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Block 1 > Metabolism 2 > Flashcards

Metabolism 2 Flashcards

1
Q

What enzymes inside the cell phosphorylate glucose?

A

Hexokinases

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2
Q

What hexokinases are low in affinity for glucose? Where are they found?

A

Hexokinase-4 (glucokinase)

Liver + pancreatic β cells

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3
Q

What hexokinases are high in affinity for glucose? Where are they found?

A

Hexokinase

Brain, RBCs + muscle

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4
Q

The affinity of a hexokinase for glucose matches the affinity of the ___ in that tissue.

A

GLUTs

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5
Q

Briefly describe the anaerobic oxidation of glucose as in erythrocytes.

A
  1. Glucose converted to G6P via HK
  2. G6P converted to F6P via isomerase
  3. F6P converted to F-1,6-BP via PFK
  4. At this point 2 ATPs have been utilised
  5. Aldolase breaks F-1,6-BP down into dihydroxyacetone-P + Glyceraldehyde-3P (isomerase can interconvert them)
  6. Further investment of inorganic phosphate
  7. Series of reactions with various phosphorylated trioses to produce pyruvate
  8. Without O2, pyruvate is converted to lactic acid
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6
Q

How many ATPs does anaerobic glycolysis produce?

A

2

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7
Q

How is glycolysis linked to other biosynthetic pathways?

A
  1. G6P can be converted to glycogen/glycoconjugates
  2. F6P can be converted to glycoconjugates too or enter the PPP to produce nucleotides (DNA, RNA)
  3. Dihydroxyacetone-P can be converted to glycerol-3-P + be used to make triglycerides + phospholipids in lipogenesis
  4. Pyruvate can go into the mitochondria + become involved in oxidation or biosynthesis OR make AAs -> proteins
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8
Q

Where is most ATP formed? What process is used to do this?

A

Inside the mitochondrial inner membrane (location of ATP synthase)

Oxidative phosphorylation (involves ETC to create a proton gradient across membrane)

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9
Q

What do NADH and FADH2 do?

A

Carry electrons (reducing power) from catabolic reactions to the site of ATP synthesis

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10
Q

When oxygen is present and mitochondria are present, what is oxidised to produce ATP?

A

NADH + pyruvate from glycolysis

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11
Q

Why are mechanisms needed to transfer NADH into mitochondria?

A

It is not permeable through the mitochondrial inner membrane + it needs to get across so cells can harvest its reducing power to form ATP aerobically

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12
Q

How do cancer cells use glucose?

A

Anaerobically even when O2 is present (Warburg effect) which means they need to use glucose at a very high rate as this is an inefficient process

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13
Q

How many ATPs can be produced aerobically?

A

~36

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14
Q

What happens to pyruvate once it is imported into the mitochondria?

A

Oxidative decarboxylation via coenzyme A to produce acetyl-CoA, NADH + CO2 (by-product)

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15
Q

What are the products of fatty acid β-oxidation?

A

Acetyl-CoA
FADH2
NADH

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16
Q

What happens in fatty acid β-oxidation briefly?

A
  1. Lipid joined to coenzyme A
  2. Series of reactions where the β-carbon changes position + single/double bonds around it
  3. β-carbon gains a OH group by adding O2 in oxidation
  4. β-carbon then gains a =O
  5. Parts of the lipid will produce Acetyl-CoA whilst the rest will join directly to coenzyme A
17
Q

Explain the mutual inhibition of glucose and fatty acid oxidation.

A

Glucose oxidation inhibits use of FA oxidation + vice versa because both processes produce Acetyl-CoA so one pathway is downregulated to avoid overproduction

18
Q

What are amino acids required for the synthesis of?

A

Proteins (structural, catalytic, signalling)

Peptides (intra- + inter-cellular communication)

Sources of carbohydrates during fasting, trauma + sepsis

19
Q

What needs to happen before amino acids can be used for glucose/lipid synthesis?

A

Deamination via a series of transamination reactions before urea formation

20
Q

What is urea?

A

Main nitrogen-containing compound excreted through the kidneys (less toxic than ammonia so requires less dilution + fluid excretion) so urea is the main route of excretion of AA groups

21
Q

What occurs during amino acid degradation?

