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Metabolism > Session 3 > Flashcards

Session 3 Flashcards

0
Q

Describe the key features of pyruvate dehydrogenase reaction

A
  • Pyruvate dehydrogenase is a large multi-enzyme complex
  • Occurs in mitochondrial matrix (pyruvate shunted across mitochondrial membrane)
  • Irreversible because of loss of Carbon dioxide - key regulatory step
  • Acetyl CoA cannot be converted back to pyruvate to form glucose in gluconeogenesis
  • PDH deficiency causes lactic acidosis
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1
Q

What happens to Pyruvate at the end of glycolysis?

A
  • Converted to Acetyl CoA by pyruvate dehydrogenase in the mitochondrial matrix
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2
Q

What cofactors does pyruvate dehydrogenase require?

A
  • FAD
  • Thiamine pyrophosphate
  • Lipoic acid
  • All act catalytically
  • Allows complicated reaction to be performed in a controlled manner
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3
Q

Why is pyruvate dehydrogenase very sensitive to vitamin B deficiency?

A
  • 4 B vitamins are involved in the reaction
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4
Q

What inhibits pyruvate dehydrogenase?

A
  • Acetyl-CoA (acetyl CoA from B oxidation of fatty acids is used in stage 3 catabolism instead of from glucose) (allosteric inhibition)
  • NADH (allosteric
  • ATP inhibition)
  • Phosphorylation
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5
Q

What activates pyruvate dehydrogenase?

A
  • Pyruvate
  • NAD +
  • ADP (allosteric)
  • Insulin (promotes dephosphorylation) - causes glucose to increase in cells
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6
Q

What is stage 3 of glucose catabolism?

A
  • TCA/Krebs cycle
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7
Q

What are the main features of the TCA cycle?

A
  • Occurs in mitochondria
  • Oxidative
  • Single pathway for the catabolism of sugars, fatty acids, ketone bodies, alcohol and amino acids
  • Acetate is converted to 2 CO2 molecules
  • Produces some energy as ATP/GTP
  • Produces precursors for other reactions
  • Only works in presence of oxygen
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8
Q

What is produced by the TCA cycle?

A
  • 6 NADH
  • 2 FAD2H
  • 2 GTP
    Per glucose mol (2 turns of cycle)
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9
Q

How is the TCA cycle regulated?

A
  • ATP/ADP ratio
  • NADH/NAD+ ratio
  • Isocitrate dehydrogenase catalysts an irreversible reaction and is allosterically inhibited by NADH and activated by ADP a
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10
Q

How many ATP molecules are produced by the TCA cycle per glucose molecule?

A
  • Approximately 32
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11
Q

Give example of intermediates used in anabolism?

A
  • Citrate -> fatty acids
  • a-ketoglutarate -> amino acids
  • Succinate -> amino acids/haem
  • Malate -> amino acids
  • Oxaloacetate -> amino acids/glucose
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12
Q

What and where do other compounds enter the TCA cycle?

A
  • Glucose, fatty acids, alcohol and some amino acids enter as Acetyl CoA
  • Amino acids also enter directly at a-ketoglutarate, Succinate, Malate and Oxaloacetate
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13
Q

How many ATP/GTP molecules have been produced from glycolysis and the TCA cycle per glyph ode molecules?

A
  • 2 from glycolysis
  • 2 from TCA cycle
  • Most of the energy is in the chemical bond energy of the e- in NADH and FAD2H
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14
Q

What has happened by the end of stage 3 catabolism?

A
  • All C-C bonds broken and C atoms oxidised to CO2

- All C-H binds broken and H atom (H+ and e-) transferred to NAD+ and FAD

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15
Q

What are the feature of stage 4 catabolism?

A
  • Takes place on the inner mitochondrial membrane
  • Involves electron transport and ATP a synthesis
  • NADH and FAD2H are re-oxidised
  • O2 is required
  • Produces large amounts of ATP
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16
Q

What processes happen in stage 4 catabolism?

A
  • Electron transport: electrons from NADH and FAD2H transferred through a range of carrier molecules to oxygen
  • Oxidative phosphorylation: free energy used to drive ATP synthesis
    Couples the energy from dissipation of the proton motive force to the synthesis of ATP from ADP
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17
Q

How many ATP a molecules are produced with the oxidation of NSDH and FAD2H?

A
  • 2 mol NADH: 5 mols ATP

- 2 mol FAD2H: 3 mols ATP

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18
Q

How is oxidative phosphorylation regulated?

