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Metabolism > Week 3 > Flashcards

Week 3 Flashcards

0
Q

What are the main things required for the TCA cycle?

A

Oxaloacetate, acetyl CoA, NAD+, FAD

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1
Q

Where does the TCA cycle occur?

A

Mitochondria.

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2
Q

Why are there no known genetic defects in the TCA cycle.

A

They would be lethal.

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3
Q

What happens to the TCA cycle in the absence of oxygen?

A

It does not function.

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4
Q

What is the ‘strategy’ of the TCA cycle?

A

Produce 6C and 5C intermediates that readily lose carbon dioxide, effectively catalysing oxidation of CH3COO- to 2CO2, and reducing NAD+ and FAD

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5
Q

What are other uses of the intermediates of the cycle?

A

Citrate is used in the synthesis of fatty acids
Alphaketoglutarate and oxaloacetate are used in the synthesis of non essential amino acids
Oxaloacetate can be used in gluconeogenesis.
4C intermediate used for Haem syntheses

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6
Q

What is the major source of replacement of intermediates of the TCA cycle that have been used in other pathways?

A

Reaction catalysed by pyruvate carboxylase - pyruvate -> oxaloacetate.

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7
Q

What regulates the rate of the TCA cycle?

A

Regulated by ATP:ADP ratio and NADH:NAD+ ratio
Isocitrate dehydrogenase catalyses early irreversible reaction in TCA cycle, allosterically inhibited by NADH and allosterically activated by ADP.

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8
Q

Describe the electron carriers involved in oxidative phosphorylation.

A

Four protein complexes spanning the inner mitochondrial membrane. Consist of flavoproteins, iron-sulphur proteins, and cytochromes.
The complexes transfer electrons with release of free energy
3 act as proton translocating complexes - FAD2H only uses two, NADH uses all three.

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9
Q

How is the proton motive force generated?

A

Proton translocating complexes use free energy to move protons from matrix of mitochondria to intermembrane space. The inner mitochondrial matrix is impermeable to protons, so an electrochemical gradient is formed.

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10
Q

Why can oxidative phosphorylation only occur in the presence of oxygen?

A

Oxygen is the terminal acceptor of electrons in the electron transport chain.

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11
Q

How is ATP synthesised in oxidative phosphorylation?

A

Protons diffuse back into the mitochondrial matrix via ATP-synthase (also known as F1F0-ATPase), driving the synthesis of ATP from ADP and Pi

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12
Q

What is the ATP/O (or P/O) ratio?

A

Number of moles of ATP per mole of NADH/FAD2H (2.5/1.5 respectively)

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13
Q

What is the efficiency of oxidative phosphorylation?

What is the remaining energy used for?

A

NADH - 31%
FAD2H - 35%
Maintains body temperature at 37 degrees Celsius.

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14
Q

List four differences between oxidative phosphorylation and substrate level phosphorylation.

A

Oxidative phosphorylation requires membrane associated complexes, substrate level phosphorylation occurs in the cytoplasm and mitochondrial matrix and requires soluble enzymes.
Oxidative phosphorylation requires oxygen, substrate level phosphorylation can occur in the absence of oxygen.
Energy coupling is indirect in oxidative phosphorylation, direct in substrate level - phosphoryl-group transfer.
Oxidative phosphorylation is the major source of ATP, substrate level is a minor source.

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15
Q

What is coupling between electron transport chain and ATP synthesis?

A

They are usually tightly coupled so one can’t occur without the other.
High [ATP] implies low [ADP], so reduced substrate for ATP synthesis.
So protons are not transported back into the matrix, the concentration in the intermembrane space increases until protons are no longer pumped out of the matrix so the electron transport chain stops.
The reverse occurs when [ATP] is low.

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16
Q

Name some uncouplers, what do they do?

A

Dinitrophenol and dinitrocresol.
Increase permeability of inner mitochondrial membrane to protons. Allow protons to diffuse back into matrix without driving ATP synthesis, so electron transport and ATP synthesis is uncoupled and proton motive force is dissipated as heat.

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17
Q

How much of the BMR is accounted for by the leakage of protons?

A

20-25%

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18
Q

What are the uncoupling proteins?

A

UCP 1-5 are proteins spanning the inner mitochondrial membrane which uncouple the electron transport chain and ATP synthesis.

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19
Q

Where is UCP-1 expressed?

A

Brown adipose tissue?

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20
Q

How does the body generate heat (without shivering) in response to a cold environment?

A

Releases noradrenaline which increases the rate of lipolysis and beta oxidation of fatty acids. This leads to the synthesis of NADH and FAD2H, which then donate their electrons to the electron transport chain and generates a proton motive force.
Noradrenaline also increases the expression of UCP1, protons reenter matrix and p.m.f is dissipated as heat.

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21
Q

Where is UCP2 found?

A

Widely distributed in body

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22
Q

Where is UCP3 found?

A

Skeletal muscle, brown adipose and the heart.

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23
Q

What inhibits the electron transport chain, and how?

A

Absence of oxygen (terminal acceptor of electrons)
Cyanide prevents oxygen accepting electrons from electron transport chain.
Rotenone
Antimycin

24
Q

What is the result of inhibiting the electron transport chain?

A

Reduced ATP synthesis and heat generation. Rapid cell death ensues.

25
Q

What are the properties of lipids?

A

Hydrophobic but soluble in organic solvents.

More reduced than carbohydrates.

26
Q

What are the three classes of lipids?

A

Fatty acid derivatives
Fat soluble vitamins
Hydroxy-methyl-glutaric acid derivatives

27
Q

What are the fat soluble vitamins?

