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MEH - SEM1 > Session 3: Carbohydrate 3 > Flashcards

Session 3: Carbohydrate 3 Flashcards

1
Q

Why does the TCA cycle not function in absence of O2?

A

because it is tightly coupled to electron transport chain

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2
Q

What is pyruvate dehydrogenase (PDH)?

A

Converts pyruvate into acetyl CoA which allows for entry of stage 3 of glycolysis (which requires acetyl CoA rather than pyruvate).
It is a key site regulation of regulation into TCA

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3
Q

What are the roles of the TCA cycle (3)?

A
  • Breaks C-C bond in acetyl CoA & oxidises the C-atoms to CO2, The H+ and e- removed from acetate are transferred to NAD+ and FAD
  • ATP/GTP production in all tissues containing mitochondria
  • Produces precursors for biosynthesis
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4
Q

How is the TCA cycle regulated?

A

Regulated by energy availability: ATP/ADP ratio & NADH/NAD+ ratio
- Signals that feed information on rate of utilisation of energy
- Regulated by isocitrate dehydrogenase => allosterically inhibited by high energy signal NADH & activated by low energy signal ADP.

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5
Q

Why does electron transport require oxygen?

A

oxygen acts as the terminal electron acceptor

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6
Q

Why does NADH have more energy than FADH2?

A

FADH2 produces less ATP because it produces a larger proton gradient
NADH has more energetic electrons

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7
Q

Which vitamins are fat-soluble?

A

A, D, E & K

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8
Q

What are the classes of lipids?

A
  • Fatty acid derivatives
  • Hydroxy-methyl-glutaric acid derivatives (C6 compound)
  • Vitamins
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9
Q

How are fatty acids more efficient stores of energy than carbohydrates?

A

They are hydrophobic so can be stored in an anhydrous form so more fuel per gram of weight

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10
Q

Why can fatty acids generate more ATP than carbohydrates?

A

they are more reduced

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11
Q

Why does fatty acid & glycerol metabolism not occur in the brain and in RBCs?

A

Brain: fatty acids do not reach brain due to blood-brain barrier
RBCs: do not have mitochondria so cannot undergo the metabolism

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12
Q

What is the main role of acetyl CoA?

A

it is a cofactor for a number of oxidative and biosynthetic reactions in intermediary metabolism

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13
Q

What is the normal plasma concentration of ketone bodies?

A

< 1mM

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14
Q

What is the plasma concentration of ketone bodies during starvation?

A

2-10 mM

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15
Q

What is the plasma concentration of pathological ketosis?

A

> 10 mM

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16
Q

What does ketone bodies’ water-soluble characteristic allow?

A

high plasma concentration & excretion in urine (ketouria)

17
Q

Where and how are ketone bodies synthesised?

A

in mitochondria of liver from acetyl CoA in excess by lypase & reductase enzymes

18
Q

How is ketone body synthesis regulated? (fed & starvation state)

A

lypase & reductase are controlled by insulin/glucagon ratio

In a fed state (high insulin/glucagon ratio) => lypase is inhibited & reductase is activated -> cholesterol synthesis

In starvation state (low insulin/glucagon ratio) => lypase is activated & reductase is inhibited -> ketone bodies

19
Q

Which tissues are ketone bodies used by?

A

peripheral tissues (muscles)

20
Q

Is the liver able to metabolise ketone bodies? What happens to them?

A

No, they are transported in the blood and used by many different cells

21
Q

What could be a reason for ketone bodies to be used as an alternative fuel?

A

way of sparring/preserving glucose eg for tissues that depend on glucose eg brain

22
Q

What could be a reason for ketone bodies to be used as an alternative fuel?

A

way of sparring/preserving glucose eg for tissues that depend on glucose eg brain

23
Q

How do dietary triglycerols generate ATP?

A
  • hydrolysed by pancreatic lipases in SI = release glycerol & fatty acids (lipolysis, cytoplasm, requires bile salts & colipase)
  • fatty acids oxidised by β-oxidation into acetyl CoA => used in TCA cycle = produce ATP.
24
Q

Describe the features of dietary triglycerols (6).

