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Med 2024-2028 > Metabolism L3.1 > Flashcards

Metabolism L3.1 Flashcards

1
Q

Diagram showing overview of Catabolism

A
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2
Q

State location of glycolysis

A

Cytosol

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3
Q

Describe the end of stage 2 catabolism

A

Pyruvate (end product of aerobic glycolysis) does not directly enter TCA cycle (stage 3 catabolism)

Pyruvate must be transported from cytosol to mitochondria via PYRUVATE TRANSLOCASE

(In mitochondrial matrix, pyruvate converted to acetyl CoA)

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4
Q

Describe how pyruvate is converted into acetyl CoA in mitochondrial matrix during end of stage 2 catabolism

A

Pyurvate undergoes oxidative decarboxylation
(IRRERVSIBLE) by pyruvate dehydrogenase

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5
Q

State cofactors required by pyruvate dehydrogenase

A

Thiamine phosphate
FAD
NAD+
CoA
Lipoic acid

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6
Q

State the source of cofactors required by pyruvate dehydrogenase

A

Vitamin B (B1, b3, B5)

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7
Q

State why converstion of pyruvate to Acetyl CoA is sensitive to vit B deficiencies

A

Pyruvate to Acetyl Coa = oxidative decarboxylation reaction by Pyruvate Dehydrogenase
This enzyme requires cofactors, (thiamine, CoA, NAD+, FAD)
These cofactors are provided from Vit B (B3, B5)

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8
Q

Diagram showing regulation of reaction catalysed by Pryuvate Dehydrogenase

A
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9
Q

How is PDH regulated (activated and inhibited) during conversion of pyruvate to acetyl CoA

A

Activated by:

  1. Pyruvate
  2. CoA
  3. NAD+
  4. ADP
  5. Insulin

Inhibited by:
1. Aceytol CoA
2. ATP
3. NADH+ + H+

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10
Q

State cause of Pyruvate Dehydrogenase Deficiency

A

Genetic defect in pyruvate dehydrogenase

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11
Q

State effects of pyruvate dehydrogenase deficiency

A

No acetyl CoA
So, no energy release in aerobic metabolim
To compensate, anaerobic metabolism occurs, (reduction of pyruvate to lactate), too much lactate then accumulates in blood, leads to LACTIC ACIDOSIS

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12
Q

Lactic acidosis recap

A
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13
Q

State where TCA cycle occurs

A

Mitochondria

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14
Q

Summary of TCA cycle

A
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15
Q

Diagram showing TCA cycle

A

Only memorise important reactions

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16
Q

Diagram showing TCA cycle: GTP (ATP) synthesis + reducing power release

A
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17
Q

Why are there 2 x TCA cycles per mole of glucose?

A

For each mole of glucose, 2 moles of pyruvate are produced in glycolysis.

Therefore, the 2 pyruvates are both oxidatvely decarboxylised into Acetyl CoA molecules.

So, 2 x Acetyl CoA, therefore, 2 rounds of TCA cycle

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18
Q

Stage 1 of TCA Cycle

A

Acetyl CoA (2C) undergoes condensation with oxaloacetate (4C) to form citrate (6C)

CITRATE SYNTHASE

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19
Q

Stage 4 of TCA Cycle

A

Oxidative decarboxylation of isocitrate (6C) to form alpha-ketoglutarate (5C)

ISOCITRATE DEHYDROGENASE

NADH + H+ produced

20
Q

Stage 5 of TCA cycle

A

Oxidative decarboxylation of alpha-ketoglutarate to form succinyl-CoA (4C)
(alpha-ketoglutarate dehydrogenase)

NADH + H+ produced

21
Q

Stage 6 of TCA cycle

A

Succinyl-CoA cleaved to form
1. Succinate
2. CoA
by subtsrate phosphorylation

THIOKINASE

(GTP formed)

22
Q

Stage 7 of TCA cycle

A

Oxidation of succinate to fumerase

Succinate Dehydrogenease
FADH2 produced

23
Q

Stage 8 of TCA cycle

A

Fumerate hydrated to malate

FUMERASE

24
Q

Stage 9 of TCA cycle

A

Malate oxidised to oxaloacertate

Malate dehydrogenease

NADH + H+ produced

25
Q

State points of regulation within TCA cycle

A

Reactions 1,4, 5

  1. Citric synthase
    Activated: Acetyl CoA
    Inhibited: Citrate
  2. Isocitrate dehydrogenase
    Activated: ADP
    Inhibited: ATP, NADH + H+
  3. alpha-ketoglutarate dehydrigenase
    Activated: ADP
    Inhibited: ATP, NADH + H+, succinyl CoA
26
Q

TCA cycle provides intermediates for anabolic processes

A
27
Q

State the location of oxidative phoshorylation

A

Mitochondria
(inner mitochondrial membrane)

