2 through a series of carrier molecules releasing energy. Some of this energy is used to pump H+ ions out of inner membrane via the proton translocating complex - which creates an electrochemical gradient (p.m.f - proton motive force). This EC grad is then used to drive protons back into the matrix across the inner membrane producing ATP

67
Q

Does ATP synthase work in both directions?

A

Yes normally in pumps H+ out of matrix, but in ETC it is used in reverse to drive ATP synthesis

68
Q

How is the ETC and ATP synthesis kept tightly coupled?

A

Because H+ have to enter via ATP synthase due to the inner mitochondrial membrane being impermeable

69
Q

What is the difference in the roles of the proton translocating complex and ATP synthase?

A

PTC - pumps H+ out of inner membrane creating a gradient

ATP synthase - drives H+ back into matrix synthesising ATP

70
Q

What happens with O at the end of the electron transport chain?

A

O binds with 2 H+ that have been released in the ETC from NADH and FADH2 to create H2O.

71
Q

Which produces more energy NADH or FADH2? How much do they produce? How many proton translocating complexes do each use?

A

NADH has more energy
NADH per 2 moles NADH - 5 ATP
FADH2 per 2 moles FADH2 - 3 ATP
NADH uses all 3, FADH2 only uses 2

72
Q

The higher the p.m.f the (more/less) ATP produced. Why?

A

More. As more H+ will drive back through to the matrix through ATP synthase producing more ATP.

73
Q

What is the substrate for ATP synthase? What happens when ATP is high and ADP is low?

A

ADP

When ATP is high and ADP is low there is no substrate so inward flow of H+ stops - no ATP produced.

74
Q

Which or both of ETC and oxidative phosphorylation are controlled by mitochondrial [ATP]?

A

Both

75
Q

What does cyanide do? Is it dangerous?

A

Inhibits oxidative phosphorylation by blocking O2 accepting electrons in the ETC - prevents ATP - lethal

76
Q

What do uncouplers do?

A

They increase the permeability of the mitochondrial inner membrane to protons - dissipate the p.m.f. so no drive for ATP synthesis

77
Q

Name 2 inhibitors of ETC

A

Cyanise CO

78
Q

Name 3 uncouplers

A

Dinitrophenol
Dinitrocresol
Fatty acids

79
Q

What happens in oxidative phosphorylation diseases?

A

Genetic defects in proteins encoded by mtDNA reduce ETC and ATP synthesis

80
Q

What does efficiency of oxidative phosphorylation depend on?

A

Coupling

81
Q

How does brown fat produce heat roughly?

A

Uses uncouplers - fatty acids that allow more energy to be released as heat

82
Q

What uncoupling protein does brown adipose contain and what is the process of ETC from ATP uncoupling?

A

Contains Thermogenic (UCP1) - in response to cold, NA activates:

1) Lipase - releases fatty acids from triacylglycerol
2) Fatty acid oxidation –> activate UCP1
3) UCP1 transports H+ back into mitochondria
4) Uncouples ETC from ATP synthesis so extra energy released as heat

83
Q

Which produces more ATP substrate level or oxidative phosphorylation?

A

Oxidative

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