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MEH > 3 - Carbohydrates + Energy Production > Flashcards

3 - Carbohydrates + Energy Production Flashcards

1
Q

explain the key role of pyruvate dehydrogenase in glucose metabolism

A

pyruvate + CoA + NAD+ → acetyl CoA + CO2 + NADH + H+

  • mitochondrial matrix (pyruvate transported from cytoplasm across mitochondrial membrane)
  • large multi-enzyme complex (5 enzymes)
  • the different enzyme activities require various co-enzymes
  • B vitamins provide the co-factors, so reaction is sensitive to vitamin B1 deficiency
  • reaction is irreversible, so a key regulatory step
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2
Q

how is pyruvate dehydrogenase (PDH) regulated

A

inhibited by
- acetyl-CoA
- NADH
- ATP
- Citrate (downstream product)

activated by
- pyruvate
- CoA
- NAD+
- ADP
- Insulin

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3
Q

describe the features of the tricarboxylic acid (TCA) cycle in metabolism

A
  • mitochondrial
  • a single pathway (single point of entry via acetyl CoA)
  • acetyl (CH3CO-) → 2CO2
  • oxidative (requires NAD+ and FAD)
  • some energy produced (2 x GTP)
  • 6 x NADH and 2 x FADH2 produced for next stage
  • CoA is released in order to be reused
  • also produces precursors for biosynthesis
  • tightly coupled to electron transport chain, so doesn’t function in absence of O2
  • 8e-s within chemical bonds in acetyl group → TCA cycle extracts these e-s and transfers them to NAD + FAD → later used in oxidative phosphorylation to generate ATP

GTP and ATP have the same energy producing capacity

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4
Q

why does the TCA cycle have so many steps?

A
  • conserve energy present in chemical bonds
  • use that energy efficiently
  • generating intermediates (used for biosynthetic reactions)
  • chemistry is easier in smaller steps
  • can control cycle by regulation of different enzymes
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5
Q

explain how the TCA cycle is regulated

A

isocitrate dehydrogenase
- isocitrate (+NAD+) → α-ketoglutarate (+CO2 and NADH)
- stimulated by ADP
- inhibited by NADH

α-ketoglutarate dehydrogenase
- α-ketoglutarate (+CoA + NAD+) → succinyl-CoA (+CO2 + NADH)
- inhibited by NADH, ATP and succinyl-CoA

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6
Q

describe the key features of electron transport and oxidative phosphorylation

A
  • electrons on NADH and FADH2 are transferred through a series of carrier molecules to oxygen (electron transport)
  • Proton translocating complexes (PTC1, PTC2 + PTC3) are involved in transferring the electrons to create the electrochemical gradient
  • 30% of energy from electron transfer is used to move H+ across the inner membrane (from mitochondrial matrix → intermembrane space)
  • this generates proton motive force (pmf) = electrochemical gradient
  • releases energy in steps
  • free energy released used to drive ATP synthesis
  • energy from the dissipation of the proton motive force is coupled to the synthesis of ATP from ADP
  • the greater the pmf, the more ATP synthesised
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7
Q

how many PTCs (proton translocating complexes) does NADH vs FADH2 use and why

A
  • electrons in NADH have more energy than those in FADH2
  • in electron transport of oxidative phosphorylation
  • NADH uses 3 PTCs, whereas FADH2 uses only 2
  • the greater the pmf ⇢ the more ATP synthesised
  • oxidation of 2 moles of NADH ⇢ synthessis of 5 moles of ATP (2.5 per molecule)
  • oxidation of 2 moles of FADH2 ⇢ synthesis of 3 moles of ATP (1.5 per molecule)
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8
Q

how are electron transport and ATP synthesis coupled together in oxidative phosphorylation?

A
  • return of protons (H+) is favoured energetically by the electrochemical potential
  • protons (H+) can only return across membrane via the ATP synthase enzyme, which drives ATP synthesis
  • ADP + Pi → ATP
  • energy from the dissipation of the proton move force is coupled to the synthesis of ATP from ADP
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9
Q

how is oxidative phosphorylation regulated

A
  • normally oxidative phosphorylation and electron transport are tightly coupled
  • both regulated by mitochondrial ATP concentration
  • high ATP = low ADP concentration
  • when concentration of ADP is low, no substrate for ATP synthase
  • therefore inward flow of H+ stops
  • concentration of H+ in the intermitochondrial space increases
  • this stops H+ pumping
  • and therefore electron transport ceases
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10
Q

what do uncouplers do to oxidative phosphorylation

and examples of uncoupling substances

A

an inhibitor of oxidative phosphorylation

  • uncouplers increase the permeability of the inner mitochondrial membrane to protons
  • ie by adding in an extra H+ transport protein into the membrane
  • means H+ enters mitochondria without driving ATP synthase
  • this dissipates the proton gradient
  • therefore reduces the proton move force
  • means there is no drive for ATP synthesis
  • no phosphorylation of ADP (no oxidative phosphorylation)
  • but: no inhibition of electron transport

