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MEH: The basics for years ahead > Session 2 > Flashcards

Session 2 Flashcards

1
Q

What are the requirements for the TCA cycle?

A
  • NAD+
  • FAD+
  • Oxaloacetate
  • Acetyl CoA
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2
Q

Where does the TCA cycle occur?

A

Mitochondria

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3
Q

What is the main function of the TCA pathway?

A
  • Oxidise carbon atoms to CO2
  • Transfer of H+ and e- to NAD+ and FAD
  • Breaking of C-C bonds in acetate
  • Production of ATP
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4
Q

What can the TCA cycle not function without?

A

-Oxygen

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5
Q

What does the intermediates in the TCA cycle allow for in terms of biosynthesis?

A
  • Amino acids
  • Haem synthesis
  • Fatty acid synthesis
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6
Q

What enzyme catalyses the conversion of pyruvate to oxaloacetate?

A

Pyruvate Carboxylase

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7
Q

What are the characteristics of pyruvate dehydrogenase?

A
  • Exist in the Mitochhondrial matrix
  • Large multi complex (5 enzymes)
  • Co-factors required leads to PDH being sensitive to vitamin B1 deficiency.
  • Reaction is irreversible so is a key regulatory step
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8
Q

What is the result of PDH deficiency?

A

Lactic acidosis

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9
Q

What are the ways in which isocitrate dehydrogenase is regulated?

A
  • Stimulated by ADP

- Inhibited by NADH and ATP

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10
Q

What are the ways in which alpha-ketoglutarate dehydrogenase is regalated?

A

Inhibited by NADH, ATP, and Succinyl-CoA

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11
Q

What are the key characteristics of stage 4 catabolism of carbohydrates?

A
  • Mitochondrial
  • Electron transport
  • NADH & FADH2 re-oxidised
  • O2 required which is reduced to H2O
  • Large amounts of energy int he form of ATP is produced
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12
Q

What is the use of reducing power in ATP synthesis?

A
  • Electrons on NADH and FADH2 transferred through a series of carrier molecules to oxygen (ELECTRON TRANSPORT)
  • Free energy released used to drive ATP synthesis (OXIDATIVE PHOSPHORYLATION)
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13
Q

What is the process of oxidative phosphorylation?

A
  • Electrons are transferred from NADH and FADH2 through a series of carrier molecules to O2 with release of energy
  • Energy used to move H+ across membrane
  • H+ gradients is established across inner mitochondrial membrane. Proton motive force established
  • Return of protons is favoured energetically by the electrochemical potential
  • Protons can only return across membrane via the ATP synthase and this drives ATP synthesis
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14
Q

Electrons in NADH have more energy than in FADH2. true/false

A

True

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15
Q

How is oxidative phosphorylation regulated?

A
  • When ATP is high (therefore ADP low) no substrate for ATP synthase
  • Inward flow of H+ stops
  • Concentration of H+ in the intermitochondrial space increases
  • Prevents further H+ pumping - stops electron transport
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16
Q

What is an example of an inhibitor of oxidative phosphorylation?

A
  • Cyanide, Carbon monoxide
  • Blocks electron transport therefore prevents acceptance of electrons. Therefore no proton motive force so no oxidative phosphorylation
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17
Q

What are examples of uncouplers of oxidative phosphorylation?

How do they work?

A

-Dinitrophenol, Dinitrocresol, Fatty Acids

  • Increases the permeability of membrane of H+
  • H+ enters mitochondria without driving ATP synthase so dissipates proton motive force. No phosphorylation of ADP as a result so no inhibition of electron transport
18
Q

What happens to energy lost during oxidative phosphorylation?

A
  • It is lost as heat.

- Efficiency of oxidative phosphorylation depends on the tightness of coupling

19
Q

What does brown adipose tissue contain that allows for heat generation in response to the cold?