A

AA R group is swapped with the R group of a ketoacid by transaminases

22
Q

How is urea synthesized in the urea cycle?

A
  1. AA transamination with α-ketoglutarate via aminotransferase producing glutamate
  2. NH3 (amine group) removed from glutamate via glutamate dehydrogenase (NAD -> NADH)
  3. Also, glutamate converted to glutamine by a synthase
  4. NH3 (amine group) removed from glutamine by glutaminase
  5. Amine groups contribute to urea synthesis
  6. Aspartate also contributes to urea synthesis
23
Q

What does alanine do when produced?

A

Cycles between muscle + liver

24
Q

What is the main aim of catabolic reactions of glucose, fatty acids and amino acids?

A

Formation of Acetyl-CoA (but not all AAs can give rise to this)

25
Q

What is the main aim of the Tricarboxylic Acid (TCA) Cycle?

A

Oxidation of Acetyl-CoA as a source of NADH + FADH2 (electron carriers) to produce CO2 in mitochondrial space

26
Q

What are the important stages of the Tricarboxylic Acid (TCA) Cycle?

A
  1. Acetyl-CoA (2Cs) + oxaloacetate (4Cs) = citrate (6Cs) + CoA recycled via citrate synthase
  2. Series of reactions changing citrate back to oxaloacetate (4C)
  3. 2Cs put in every cycle at beginning via Acetyl-CoA released as 2CO2s
  4. 3NADH, FADH2 + GTP produced
27
Q

What else is the Tricarboxylic Acid (TCA) Cycle involved in?

A

Many other metabolic processes may involve only parts of it:
- Anapleurotic roles in the liver
- Acetyl-CoA used to make ketone bodies e.g. in liver too
- All AAs feed in to the cycle which generates energy, gluconeogenesis
+ lipid metabolism

28
Q

What is anapleurosis?

A

Replenishing of intermediates in the TCA cycle that have been extracted for biosynthesis

29
Q

How is the urea cycle linked to the Tricarboxylic Acid (TCA) Cycle?

A

Oxaloacetate from TCA cycle converted to aspartate which goes into urea cycle

Fumarate from urea cycle joins the TCA cycle

30
Q

What is the main aim of the electron transport chain (ETC)?

A

Conversion of energy harnessed from oxidation processes as NADH (from TCA cycle, FA β-oxidation + malate shuttle in glycolysis) + FADH2 (from TCA cycle, FA β-oxidation + G3P shuttle in glycolysis) into a usable form of high energy compound; ATP

31
Q

What occurs in the electron transport chain (ETC)?

A
  1. NADH comes in first as FADH2 is not as useful
  2. Electrons transferred into a chain in the membrane which carries electrons from high to low energy state
  3. Electrons go through series of carriers + inner mitochondrial membrane spanning transporters (I, III + IV (also II but not important))
  4. The energy gained from this used to pump protons (H+) against their concentration gradient into intermembrane space across matrix
  5. 2 electrons join with O2 + 2Hs = H2O (by-product)
  6. ATP synthase allows H+ to flow back down concentration gradient producing energy (ATP) through ADP phosphorylation
  7. ATP transported out of mitochondria, across inner membrane + into cytoplasm via a ATP-ADP carrier
32
Q

How is the Electron Transport Chain (ETC) coupled to ATP synthesis?

A

For each 2 electrons transported across complex I + III, 4 proteins ejected across inner mitochondrial membrane by each complex

ATP synthase requires 3 proteins flowing down their concentration gradient to synthesize 1 ATP - 4th proton symported with each ATP across the inner membrane in exchange for 1 ADP

33
Q

What is the Cori cycle briefly?

A

When lactate is produced from anaerobic glycolysis goes back to the liver + is converted back to glucose so glucose gets another change to gain more energy aerobically

34
Q

What other intermediates can be produced by the Electron Transport Chain (ETC)?

A

ROS which can react with anything e.g. DNA causing cell damage + ageing

35
Q

How can proton influx be uncoupled from ATP synthesis? What is the consequence of this?

A

UCP1

Dissipation of the proton (H+) gradients results in release of heat resulting in non-shivering thermogenesis in brown adipose tissue - useful as part of homeostasis if your cold as fat tissue takes the energy + uses it differently to create heat

Block 1 (54 decks)

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