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Metabolism > Carbohydrate glycolysis > Flashcards

Carbohydrate glycolysis Flashcards

1
Q

why do reaction pathways happen in small steps?

A
  • energy conservation
  • interconnection by producing useful intermediates
  • fine control
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2
Q

Why can rate of glycolysis be used to detect cancer cells?

A

rate of glycolysis is 200x faster in cancer cells, so radioactive deoxyglucose can be given and detected by PET scan

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3
Q

What 3 enzymes are most important in control of glycolysis?

A

Hexokinase, PFK, Pyruvate kinase

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4
Q

What is the overall goal of phase 1 of glycolysis?

A

Add neg charge to glucose so it cant diffuse out the cell. Done by converting glucose to fructose 1,6 bisphosphate

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5
Q

What is the role of hexokinase in glycolysis?

A

Converts glucose to glucose 6 phosphate. Shows product inhibition so when lots of G6P, its activity will be reduced.

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6
Q

what is differences between hexokinase and glucokinase?

A

Glucokinase only found in liver, is higher affinity for glucose and doesn’t show product inhibition

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7
Q

What is the role of phosphofructokinase (PFK) in glycolysis?

A
  • In 3rd step of glycolysis
  • creates fructose 1,6, bisphosphate
  • Is a key regulator (stimulated by AMP, insulin, NAD+ ect, inhibited by ATP, glucagon, citrate ect)
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8
Q

What is the role of Pyruvate kinase in glycolysis?

A
  • Enzyme for the last step of glycolysis (10th step), creating pyruvate
  • inhibited by low insulin: glucagon ratio (when low insulin its inhibited)
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9
Q

What is the overall reaction of glycolysis?

A

Glucose–> 2x pyruvate + 2x NADH + 2x ATP

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10
Q

What type of phosphylation occurs in glycolysis?

A

Substrate level phosphylation- PO4 donated from ATP

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11
Q

Which steps in glycolysis are reversible and why?

A

1, 3 and 10. They all have a large -ve Gibbs free energy change

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12
Q

Why is 1,3 bisphosphate glycerate (intermediate 7 in glycolysis) an important intermediate?

A

It is converted to 2,3 bisphosphate glycerate by BPG mutase. 2,3 BPG is important in decrease the affinity of Hb for oxygen. more BPG produced when cells respiring lots so more oxygen released for this process

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13
Q

Dihydroxyacetone can also be produced as the 5th intermediate in glycolysis. Why is it significant?

A

It can be oxidised to produce glycerol phosphate (or visa versa) in fat acid synthesis- also gives route into glycolysis for fat breakdown.

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14
Q

In what way is NAD a regulator of glycolysis

A

NAD is needed at step 6 of glycolysis but there is only so much NAD and NADH in the cell, when all NAD is converted to NADH, glycolysis will slow down.

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15
Q

In what conditions may NAD+ run out completely?

A

When no O2 so ECT cannot be drive to reduce NADH.

Also in RBCs and WBCs that have no mitochondria for ECT

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16
Q

How is NAD+ recreated to drive glycolysis when anerobic condtions/ in RBCs and WBCs?

A

NADH and H+ used to reduce pyruvate into NAD+ and lactate

17
Q

How can lactate be removed?

A

Taken to heart which convert it back into pyruvate.

Or to liver which can convert it back to pyruvate and used for energy or regenerating glucose.

18
Q

When is the ability of liver to convert lactate back into pyruvate impaired?

A

Liver disease, low thiamine (vitamin), alcohol poisoning and enzyme deficiency disorders

19
Q

What is normal, hyperlactaemia and lactic acidosis ranges for plasma lactate concentration?

A

Normal- 1mM
Hyperlactaemia- 2- 5mM
Lactic acidosis- 5 + mM

20
Q

What is the difference between lactic acidosis and hyperlactaemia?

A

In hyperlactaemia there is no change in blood ph as the kidneys can buffer the blood
In lactic acidosis the blood is no longer buffered and they get really ill

21
Q

What 3 enzymes are important in galactose catabolism?

A

galactose kinase, uridyl transferase, UDP galactose epimerase

22
Q

What two products can be made form galactose metabolism and what are their functions?

A

Glucose 1-phosphate- enters glycolysis

Glycogen- storage

23
Q

outline galactose metabolism into G1P and glycogen.

A

Galactose converted to galactose 1P by galactose kinase. Uridyl transferase converts this to G1P OR UDP galactose epimerase can convert this (via a few intermediates) to glycogen.

24
Q

What are symptoms of galactasaemia?

A

Cataracts, low blood glucose (high galactose), sugar in urine, hepatomegaly, jaundice, diarrhoa, vomiting, weight loss

25
Q

What organ is responsible for galactose and fructose metabolism?

A

Liver

26
Q

How is galactosaemia treated?

A

Low galactose (so lactose) diet.

27
Q

What 4 enzymes are involved in fructose pathway?

A

Fructokinase
Aldolase
Triosekinase
TPI

28
Q

Outline fructose metabolism

A

Fructokinase catalyses substrate level phosphylation of fructose. Aldolase creates two intermediates. One is substrate level phyophylated with help of triosekinase, the other converted to the end product by TPI. These two products are the same and enter glycolysis.

29
Q

What is the consequences of fructokinase deficiency?

A

Essential fructose urea- fructose in urine but no signs or symptoms

30
Q

What is the consequence of aldolase missing? How do you treat it?

A

Fructose 1P builds up, accumulates in liver and causes liver damage.
Treat by removal of fructose from diet

31
Q

what does the pentose sugar pathway start with and where does this come from?

A

Glucose 6P- 2nd intermediate from glycolysis

32
Q

What is the role of the pentose sugar pathway?

A

Source of NADPH (a reducing agent, needed in maintaining GSH levels and detoxification reactions)
Produces 5 carbon ribose sugar for DNA, RNA and nucleotides

33
Q

What enzyme is needed to convert G6P into the first intermediate in the pentose phosphate pathway?

A

Glucose 6 phosphate dehydrogenase

34
Q

Other than a ribose sugar, what is produced from the pentose phosphate pathway?

A

CO2 and NADPH

35
Q

Why does galactosaemia lead to cateracts?

A

Galactasose builds up in blood and so aldose reductase converts it to galacticol with NADPH.
This increases the osmotic pressure and so water moves into the eye.
Also NADPH used to defence against free radicals using GSH reduced, so crystallin protein in lens of eye denatured

36
Q

Why is galactokinase deficiency less severe than uridyl transferase of UDP galactose epimerase deficiency?

A

becuase galatcose 1 P can still be made and removed when required and it wont build up, so you only get cateracts from galactose build up

37
Q

What other impacts do UDP galctose epimerase and uridyl transferase have and why?

A

galactose 1P builds up in liver, kidneys and brain leaving to their damage and failure from phosphate imbalences
Therefor: hepatomegaly, renal failure, vomiting, seizure, brain damage, hypoglycaemia

38
Q

Why do heinz bodies occur in G6PHD deficiency?

A

G6PHD needed for NADPH production in pentose phosphate pathway.
less NADPH means less protection from free radicals by GSH protection mechanism
More stress and damage to Hb in RBCs cause Hb to aggregate and so stains darker (these RBCs removed in spleen)

Metabolism (8 decks)

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