A

-Contains thermogenin (UCP1)

  • In response to the cold, noradrenaline activates
  • Lipase triggers release of fatty acids from TAG
  • Fatty acid oxidation occurs so NADH and FADH2 are formed.
  • Electron transport can occur
  • UCP1 transport H+ back into mitochondria
  • Electron transport is uncoupled from ATP synthesis. Energy from the p.m.f is released as EXTRA HEAT
20
Q

Oxidative VS Substrate level Phosphorylation

A

Oxidative phosphorylation

  • Requires membrane associated complexes
  • Energy coupling occurs indirectly through generation & subsequent utilisation of proton gradients
  • Cannot occur in the absence of O2
  • Major process for ATP synthesis in cells requiring large amounts of energy

Substrate level phosphorylation

  • Requires soluble enzymes
  • Energy coupling occurs directly through formation of high energy hydrolysis bone
  • Can occur to a limited extent in the absence of O2
  • Minor process for ATP synthesis in cells requiring large amounts of energy
21
Q

What are the benefits of TAGs that allow it to be stored?

How is storage and mobilisation control?

A
  • Hydrophobic therefore stored in anhydrous form in a specialised tissue called adipose tissue.
  • Controlled by hormones
22
Q

When are TAGs utilised?

A
  • Utilised in prolonged exercise, starvation and during pregnancy
  • Released as fatty acids when need and carried to tissues as albumin-fatty acid complex
23
Q

How are TAGs in the diet metabolised and transported?

A
  • TAGs in diet are hydrolysed by pancreatic lipase in small intestine to fatty acids and glycerol
  • They are recombined back to TAGs in the G.I tract and packaged into lipoprotein particles (CHYLOMICRONS)
  • They are released into circulation via lymphatics
  • They are then carried to adipose tissue and stored as TAGs
24
Q

How does fatty acid catabolism occur?

A

-Occurs in the mitochondria

  1. Fatty acid is activated by linkage to co-enzyme A outside the mitochondrion by the action of ‘fatty acyl CoA synthase’
  2. The fatty acids is transported across the inner mitochondria membrane using a carnitine shuttle
  3. Fatty Acid cycles through a sequence of oxidative reactions with 2 carbons being removed each cycle
25
Q

How is the fatty acid oxidation regulated via the carnitine shuttle?

A

-Inhibition by malonyl CoA

Defects can also occur in the transport system leading to exercise intolerance and lipid droplets in muscle

26
Q

Main points of Fatty acid metabolism?

A
  • Mitochondrial
  • Cycle of reactions
  • Removal of 2C units per cycle
  • Oxidation
  • H+ and e- transferred to NAD+ and FAD
  • Stops in absence of O2
  • No ATP synthesis
27
Q

What enzyme is used to convert glycerol to glycerol phosphate?

A

-Glycerol kinase

28
Q

Where is glycerol metabolised?

A

Glycerol is transported in the blood to the LIVER

29
Q

Which molecule acts as the main convergence point for catabolic and anabolic pathways?

How are they linked?

A

Acetyl CoA

-Acetyl is linked to coenzyme A via S-atom

30
Q

What vitamin does CoA contain?

A

Vitamin B5

31
Q

What are 3 types of ketone bodies?

A
  • Acetoacetate
  • Acetone
  • Beta-hydroxybutyrate
32
Q

What are key ranges of ketone bodies?

A
  • Normal plasma ketone body concentration = <1mM
  • Stavation ketone body concentration = 2-10 mM (physiological ketosis)
  • Untreated Type 1 diabetes = >10 mM
33
Q

What do statin drugs act on?

A

HMG-CoA Reductase

34
Q

Which enzyme is used to form cholesterol from acetyl CoA?

A

HMG-CoA reductase

35
Q

Which enzyme is used to form ketone bodies from acetyl CoA?

A

Lyase enzyme

36
Q

What are inhibitors of isocitrate dehydrogenase and alpha-ketoglutarate dehydrogenase in the TCA cycle?

A
  • Low NAD+ substrate availability

- NADH product inhibition

37
Q

What is activated when insulin/glucagon ratio is high?

HMG-CoA Reductase or Lyase

A

HMG-CoA reductase is activated

Lyase is inhibited

38
Q

What is activated when insulin/glucagon ratio is low?

HMG-CoA Reductase or Lyase

A

HMG-CoA reductase is inhibited

Lyase is activated

39
Q

What are the characteristics of ketone bodies?

A
  • Water soluble molecules
  • Permits relatively high plasma concentrations
  • Alternative substrate
  • Above renal threshold, ketonuria occurs
  • Acetoacetate and beta hydroxybutyrate are relatively strong organic acids so can lead to ketoacidosis
  • Volatile acetone may be excreted via the lungs
40
Q

What is ketonuria?

A

Ketone excreted in the urine

MEH: The basics for years ahead (2 decks)

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