Midterm 2 Flashcards

1
Q

Where does glycolysis take place?

A
  • cytoplasm
  • aerobic: cardiac muscle, brain, liver
  • anaerobic: RBC, muscle
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2
Q

How is glycolysis regulated?

A
Phosphofructokinase:
\+ F, 2-6 P, AMP
- ATP, citrate, H
Pyruvate kinase:
\+ F, 1-6 P
- ATP, alanine
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3
Q

Energy Production of glycolysis

A
glucose -> glucose-6-P = -1 ATP
fructose -> fructose 1-6 PP = -1 ATP
1,3 bisphosphofructose (x2) -> 3PG = +1 ATP
PEP -> pyruvate (x2) = +1 ATP 
net = +2 ATP
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4
Q

Where does glyconeogenesis take place?

A
  • cytoplasm
  • liver (kidney, especially in prolonged
    starvation)
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5
Q

How is glyconeogenesis regulated?

A
Pyruvate carboxylase
\+ acetyl CoA
Fructose, 1-6 P
\+ ATP, citrate
- AMP
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6
Q

What is gluconeogenesis?

A

Gluconeogenesis is the synthesis of
glucose/ glycogen by non-carbohydrate
precursors (lactate, glycerol, amino acids
and in Ru propionate)

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7
Q

Energy Balance of GNG?

A

2 lactate + 7 ATP -> 1 glucose unit + 7 ADP

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8
Q

Amino acids of GNG?

A

Almost all amino acids are glucogenic (except leucine)
Alanine -> pyruvate
Glutamic acid -> alpha-keto glutarate
Aspartic acid -> oxaloacetate

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9
Q

Hormonal control of GNG?

A
  • Glucagon: +GNG - Stimulates mobilisation of aa. in muscle. Stimulates uptake of aa in the liver. Raises cAMP levels in adipose cells.
  • Glucocorticoids: + GNG - Favours synthesis of glucose by aa.
  • Insulin: -GNG - Antagonist of glucagon.
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10
Q

Oxidation of pyruvate to AcCoA

  1. What kind of reaction is it?
  2. Where does it happen?
  3. Reaction equation
  4. What does it require?
  5. Regulation?
A
  1. Oxidative decarboxylation
  2. Mitochondrial matrix
  3. Pyruvate + HSCoA + NAD+ -> AcCoA + CO2 + NADH + H+
  4. Requires the pyruvate dehydrogenase complex:
    - Enzymes: pyruvate decarboxylase, dihydrolipyl transacetone, dihydrolipoic acid dehydrogenase
    - Cofactors: thiamine (TPP), pantothenic acid (HSCoA), nicotinic acid (NAD+), riboflavin (FAD), lipoic acid
  5. Pyruvate dehydrogenase complex is inhibited by ATP.
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11
Q

Citric acid cycle

  1. Another word for it?
  2. Where?
  3. Energy gain?
  4. Regulation
A

1.Tricarboxylic acid cycle
2.Mitochondrial matrix (not in RBCs)
3.3NADH + H + = 9 ATP
1FADH2 = 2 ATP
1 GTP
= 12ATP x 2 = 24 ATP
4.Citrate synthase: + ADP, NAD, - ATP, NADH, Isocitrate dehydrogenase: - ADP, NADH, Succinate dehydrogenase: + succinate, - oxaloacetate

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12
Q

THE RESPIRATORY CHAIN

  1. What is it?
  2. Where?
A
  1. A series of e- carriers which are red. and ox. The released E can be used to form ATP via ox.ppr.
  2. inner membrane of mitochondria
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13
Q

Steps of resp.chain

A

1.From the glycerol phosphate shuttle NADH+H+ is
ox. to NAD+ by substrate dehydrogenase
2.The 2 e- generated are used to red. the FMN -> FMNH2 by NADH dehydrogenase in the Fe-S complex 1 (4H+)
3.The e- are transferred to coQ. Oxidised = ubiquinone, reduced = coQ.
4.Between CoQ and oxygen are the cytochromes which are e- carrying proteins that contain a haem prosthetic
group. The iron atom in the haem alternates between a
red. Fe2+ and ox. Fe3+ state.
5-8: -CoQ —Fe3+ -> Fe2+ —>cytochrome B (Complex III)
-cytochrome B —Fe2+ -> Fe3+ —> cytochrome C
-cytochrome C —Fe3+ -> Fe2+ —cytochrome a + a3 (Cu2+
Complex IV)
-cytochrome a + a3 is reoxidised by O2 and prod. H2O