A
  • High ATP/low ADP: lack of substrate (inhibition)
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19
Q

What are uncouplers?

A
  • Increase the permeability of the inner mitochondrial membrane to protons
  • Dissipate the protons gradient, reducing the protein motive force
  • No drive for ATP synthesis
  • Eg dinitrophenol, dinitrocresol
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20
Q

What are inhibitors?

A
  • Block electron transport
  • Prevents O2 accepting electrons
  • Eg cyanide, carbon monoxide
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21
Q

What are uncoupling proteins?

A
  • Proteins that uncouple electron transport chain from ATP production to produce heat
  • UCP1-5
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22
Q

Where are uncoupling proteins located?

A
  • Inner mitochondrial membrane and allow a leak of protons back across
  • UCP 1 (thermogenin) is in brown adipose tissue - important in non-shivering thermogenesis
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23
Q

How non-shivering thermogenesis occur in brown adipose tissue?

A
  • In response to cold, noradrenaline is released from the sympathetic nervous system
  • Stimulates lipolysis releasing fatty acids for B-oxidation
  • Forms NADH and FAD2H, driving electron transport and proton motive force
  • Noradrenaline also activates UCP1, allowing protons to re-enter matrix, dissipating proton motive force as heat
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24
Q

What are other functions of the UCP proteins?

A
  • UCP2 is widely distributed in the body, could be linked to diabetes, obesity, metabolic syndrome and heart failure
  • UCP3 is found in skeletal muscle, brown adipose tissue, and is involved in modifying fatty acid metabolism and protecting against reacting species damage
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25
Q

What are the key features of lipids?

A
  • Structurally diverse
  • Hydrophobic - mostly insoluble in water
  • Contain C, H and O (phospholipids contain P and N)
  • More reduced that carbohydrates - release more energy when oxidised, requires more Oxygen for oxidation
26
Q

What are the classes of lipids?

A
  • Fatty acid derivatives
  • Hydroxy-methyl-glutaric acid derivatives (c6 compound)
  • Vitamins
27
Q

What lipids are in fatty acid derivative class?

A
  • Fatty acids: fuel molecule
  • Triacylglyerides: fuel storage and insulation
  • Phospholipids: components of membranes and plasma lipoproteins
  • Eicosanoids: local mediators
28
Q

What lipids are in the hydroxy-methyl-glutaric acid derivatives

A
  • Ketone bodies: water soluble fuel molecules

- Cholesterol: membranes and steroid hormone synthesis

29
Q

What lipids are in the vitamin class?

A
  • A, D, E and K
30
Q

What are the main features of triacylglyerides?

A
  • Hydrophobic
  • Can be stored in anhydrous form
  • Stored in adipose tissue
  • Utilised in prolonged exercise, starvation, pregnancy
  • Storage/mobilisation under hormonal control
31
Q

Where does stage 1 of triacylglyceride occur?

A
  • GI tract

- Extracellular

32
Q

What happens during stage 1 of triacylglyceride catabolism?

A
  • Hydrolysed by pancreatic lipases in small intestine

- Forms fatty acids and glycerol

33
Q

What happens to fatty acids from triacylglyerides?

A
  • Converted back to triacylglyerides in GI tract
  • Packaged into lipoprotein particle: chylomicrons
  • Released into circulation via lymphatics
  • Carried to adipose tissue where it is stored as triacylglyeride
  • Released as fatty acids when needed
  • Carried to tissues as albumin-fatty acid complex
34
Q

What happens in adipose cells when extracellular glucose is low?

A
  • Fatty acids are released (on albumin) as an alternative fuel
35
Q

How is triacylglyeride storage controlled?

A
  • Hormonal control
36
Q

What hormones activate triacylglyeride storage?

A
  • Insulin
37
Q

What hormones inhibit triacylglyeride storage?

A
  • Glucagon
  • Adrenaline
  • Cortisol
  • Growth hormone
  • Thyroxine
38
Q

What happens to glycerol after it is hydrolysed from dietary triacylglyerides?

A
  • Enters bloodstream and is transported to the liver

- Is converted to glycerol phosphate

39
Q

Describe the conversion of glycerol to glycerol phosphate

A
  • Glycerol -> glycerol phosphate
  • ATP -> ADP
  • Glycerol kinase
40
Q

What happens to the glycerol phosphate after conversion from glycerol?

A
  • Used in triacylglyeride synthesis

- Converted to dihydroxyacetone phosphate (NAD+ -> NADH) and enters glycolysis

41
Q

What are features of fatty acids?

