NP19 Molecular and physiological regulation

15 important questions on NP19 Molecular and physiological regulation

The pathway from pyruvate to Acetyl-CoA:
  1. Produces lactic acid
  2. Is part of gluconeogensis
  3. Is metabolically irreversible
  4. Requires more energy than it produces

3. Is metabolically irreversible

The pathway from pyruvate to Acetyl-CoA:
  1. Produces lactic acid
  2. Is part of gluconeogensis
  3. Is metabolically irreversible
  4. Requires more energy than it produces

3. Is metabolically irreversible

Which of these statements is true?
  • 1. at least 4 of the 16.5 ATP formed by the complete oxidation of glycerol (via dihydroxyacetone phosphate) are obtained by substrate level phosphorylation
  • 2. Alanine, tryptophan and iso-leucine are glycogenic amino acids

  1. None
  2. Both
  3. 1
  4. 2


4. Only statements 2 is true

1. Is false it is 3
2. True
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Which of these statements is true?
  • 1. at least 4 of the 16.5 ATP formed by the complete oxidation of glycerol (via dihydroxyacetone phosphate) are obtained by substrate level phosphorylation
  • 2. Alanine, tryptophan and iso-leucine are glycogenic amino acids

  1. None
  2. Both
  3. 1
  4. 2


4. Only statements 2 is true

1. Is false it is 3
2. True

Glucogenic amino acids can follow two metabolic pathways: gluconeogenesis or direct oxidation. Which component is, in most cases, a common intermediate for both pathways?
  1. 3-phospho-glyceraldehyde
  2. Phospho-enol pyruvate
  3. Pyruvate
  4. Acetyl-CoA

2. Phospho-enol pyruvate

Glucogenic amino acids can follow two metabolic pathways: gluconeogenesis or direct oxidation. Which component is, in most cases, a common intermediate for both pathways?
  1. 3-phospho-glyceraldehyde
  2. Phospho-enol pyruvate
  3. Pyruvate
  4. Acetyl-CoA

2. Phospho-enol pyruvate

Rank these fatty acids for their ATP yield upon complete oxidation!
Start with the lowest
  1. (C18:0) < (C16:0) < (18:2) < (C18:3)
  2. (C18:0) < (C16:0) < (18:3) < (C18:2)
  3. (C16:0) < (C18:0) < (18:2) < (C18:3)
  4. (C16:0) < (C18:3) < (18:2) < (C18:0)

4. (C16:0) < (C18:3) < (18:2) < (C18:0)

What is the metabolic rate per organ?

BMR: 6-7 kJ/min ± 2000-2500 kcal/day

RMR tissues (per kg tissue) --> SEE IMAGE

Brain, liver, heart, kidneys: ± 60% of REE
  • weight of organs <6% of body weight
  • Skeletal muscle: 40%-50% of BW, 18-25% REE
  • Human adult: REE ! 25 kcal/kg weight day

What uses your brain with a metabolic rate when fasting (initial)

Brain uses 4-5 g glucose/hr  - 96-120/day

Blood level: ± 5mM = 0.9 gram/L


hepatic glucose production: 180 g/day
  • thus, brain consumes 2/3 of hepatic glucose
  • both glycogenolysis and gluconeogenesis (50%)

induced by glucagon, inhibited by insulin

Which organs play a large role in gluconeogenesis when
  • Post-absorptive state - standard (starch) diet
  • Fasting (24-48h)
  • Post-absorptive state - protein-enriched diet

  • Post-absorptive state - standard (starch) diet
    • liver 70-75%
  • Fasting (24-48h)
    • kidney 50-55%
  • Post-absorptive state - protein-enriched diet
    • kidney 40-45%

What are the cellular regulations of different pathways?

  1. Glycolysis/glycogenesis: HK, PFK and PK/GyS
  2. Pyruvate fate: PDH, PCK
  3. Gluconeogenesis: PEPCK
  4. TCA cycle: CS
  5. Fatty acid import into mitt's: Cpt1a by Malonyl-CoA
  6. TG lipolysis/lipogenesis
  7. Protein metabolism: N-balance, protein turn-over

PDHC phosphorylation =

What happens when there is lots of acetyl-CoA and NADH?

It will activate the PDH kinases, where ATP is used to make the PDHC inactive

Gluconeogenesis / glycogenolysis =

+ what inhibited and activates the processes

Insulin inhibites
  • Pyruvate carboxylase
  • PEPCK (phosphoenolpyruvate carboxykinase)
  • Fructose-1,6-biphosphatase
  • Glucose-6-Phosphatase
  • Glycogen Phosphorylase


Glucagon/cortisol activates
  • Pyruvate carboxylase
  • PEPCK (phosphoenolpyruvate carboxykinase)
  • Fructose-1,6-biphosphatase
  • Glycose-6-Phosphatase


Glucagon alone activates
  • Glycogen Phosphorylase
  • Pyruvate kinase

What is a role for leptin in oxidation of fatty acids?

Adipose tissue secrets leptin

leptin signal form the muscle --> AMPK

AMPK-Pactive --> ACC

ACC-Pinactive --> no malonyl CoA --> no cytoplasmic fatty acids


Leptin --> increases FFA oxidation

What happens in the absence of (or resistance to) leptin?

ACC converts Acetyl-CoA into malonyl-CoA  --> more fatty acid storage

FA can not enter mitochondria


No oxidation --> fat storage increases --> disturbed insulin-stimulated glucose uptake

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