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14
Q

OXIDATIVE PHOSPHORYLATION

  1. Where?
  2. Role?
  3. What does it do?
  4. Role of NADH + H+ and FADH2
  5. What is the net result?
A

1.inner membrane of mitochondria
2.to generate ATP
3.Generates a proton gradient across the inner mitochondrial membr. Once established, the protons will flow through the ATPase complex back into the mitochondrial matrix. As they lose E, this E is utilised by the ATPase complex to phosphorylase and therefore generate ATP (11 molecules).
4.serve as H/e- donors and cofactors for the protein complexes in the electron transport chain.
5.an influx of protons into the inter membranous
space.

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15
Q

Uncouplers of ox.ppr?

A

Protons pumped out are carried by the uncoupler back to the matrix preventing a pH/ electrical gradient.

  • Thermogenin: in brown adipose tissue of newborns and hibernating mammals. Stimulates resp. and heat prod. (non-shivering thermogenesis).
  • Dinitrophenol: a yellow toxin that affects cattle
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16
Q

Transamination

  1. Why do we have it?
  2. What does it do?
  3. What catalyses it?
A

1.Aa can´t be stored by the body, so a surplus is degraded and excreted as urea, while their carbon skeletons are converted into major metabolic
intermediates.
2.Ultimately all amino groups are collected by alpha-keto
glutarate yielding glutamate. Glutamate enters the
mitochondria where:
A. It is deaminated by L-glutamate dehydrogenase or
B. Its amino group is transferred to oxaloacetate to yield
aspartate
3.Transaminases

17
Q

Oxidative deamination?

  1. What is it?
  2. Regulation?
  3. Localisation?
A

1.The alpha-amino groups from the aa. end up as the amine group of L-glutamate. Glutamate undergoes oxidative deamination by mitochondrial L-glutamate
dehydrogenase.
2.+ ATP, GTP, - ADP, GDP
3.liver

18
Q

THE UREA CYCLE

  1. localisation?
  2. regulation?
  3. Reaction equation?
A

1.only in the liver. Mitochondria until citrulline leaves to the cytosol
2.carbamoyl phosphate synthetase + N-acetyl glutamate
3.CO2 + NH3 + 3ATP + 2H2O -> urea + 2ADP + 2Pi
+ AMP + PP

19
Q

LIPOLYSIS

  1. localisation
  2. What is it?
  3. Enzyme?
A
  1. adipose tissue
  2. the breakdown of fats and other lipids by hydrolysis to release fa.
  3. Hormone-sensitive lipase
20
Q

What is adenylate cyclase in the lipolysis, how is it activated and what does it cause?

A

Catalyses the synthesis of cAMP.
Activated when adrenaline, noradenaline, glucagon or ACTH bind to receptors on the cell membr. cAMP activates protein kinase A which activates after a cascade of reactions hormone-sensitive lipase.

21
Q

Lipogenesis

1.localisation?

A

1.cytoplasm and adipose tissue, liver, mammary gland

22
Q

BETA-OXIDATION

  1. What does it do?
  2. Regulation?
  3. Example?
  4. Energy yield?
  5. Localization?
A

1.Triacylglycerides are split into fa. and glycerol. Fa. are transported into mitochondria in the blood bound to albumin.
2.Regulation: CAT 1
(+) allosterically and by high conc. of free fa.
(+) adrenaline and glucagon indirectly
(-) by malonyl CoA
(-) insulin indirectly
3.Example: palmitoyl CoA (C = 16, 7 cycles (n/2 - 1))
4.Energy yield of palmiotyl CoA:
8 acetyl CoA 8 x 12 = 96 ATP
7 FADH2 7 x 2 = 14 ATP
7 NADH 7 x 3 = 21 ATP
= 131 ATP
Energy yield of stearic acid (+2C)
1 acetyl CoA = 12 ATP
1 FAHD2 = 2 ATP
1 NADH = 3 ATP
= 17 ATP per cycle
5. mitochondrial matrix, liver and muscle (skeletal and cardiac)