Gluconeogenesis -- FA13 pg 97

[MedicalBeast]

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On page 97 of First Aid 2013, it says that Gluconeogenesis is positively regulated by ATP. I am having trouble understanding why increasd ATP would cause gluconeogenesis. I understand why high ATP would inhibit glycolysis, but then why would it promote gluconeogenesis? Could someone help explain this?

Thank you

 

[withrye]

Solely in the liver, which is the primary site of gluconeogenesis. High ATP means that energy and precursors are abundant, so why not use them to make glucose (and glycogen) for later? When ATP is low, your primary goal is to make more ATP, so you rev up glycolysis and downregulate gluconeogenesis.

 

[MedicalBeast]

thanks, makes sense now

 

[Donald Juan]

Solely in the liver, which is the primary site of gluconeogenesis. High ATP means that energy and precursors are abundant, so why not use them to make glucose (and glycogen) for later? When ATP is low, your primary goal is to make more ATP, so you rev up glycolysis and downregulate gluconeogenesis.

I don't fully agree. Gluconeogenesis is done to raise blood glucose levels when they are low, not to replenish glycogen; it's not done for the later, it's done for the right now. Glycogenesis occurs when blood glucose levels are high.

But yes, the important part is high ATP/low AMP = + gluconeogenesis, - glycolysis (and vice versa). Remember that when the body is starved, the liver receives a large amount of fatty acids from the lipolysis that is occuring in adipocytes which is what increases the ATP levels in the liver as glucose levels are dropping.

 

[Jonari]

On page 97 of First Aid 2013, it says that Gluconeogenesis is positively regulated by ATP. I am having trouble understanding why increasd ATP would cause gluconeogenesis. I understand why high ATP would inhibit glycolysis, but then why would it promote gluconeogenesis? Could someone help explain this?

Thank you

From what I understand is that in order for ggenesis to occur, you need ATP for the cycle to run. You get the ATP from another pathway, which is basically fueling ggenesis, and that pathway is from beta-oxidation of fatty acids taking place in the mitochondria.

B-ox gives you 5 ATP for every cycle of b-ox. In add'n to that, the last two acetyl-coas go into the TCA cycle to generate additional ATP, however keep in mind that the latter is not part of b-ox.

ATP regulates ggenesis at the level of the enzyme F2,6BPase. Funny right, because ATP simultaneously inhibits PFK-1, the same enzyme which is working in the mirrored pathway of glycolysis. Hope that makes sense.