A
  • Saturated/unsaturated
  • Amphipathic
  • Some essential fatty acids eg linolenic acid
  • Reduced and hydrophobic (good for energy storage)
42
Q

Where does stage 2 of lipid metabolism occur (fatty acids)?

A
  • Mitochondria
43
Q

What happens in fatty acid catabolism?

A
  • Fatty acids are activated outside the mitochondrion (by linking to CoA)
  • Transported across inner mitochondrial membrane by the carnitine shuttle
  • Cycles through sequence of oxidative relations, removing a C2 at each cycle
44
Q

What happens during fatty acid activation?

A
  • Occurs outside of mitochondria
  • Linked to CoA by fatty acyl CoA synthase
  • Requires ATP a
45
Q

When do triacylglyerides in adipose tissue undergo lipolysis?

A
  • Stress eg aerobic exercise, starvation, lactation
46
Q

How is lipolysis of triacylglyerides in adipose tissue controlled?

A
  • Enzyme hormone-sensitive lipase
47
Q

What activates lipolysis?

A
  • Glucagon
  • Adrenaline
  • Cortisol
  • Growth hormone
  • Thyroxine
48
Q

What inhibits lipolysis?

A
  • Insulin
49
Q

Why do activated fatty acids need the carnitine shuttle to cross the mitochondrial membrane?

A
  • Are hydrophobic
50
Q

What are the features of the carnitine shuttle?

A
  • Regulates rate of fatty acid oxidation as controls entry into mitochondria
  • Inhibited by malonyl CoA (prevents newly synthesised fatty acids in cytoplasm from immediately being transported into mitochondria and oxidised)
  • Defects: poor exercise tolerance and high levels of triacylglyerides in muscle cells
51
Q

What does the B oxidation of fatty acids require?

A
  • Mitochondrial NAD+ and FAD

- Oxygen presence

52
Q

What are the features of b oxidation?

A
  • Oxidises
  • Removes 2C (acetate) each cycle
  • No direct synthesis of ATP
  • All intermediates are linked to CoA and C atoms of fatty acid are converted to Acetyl CoA
  • More energy derived from fatty acid oxidation than glucose oxidation
53
Q

Where doesn’t b oxidation occur?

A
  • Brain
  • Red blood cells
  • White blood cells
54
Q

What happens to Acetyl CoA (catabolism and anabolism)?

A
  • CO2
  • Fatty acids -> triacylglyerides/phospholipids
  • Hydroxymethyl glutaric acid (HMG) -> ketone bodies/cholesterol (-> steroid hormones)
55
Q

What ketone bodies are there?

A
  • Acetone
  • Acetoacetate
  • B-hydroxybutyrate
56
Q

What are the different levels of ketones in the blood plasma?

A
  • Normal: 10 mM
57
Q

Where are ketone bodies synthesised?

A
  • Acetoacetate and B-hyroxybutyrate: liver

- Acetone: spontaneous decarboxylation of Acetoacetate

58
Q

What are the properties of ketone bodies?

A
  • Water-soluble (allows high plasma concentrations and excretion in urine (ketouria)
  • Acetoacetate and B-hydroxybutyrate can cause ketoacidosis in high concentrations in plasma
  • Acetone is volition and can be excreted by lungs (can be smelt on breath of untreated type 1 diabetics)
59
Q

How are ketone bodies synthesised?

A
  • Acetyl~CoA -> Hydroxymethyl glutaryl CoA (HMG~CoA) (synthase)
  • HMG~CoA -> mevalonate (HMG~CoA reductase) -> cholesterol
  • HMG~CoA -> Acetoacetate (Lyase) -> acetone/B-hydroxybutyrate
60
Q

How is ketone body synthesis regulated?

A
  • Fed state ie high insulin:glucagon ratio: Lyase is inhibited/reductase is activated; Cholesterol synthesis activated
  • Starvation/diabetes ie low insulin: glucagon ratio: Lyase is activated/reductase inhibited; ketone body synthesis
61
Q

What does ketone body synthesis require?

A
  • Excessive lipolysis of in adipose tissue to supply substrate of fatty acids
  • Low plasma insulin:glucagon ratio usually due to a fall in insulin
62
Q

What uses ketone bodies?

A
  • All tissues containing mitochondria including CNS
63
Q

What happens to ketone bodies?

A
  • Converted to Acetyl CoA

- Oxidised in stage 3 of catabolism

Metabolism (11 decks)

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