NP8 Gluconeogenesis, PPP
12 important questions on NP8 Gluconeogenesis, PPP
Why/for what is there a pentose phosphate cycle?
NADPH
- You need NAPDH for fatty acid synthesis
High in tissues:
- liver
- mammary gland
- adipose
Glycolysis - isomerization --> fructose -6-phosphate with the pentose phosphate cycle
3 mol glucose of glucose-6-phosphate gives
- 6 mol NADPH
- 3 mol CO2
- 2 mol fructose 6-phosphate
- 1 mol glyceraldehyde-3-phosphate
What is the difference between PPP and glycolysis?
- 3 G-6-P -> 2 F-6-P + GA3P + 6 NADPH + 3 CO2
Glycolysis
- 2 G-6-P --> 2 F-6-P
- 1 G-6-P --> 2 mol GA3P - 1 ATP
- 1 mol GA3P for complete oxidation: + 3.5 (GA3P -> pyruvate) + 12.5 ATP = 16 ATP (+3 CO2)
- in total: 3 G-6-P -> 2 F-6-P + GA3P + 15 ATP (+ 3 CO2)
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What is the meaning of energetics of reverse reactions?
- energy invested in the forward reaction is released in the backward reaction
Substrate cycle (tourniquet principle; go in 'pay' / go out 'free')
- energy invested in the forward reaction is NOT released in the backward reaction
Energetics of glucose substrate cycling [the ATP difference]
overall -6
What are the costs of oxaloacetate mito membrane transport?
- oxaloacetate occurs in both the cytoplasm and the mitochondrion, but cannot pass the mitochondrial membrane
- to pass the membrane oxaloacetate is converted to malate (NADHm; 2.5 ATP) and back (NADHc; 1.5 ATP)
- the costs of oxaloacetate mito membrane transport, as substrate cycle, are 1 ATP
Glucose substrate cycling costs related to the level
- glucose -- 0
- glucose- 6P
- fructose - 1,6 diP
- PEP
- Pyruvate
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energy loss (glucose --> level --> glucose) - X ATP
- glucose --> 0 ATP
- glucose- 6P --> -1 ATP
- fructose - 1,6 diP --> -2 ATP
- PEP --> -2 ATP
- Pyruvate --> -6 ATP
When is pyruvate converted into Acetyl-CoA or Oxaloacetate?
- High level of Acetyl-CoA: change to Oxaloacetate
- High AMP (so low ATP): stimulation of citric acid cycle condensation oxaloacetate + acetyl-CoA
- Low AMP (so high ATP): stimulation of gluconeogenesis oxaloacetate is converted to PEP; inhibition glycolysis
Glycolysis of lactate / lactic acid
- Pasteur effect" 15x increase in glucose utilisation
- Metabolic pathway by which glucose is converted to lactic acid (anaerobic respiration)
- oxygen is not used/needed in the process
- NADH + H+ + pyruvic acid --> lactic acid + NAD+
- prude 2 ATP/glucose molecule
Glycolysis: the anaerobic metabolism of glucose
Lactate in the muscle will go to the liver and will be converted back into glucose
muscle: glucose --> 2 ATP + 2 lactate
liver: 2 lactate + 8 ATP --> glucose
extra costs: anaerobic glycolysis as substrate cycle 6 ATP
8 ATP is derived from fatty acid oxidation in the liver -- Beta-ox fatty acids
Some tissues better adapt to anaerobic conditions, which ones and why/how
- RBCs do not contain mitochondria and ONLY use the lactic acid pathway
- Occurs in skeletal muscles and heart when ration of oxygen supply to oxygen need falls below critical level
- skeletal muscle
- normal daily occurrence
- does not harm muscle tissue
- cardiac muscle normally respires aerobically
- myocardial ischemia occurs under anaerobic conditions
Pasteur effect
what it the ration in ATP yield of aerobic and anaerobic breakdown of glucose?
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