A
  • Derived from glycerol => glycerol -> triglycerol = esterification
  • Hydrophobic
  • Stored in anhydrous form
  • Stores in adipose tissue
  • Used in prolonged exercise, starvation & pregnancy
  • Storage/mobilisation under hormonal control
25
Q

How do uncoupling proteins (UCP) work? Give an example

A

they uncouple electron transport chain from ATP production to produce heat
located in inner membrane & allow leak of protons across membrane = reduces pmf and stops synthesis of ATP.

Example: brown adipose tissue contains UCP1 - infants breakdown brown adipose tissue to generate heat

26
Q

How do uncoupling substances work?

A
  • They increase permeability of inner mitochondrial membrane to protons
  • Protons enter mitochondria without driving ATP synthetase.
  • Dissipates proton gradient (provide alternative route for H+ to penetrate back into inner membrane)
  • No phosphorylation of ADP so oxidative phosphorylation is inhibited but ET continues

=> processes uncoupled & pmf of energy = heat

27
Q

How & why does uncoupling occur in some tissues?

A

The mitochondrial concentration of ATP regulates oxidative phosphorylation and electron transport, when high [ATP]:
o [ADP] is low & ATP synthesis stops due to lack of substrate
o Inward flow of H+ stops and [H+] in intramitochondrial space increases
o Prevents further H+ pumping/translocation = ET stops
o Reverse occurs when [ATP] is low

28
Q

Where does electron chain transport occur?

A

inner membrane of mitochondria

29
Q

How does ATP synthesis work?

A
  • Energy derived from proton gradient (pmf) produced by electron transport
  • Protons can only re-enter mitochondrial matrix via ATP synthase complex driving synthesis of ATP from ADP + Pi
  • Higher the pmf = more ATP synthesised (ATP/O ratio or P/O ratio)
  • Oxidation of 2 moles of NADH => synthesis of 5 moles of ATP (P/O = 2.5)
  • Oxidation of 2 moles of FADH2 => synthesis of 3 moles of ATP (P/O = 1.5)
30
Q

What is electron transport?

A

Electrons on NADH & FADH2 are transferred through a series of carrier molecules to oxygen => energy is released in steps & oxygen is required

31
Q

How does electron transport work?

A
  • Protons are pumped across membrane
  • Proton translocating complexes use the free energy (derived from electron transport) to move H+ from the matrix of the mitochondria to the intermembrane space.
  • membrane = impermeable to protons and as electron transport proceeds the proton concentration on the outside of the inner membrane increases
  • proton translocating complexes transform the chemical bond energy of the electrons into an electro-chemical potential difference of protons = proton motive force (pmf)
  • greater the chemical bond energy of electrons = more protons can be translocated = greater the pmf
  • NADH produces more energy than FADH2 so used 3PTCs whilst FADH2 uses only 2
  • Needs oxygen as it acts as the terminal electron acceptor
32
Q

What happens by the end of stage 3 of catabolism?

A
  • All the C-C bonds have been broken and the C-atoms oxidised to CO2.
  • All the C-H bonds have been broken and the H-atoms (H+ + e-) transferred to NAD+ and FAD.
33
Q

What is oxidative phosphorylation and where does it occur?

A

ATP synthesis is coupled to the movement of electrons through the mitochondrial electron transport chain
Final stage of catabolism
Involves electron transport & ATP synthesis (oxidative phosphorylation)
Occurs in inner mitochondrial membrane

34
Q

Compare & contrast oxidative phosphorylation (OP) and substrate-level phosphorylation (SLP)

A
  • OP requires membrane-associated complexes (inner mitochondrial membrane) whilst SLP requires soluble enzymes (cytoplasmic & mitochondrial matrix)
  • OP = indirect energy coupling whilst SLP = direct energy coupling
  • OP cannot occur in absence of O2 whilst SLP can occur to limited extent in absence of O2
  • OP is a major process for ATP synthesis in cells which require a lot of energy whilst SLP is a minor process for ATP synthesis in cells which require a lot of energy

MEH - SEM1 (6 decks)

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