Examples: dinitrophenol, dinitrocresol, fatty acids

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11
Q

what are the different types of oxidative phosphorylation inhibition

and examples of substances

A

inhibition of electron transport
- eg cyanide and carbon monoxide
- cyanide is found in cassava, stones and seeds of fruits etc
- prevents acceptance of electrons by O2
- block flow of electrons (no electron transport and no oxidative phosphorylation)
- lethal

uncouplers
- eg dinitrophenol, dinitrocresol + fatty acids
- increase permeability of membrane to H+
- H+ enters mitochondria without driving ATP synthase
- no phosphorylation of ADP
- therefore no oxidative phosphorylation but electron transport continues
- more detail on another card

ox/phos diseases
- genetic defects in proteins encoded by mtDNA
- (some subunits of the PTCs and ATP synthase)
- causes a decrease in electron transport and ATP synthesis

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12
Q

how + why does uncoupling occur in brown adipose tissue

and where is brown adipose tissue found?

A
  • brown adipose tissue contains thermogenin (UCP1)
  • UCP1 is a naturally-occuring uncoupling protein
  • in response to cold, noradrenaline activates…
  1. lipase relases fatty acids from triacylglycerol
  2. fatty acid oxidation ⇢ NADH/FADH2 ⇢ electron transport
  3. fatty acids activate UCP1
  4. UCP1 transports H+ back into mitochondria

…therefore electron transport uncoupled from ATP synthesis
- energy from pmf is then released as extra heat
- brown adipose tissue is found in newborn infants (to maintain heat, particularly around vital organs)
- also found in hibernating animals (to generate heat to maintain body temperature)
- there are a family of UCPs, which have a role in heat generation by uncoupling, but may have other functions

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13
Q

compare the processes of oxidative phosphorylation + substrate level phosphorylation

oxidative phosphorylation = OP substrate level phosphorylation = SLP

A

oxidative phosphorylation
- requires membrane associated complexes (inner mitochondrial membrane)
- energy coupling occurs indirectly through generation + subsequent utilisation of a proton gradient (pmf)
- 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 (cytoplasmic + mitochondrial matrix)
- energy coupling occurs directly through formation of high energy of hydrolysis bond (phosphoryl-group transfer)
- can occur (to a limited extent) in the absence of O2
- minor process for ATP synthesis in cells requiring large amounts of energy

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14
Q

describe the various classes of lipids

and give examples of each

A

fatty acid derivatives
- fatty acids (fuel molecules)
- triacylglycerols (fuel storage and insulation)
- phospholipids (components of membranes and plasma lipoproteins)
- eiosanoids (local mediators ie signalling molecules)

hydroxy-methul-glutaric acid derivatives (C6 compound)
- ketone bodies (C4), water soluble fuel molecules
- cholesterol (C27), maintains fluidity of plasma membrane and role in steroid hormone synthesis
- cholesterol esters, cholesterol storage
- bile acids and salts, lipid digestion

vitamins → these are lipid derived and are fat soluble
- Vitamin A, D, E + K

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15
Q

describe how dietary triacylglycerol is broken down and stored

A
  • taken in + broken down by pancreatic lipases → fatty acids + glycerol
  • converted back to triglycerides in GI tract
  • packaged into lipoprotein particle to stabilise
  • form chylomicrons that are packages of lipoproteins and fatty acids
  • released into circulation via lymphatic system
  • carried to adipose tissue
  • stored as triglyceride
  • rekeased as fatty acids + glycerol when needed
  • carried to tissues as albumin-fatty acid complex
  • glycerol is water soluble
  • fatty acid is bound to albumin to enable it to be carried to tissues
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16
Q

general features of triacylglycerols

A
  • lipolysis triacylglycerol → fatty acids + glycerol
  • esterification glycerol + fatty acids → triacylglycerol
  • triacylglycerols are hydrophobic
  • therefore stored in an anhydrous form (in conditions with no water, more efficient this way)
  • stored in specialised tissue = adipose
  • utilised in prolonged exercise, starvation, during pregnancy
  • storage/mobilisation is under hormonal control
17
Q

