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Physiology Metabolism > Metabolism 3: CAC > Flashcards

Metabolism 3: CAC Flashcards

1
Q

Where is Acetyl CoA formed?

A

Mitochondria

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2
Q

What can Acetyl-CoA be used for?

A

ketone bodies, CAC, fatty acids, sterols

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3
Q

What can form Acetyl-CoA

A 
Pyruvate (oxidaiton)
Fatty Acids (beta ox)
Amino acids (Deamination and oxidation)
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4
Q

What are the 3 places we get NADH in the TCA cycle?

A

Isocitrate ->a-ketoglutarate
a-ketoglutarate->succinyl-CoA
Malate -> Oxaloaceteate

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5
Q

Where do we get GTP formed in TCA cycle?

A

Succinyl CoA -> Succinate

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6
Q

Where do we get FADH2 formed in TCA cycle?

A

succinate -> fumarate

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7
Q

List the sequence of substances of hte TCA cycle starting from Pyruvate

A

pyruvate -> Acetyl CoA -> citrate -> isocitrate ->a-ketoglutarate -> succinyl CoA -> succinate -> fumarate -> malate -> oxaloacetate

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8
Q

Where does CAC take place?

A

Primarily in the mitochondria inner membrane and matrix where hte CAC enzymes are located

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9
Q

How do we go from a 6C compound to oxaloacetate, a 4C compound at the end of CAC

A

Lose 2 C in form of carbon dioxide via oxidation

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10
Q

What happens to the NADH generated?

A

Used within mitochondria in the ETC rxn to generate ATP, which is then exported out of the mitochondria as ADP is imported in

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11
Q

In total, what is generated in cycle of the CAC

A

3 NADH, 1 FADH2, 1 GTP, 2CO2

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12
Q

How many ATP/GTP is generated by 1 round of CAC

A

10 (9 ATP: 7.5 from 3 NADH, 1.5 from FADH2 and 1 GTP)

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13
Q

Where does the ATP come from?

A

Electron transfer from substrates to molecular Oxygen provides energy to create ATP as well as water

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14
Q

What are the course control regulations of the citric acid cycle?

A

Major mechanism for regulation; important for exercise, flight or fight response
levels of ADP(rate limiting):

NADH, FADH2,

Acetyl CoA: related to PDH and transport of fatty acids to mitochondria

Oxaloacetate: affected by pathways depleting CAC intermediates

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15
Q

What are the fine control regulators of the CAC?

A

Under baseline condition: no desperate need for energy
Allosteric regulation
Isocitrate dehydrogenase
a-ketoglutarate dehydrogenase

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16
Q

Does higher concentration of ATP, GTP, and NADH stimulate or inhibit CAC?

A

inhibits

17
Q

Does higher concentration of ADP and calcium stimulate or inhibit CAC?

A

stimulate

18
Q

What are the activators /inhibitors for isocitrate dehydrogenase

A

Fine control regulation
Activator: ADP
Inhibitors: ATP, NADH

19
Q

What are the activators/inhibitors for a-ketoglutarate dehydrogenase?

A

Fine control regulation
Activator: Calcium
Inhibitor: NADH, Succinyl CoA, ATP, GTP

20
Q

What happens wiht high cellular activity in course control

A

ATP decreases and ADP increases -> increases CAC activity

21
Q

What happens with low oxygen in course control

A

Increased NADH, FADH2 -> lack of NAD+ and FAD will decrease CAC

22
Q

What CAC intermediate contributes to fatty acid and sterol synthesis?

A

Citrate

23
Q

What CAC intermediate contributes to amino acid synthesis?

A

a-ketoglutarate

Oxaloacetate

24
Q

What CAC intermediate contributes to gluconeogenesis?

A

Malate

25
Q

What CAC intermediate contributes to heme synthesis?

A

Succinyl CoA

26
Q

What can replenish a-ketoglutarate in the CAC

A

amino acid (glutamate)

27
Q

What can replenish succinyl coA in the CAC

A

Valine and Isoleucine -> propioniyl CoA -> Succinyl CoA

28
Q

What can replenish fumarate in the CAC

A

amino acids (aspartate, phenylalanine, tyrosine)

29
Q

What can replenish oxaloacetate in the CAC

A

Aspartate

30
Q

What can replenish pyruvate?

A

Amino acids

31
Q

What casues PDH deficiency?

A

mutations in E1 alpha gene -> E1 becomes inactive

Inherited in X linked dominant (all others are autosomal recessive)

32
Q

What is typically seen with PDH deficiency in children?

A

inc serum lactate, pyruvate, alanine
chronic lactic acidosis
cyst formation

33
Q

How is PDH deficiency treated?

A

dietary supplementation with thiamine, carnitine, and lipoic acids

34
Q

What causes fumarase deficiency?

A

Mutations in the fumarase gene and disrupts the conversion of fumarate to malate and thus the CAC

35
Q

What are some sx seen with fumarase deficiency?

A

Severe Neurological Impairment: Encephalopathy, Dystonia

Increased urinary excretion of fumarate, succinate, a-ketoglutarate, citrate

36
Q

What are treatments for fumarase deficiency

A

no effective treatment currently

37
Q

What can fluoroacetate (rat poison) do?

A

Directly inhibits aconitase which converts citrate to cis aconitate in the CAC before changing to isocitrate

Inhibits the CAC

Physiology Metabolism (11 decks)

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