Energy I Flashcards

1
Q

Why do we need energy

A

Metabolism

  1. Synthesis of new molecules
  2. Establishing ion gradients
  3. Mechanical work
  4. keeping warm
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2
Q

Define catabolism

A

The breakdown of complex molecules to release energy to carry out mechanical work

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3
Q

Catabolism pathway

A

Carbohydrates, fats proteins > degradation > heat

02 to CO2

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4
Q

Anabolism

A

Synthesis of new molecules from less complex compounds

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5
Q

Anabolism pathway

A

Amino acids, nucleotides, sugars and fats > biosynthesis > new cells

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6
Q

What does ATP do

A

Acs as both an acceptor and donator of energy

It acts a short term reservoir of energy

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7
Q

What are the major oxidative pathways

A
  1. Glycolysis
  2. Citric acid cycle
  3. Electron transport coupled to oxidative phosphorylation
  4. Fatty acid oxidation
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8
Q

Glycolysis pathway

A
  1. Glucose is phosphorylated into glucose-6-phosphate using 1 ATP
  2. Which is then isomerised into fructose-6-phosphate
  3. This is then phosphorylated into fructose 1,6 bisphosphate using 1 ATP
  4. This splits into two 3 carbon molecules; dihydroxyacetone phosphate and glyceraldehyde-3-phosphate
  5. These molecules are made into phosphoenol pyruvate as NAD+ and Pi are made into NADH and one ATP is generated from ADP and Pi
  6. This is then made into pyruvate as 1 ATP is generated again
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9
Q

What are the overall net gain of glycolysis

A
  • 2 ATP molecules

- 2 NADH molecules

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10
Q

Where can glycolysis be regulated and how

A

Where there are enzymes catalysing irreversible reactions

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11
Q

How are these enzymes regulated

A
  1. Reversible binding of allosteric effectors
  2. Covalent modification
  3. transcription
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12
Q

What are the 3 regulatory kinases used and how they regulated

A
  1. Hexokinase - Regulated by its product, G-P-6
  2. Phosphate-fructokinase - Regulated by ATP, citrate and H+ and stimulated by F26BP and AMP
  3. Pyruvate kinase - regulated by ATP
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13
Q

How is PFK (phosphate-fructokinase) inhibited

A

High concentrations of ATP inhibit PFK by lowering the affinity for its substrate fructose-6-phosphate
Its also inhibited by low pH
Inhibition of PF leads to inhibition of hexokinase because of the backup of substrates

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14
Q

What are the differences between hexokinase and glucokinase

A
  1. Glucokinase has a higher Km so its only really active at high glucose concentrations
  2. Hexokinase is inhibited by G-P-6 but glucokinase isn’t
  3. Glucokinase is induced by insulin
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15
Q

How are tumours and exercising muscles similar

A

Both rely on anaerobic respiration for the generation of ATP

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16
Q

What is a limiting factor of anaerobic respiration

A

NAD+ since it limits the production of pyruvate

17
Q

How is NAD+ resynthesised

A

Lactate is made from pyruvate so NADH is metabolised back into NAD+

18
Q

Why does muscle fatigue and how does it counteract it

A

Lactate is highly acidic because of H+ ion production
Low pH is an inhibitor of glycolysis
The muscle overcomes this by exporting lactate back to the liver, here it is metabolise back to glucose

19
Q

Why do tumours use glycolysis

A

When tumours outgrown their blood supply, oxygen delivery is reduced and therefore tumour cell metabolism reverts to glycolysis

20
Q

How does tumour physiology change to accommodate glycolysis

A

A reduction in O2 leads to he activation of the transcription factor HIF-1 alpha
HIF-1 alpha regulates the expression of a number of enzymes in the glycolytic pathway such as hexokinase and phosphate-fructokinase
HIF-1 alpha also leads to blood vessel growth