fatty acid catabolism

A
  • when body is subjected to stress situations, adipose tissues are hydrolysed by hormone-sensitive lipase to carry out lipolysis
  • this causes release of fatty acids + glycerol that diffuse from the tissue
  • activated by adrenaline, glucagon, growth hormone, cortisol and thyroxine
  • inhibited by insulin
  • FA is activated
  • this occurs outside mitochondria (in cytoplasm), by linking to coenzyme A
  • Transported across the inner mitochondrial membrane using a carnitine shuttle
  • FA cycles through sequences of oxidative reactions (β oxidation)
  • each cycle, 2 carbons are removed, reducing the fatty acid chain by 2
18
Q

what are carnitine shuttles

A
  • transports fatty acyl CoA across the mitochondrial membrane
  • this is because activated fatty acids (fatty acyl CoA) do not readily cross the inner mitochondrial membrane
  • Carnitine acyltransferases (CAT1 + CAT 2) exchange acyl carnitine (from intermembrane space) for carnitine (mitochondrial matrix) across the mitochondrial membrane
  • regulated (by levels of AMP + insulin), so controls the rate of FA oxidation
  • CAT 1 inhibited by malonyl CoA (biosynthetic intermediate)
19
Q

what is β-oxidation

A
  • the process by which fatty acids are oxidised to release energy
  • oxidises the fatty acid and removes a C2 unit (acetate)
  • the shortened fatty acid is cycled through the reaction sequence repeatedly removing a C2 unit each turn of the cycle until only two carbon atoms remain
  • the reaction sequence requires mitochondrial NAD+ and FAD
  • cannot occur in the absence of O2 (as need to re-oxidise NADH and FADH2 formed in stage 4 of catabolism)
  • no direct synthesis of ATP by the pathway
  • all intermediates in pathway are linked to coenzyme A
  • all C atoms of the fatty acid are converted to acetyl CoA
20
Q

what are the three ketone bodies produced by the body

A
  • acetoacetate (synthesised in liver from acetyl CoA)
  • β hydroxybutyrate (synthesised in liver from acetyl CoA)
  • acetone (arises from spontaneous, non-enzymatic, decarboxylation of acetoacetate)
21
Q

what are ketone bodies and why are they formed

A
  • water soluble molecules (allows high plasma concentrations and excretion in urine)
  • may cause acidosis in high concentrations (acetoacetate and β hydroxybutyrate)
  • acetone is volatile and may be excreted via the lungs
  • ketone bodies are synthesised in liver mitochondria by the actions of lyase and reductase enzymes
  • these are reciprocally (ie one is activated and the other is inhibited) controlled by the insulin/glucagon ratio
  • ketone bodies are important fuel molecules that can be used by all tissues containing mitochondria
  • rate of utilisation is proportional to the plasma concentration
  • they are converted to acetyl CoA and this is subsequently oxidised via stage 3 of catabolism

the synthesis of ketone bodies requires both of the following
- fatty acids to be available for oxidation in the liver following excessive lipolysis in adipose tissue (this supplies the substrate)
- the plasma insulin:glucagon rato to be low (usually due to fall in insulin), as this activates lyase and inhibits reductase

22
Q

what are ketone bodies and why are they formed

A
  • water soluble molecules (allows high plasma concentrations and excretion in urine)
  • may cause acidosis in high concentrations (acetoacetate and β hydroxybutyrate)
  • acetone is volatile and may be excreted via the lungs
  • ketone bodies are synthesised in liver mitochondria by the actions of lyase and reductase enzymes
  • these are reciprocally (ie one is activated and the other is inhibited) controlled by the insulin/glucagon ratio
  • ketone bodies are important fuel molecules that can be used by all tissues containing mitochondria
  • rate of utilisation is proportional to the plasma concentration
  • they are converted to acetyl CoA and this is subsequently oxidised via stage 3 of catabolism

the synthesis of ketone bodies requires both of the following
- fatty acids to be available for oxidation in the liver following excessive lipolysis in adipose tissue (this supplies the substrate)
- the plasma insulin:glucagon rato to be low (usually due to fall in insulin), as this activates lyase and inhibits reductase

23
Q

why is acetyl CoA important

A
  • produced by the catabolism of fatty acids, sugars, alcohol and certain amino acids
  • can be oxidised via stage 3 of catabolism
  • important intermediate in lipid biosynthesis
  • most lipids can be synthesised

MEH (19 decks)

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