A

A, D, E and K

28
Q

What are the fatty acid derivatives?

A

Fatty acids
Triacylglycerols
Phospholipids
Eicosanoids

29
Q

What are the hydroxy-methyl-glutaric acid derivatives?

A

Ketone bodies
Cholesterol
Cholesterol esters
Bile acids and salts

30
Q

What is the function of the triacylglycerols?

A

Storage of fuel for prolonged starvation, pregnancy and sustained exercise.

31
Q

How is fat storage regulated?

A

Hormonally - insulin promotes

Glucagon, adrenaline, cortisol, growth hormone and thyroxine inhibit

32
Q

What is the first stage of metabolism of triacylglycerols?

A

Hydrolysed by pancreatic lipase in the small intestine to release glycerol and fatty acids. Requires bile salts and colipase.

33
Q

What is the fate of glycerol?

A

Enters the blood stream and transported to the liver.
Phosphorylated (catalysed by glycerol kinase)
Then either used for TAG synthesis, or oxidised (NAD+ -> NADH) to dihydroxyacetone phosphate and enters glycolysis.

34
Q

What are the properties of the most common fatty acids in the body?

A

Long chain fatty acids with an even number of carbon atoms (14-18)

35
Q

Which fatty acids are essential?

A

Polyunsaturated fatty acids as they can’t be synthesised.

36
Q

What is the significance of arachidonic acid?

A

Used in synthesis of eicosanoids including prostaglandins.

37
Q

How are fatty acids transported to the tissues?

A

Non covalently bound to albumin (called none esterified fatty acids or free fatty acids)

38
Q

Which tissues cannot use fatty acids as a fuel?

A

Red blood cells - don’t have mitochondria to oxidise fatty acids
Central nervous system -fatty acids can’t cross blood brain barrier.

39
Q

What is CoA?

A

Complex molecule containing pantothenic acid and free SH group.

40
Q

What is fatty acid activation?

A

Fatty acids bound to S atom in CoA forming high energy of hydrolysis bond.
Requires ATP and catalysed by fatty acyl CoA synthase. Produces AMP, fatty acyl~CoA and 2 Pi

41
Q

Where does fatty acid activation occur?

A

Cytoplasm

42
Q

How are activated fatty acids transported into the mitochondria, and why is this important?

A

Carnitine shuttle. Activated fatty acids cannot easily cross inner mitochondrial membrane, carnitine shuttle controls entry of fatty acids into mitochondria which regulates fatty acid oxidation.

43
Q

What inhibits transport of activated fatty acids into mitochondria and why is this important?

A

Malonyl CoA. Significant as this is an intermediate of fatty acid synthesis and so prevents newly synthesised fatty acids being oxidised.

44
Q

What is the consequence of a defective fatty acid transport system?

A

Poor exercise tolerance and excess triacylglycerols in their muscles.

45
Q

What is required for oxidation of fatty acids?

A

CoA, water, mitochondrial NAD+ and FAD, ATP

46
Q

What is the fate of the carbons in a fatty acid that is oxidised?

A

Converted to acetyl CoA

47
Q

What are the products of fatty acid oxidation?

A 
NADH and FAD2H for electron transport chain
Acetyl CoA
Pi
H
AMP
48
Q

Where does beta oxidation of fatty acids occur?

A

Mitochondrial matrix

49
Q

What are the three ketone bodies?

A

Beta hydroxybutyrate
Acetone
Acetoacetate

50
Q

Where are the ketone bodies synthesised?

A

Acetoacetate and beta hydroxybutyrate are synthesised in the liver from Acetyl CoA
Acetone produced from spontaneous decarboxylation of acetoacetate.

51
Q

What is the normal concentration of ketone bodies in the blood, and in what circumstances can it increase?

A

10 mmol/L - pathological ketosis)

52
Q

What are the consequences of ketones being water soluble?

A

Allows high plasma concentrations and their excretion in urine (ketonuria)

53
Q

What are the implications of the smell of nail varnish remover / pear drops on someone’s breath?

A

Acetone is volatile and may be excreted via the lungs if present in high concentrations, such as in DKA

54
Q

How are ketone bodies synthesised?

A

In the liver - 3 Acetyl CoA-> hydroxymethyl glutaryl CoA (catalysed by hydroxymethyl glutaryl CoA synthase)
Then hydroxymethyl glutaryl CoA -> acetoacetate (catalysed by hydroxymethyl glutaryl CoA lyase)
Acetoacetate -> acetone and beta hydroxybutyrate

55
Q

How is the synthesis of ketone bodies regulated?

A

Alternative pathway for hydroxymethyl glutaryl CoA is:
hydroxymethyl glutaryl CoA -> mevalonate (catalysed by hydroxymethyl glutaryl CoA reductase) -> cholesterol
Two pathways are reciprocally controlled - high insulin to glucagon ratio promotes activity of reductase and inhibits lyase
Low insulin to glucagon ratio inhibits reductase and activates lyase
Also requires fatty acids from lipolysis.

56
Q

Which tissues can use ketone bodies and how?

A

All tissues with mitochondria including CNS. Convert them into Acetyl CoA, enters TCA cycle.

57
Q

How are lipids transported in the blood?

A

98% in lipoproteins

2% bound to albumin (mainly FAs, limited capacity therefore doesn’t exceed 3mmol/L)

59
Q

What is the structure of a lipoprotein?

A

Spherical particles with hydrophilic coat containing phospholipids, apoproteins and cholesterol, and hydrophobic core containing TAGs and cholesterol esters.

Metabolism (9 decks)

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