28
Q

State conditions required for oxidative phosphorylation

A

O2

29
Q

Summarise oxidative phosphorylation

A

Electrons from NADH+ + H+ and FADH2 transferred to O2.
The carriers above are now re-oxidised to NAD+, FAD)
Free energy from electron transport drives synthesis of ATP

30
Q

Describe oxidative phosphorylation

A

2 phases: 1. Electron transport 2. ATP synthesis

Electrons transferred from NADH+ + H+ and FADH2 through series of protein complexes to O2
(IN MORE DETAIL: PCI + PCII pass electrons from NADH+ + H+ and FADH2 TO PCIII and PCIV. PCIV passes electrons to oxygen, which forms water). PCI, PCIII, PCIV pump H+ from matrix to intermembrane space using free energy released during electron transport)

This releases energy

30% of this energy used to move H+ across membrane and rest is lost as heat

Movement of H+ creates H+ conc gradient cross inner membrane (proton motive force)

H+ conc gradient dissipated (reduced) by ATP synthase

H+ pumped into matrix (favoured by electrochemical gradient)

Energy released from flow of H+ used by ATP synthase to synthesise ATP from ADP and Pi.

31
Q

Energetics of oxidative phosphorylation

A
32
Q
A
33
Q

Describe the net synthesis of ATP from glucose

A
34
Q

Compare oxidative vs substrate level phosphorylation

A
35
Q

Describe Regulation of oxidative phosphorylation

A

High ATP - Rate of oxidative phosphorylation decreased.
No substrate for ATP synthase.
Conc. of H+ atoms No, inward flow of H+ atoms stops. Prevents firther H+ pump, stops electron transport

Low ATP - Rate of oxidative phosphorylation increased

36
Q

Describe what factors affect the efficiency of oxidative phosphorylation

A

Tightness of coupling og electron transport to ATP synthesis.

Coupling depend s on tissues:

  • Higher in tissues with higher energy demand (exercising muscle tissue)

Uncoupling occurs in brown adipose tissue.
Therefore, oxidative phosphorylation is less efficient
This allows extra heat generation rather than ATP

37
Q

State conditions under which oxidative phosphorylation can be inhibited

A
  1. Anaerobic
  2. Excessive reactive oxygen species
  3. Cabron monoxide, cyanide (inhibit electron transport)
    Cyanide - prevents acceptance of electrons by O2
    therefore, no electrochemical gradient across mitochondrial membrane, no ATP synthesis
    Leads to death
38
Q

State the role of synthetic uncouplers

A

e.g. 2,4 dinitrophenol (DNP)

(uncoupling electron transport from ATP synthesis)

  1. Increase permeability of mitochondrial inner membrane to H+
  2. Dissipates H+ conc gradient
  3. No movement of H+ / No proton motive force
  4. Uncouples electron transport from ATP synthesis
  5. No ATP synthesis,increased heat production, leads to death
39
Q

Why was DNP used medically as a weight loss drug?

A

Increased metabolic rate, increase heat production

40
Q

Why was DNP banned from human consumption?

A

e.g. 2,4 dinitrophenol (DNP)

(uncoupling electron transport from ATP synthesis)

  1. Increase permeability of mitochondrial inner membrane to H+
  2. Dissipates H+ conc gradient
  3. No movement of H+ / No proton motive force
  4. Uncouples electron transport from ATP synthesis
  5. No ATP synthesis,increased heat production, leads to death
41
Q

Describe the process of uncoupling in brown adipose tissue

A

Brown adipose tissue has UCP1 (uncoupling protein - thermogenin) (present in inner mitochindrial membrane)

UCP-1 activated in response to cold / stress
1. Noradrenaline released from sympathetic nervous system
2. Binds to beta adrenergic receptros on BAT
3. Stimulates hydrolysis of triacylglycerols relasing fatty acids
4. Fatty acids oxidised in mitochondria, providing reducing power for oxidatiove phosphorylation
5. Fatty acids activate UCP1, transports H+ from intermembane space into matrix, but no ATP synthesis
6. Electron transport uncoupled from ATP synthesis. Energy from dissipation of H+ conc gradient used to generate heat

This process is known as NON-SHIVERING THERMOGENESIS.

42
Q

State causes of oxidative phosphorylation diseases

A

Mutations in mitochondrial DNA (greater mutation rate than nuclear DNA)

43
Q

State causes and symptoms of Leber hereditary optic neuropathy (LHON)

A

Mutation in gene coding for PTC 1

Presnets with loss of vision

44
Q

State causes and symptoms of Leigh syndrome (subacute necrotising encephalopathy)

A

Mutation in gene coding for ATP synthase

Presents with progressive loss of mental and physical abilities in infancy

45
Q
A

Med 2024-2028 (56 decks)

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