Really simple gluconeogenesis q

[EdwardKim]

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In gluconeogenesis, it seems that the enzymatic steps are induced via high energy molecules such as Acetyl CoA (pyruvate carboxylase) and ATP/Citrate (fructose 1,6 bphosphatase). Fructose 1,6 BPhosphatase is also inhibited by AMP and fructose 1,6 bp.

Why is this the case? Shouldn't you want to ramp up gluconeogenesis in low energy state where AMP is high?

 

[Boardz]

In gluconeogenesis, it seems that the enzymatic steps are induced via high energy molecules such as Acetyl CoA (pyruvate carboxylase) and ATP/Citrate (fructose 1,6 bphosphatase). Fructose 1,6 BPhosphatase is also inhibited by AMP and fructose 1,6 bp.

Why is this the case? Shouldn't you want to ramp up gluconeogenesis in low energy state where AMP is high?

Are you sure fructose 1,6 Bisphosphatase is inhibited by AMP?

 

[GTP]

Are you sure fructose 1,6 Bisphosphatase is inhibited by AMP?

Yes it is. I don't remember much about this topic but I remember a teacher saying there is a huge energy requirement for gluconeogenesis. Could this by why it's inhibited by amp? Someone else should explain this better. Sorry OP

 

[Boardz]

Yes it is. I don't remember much about this topic but I remember a teacher saying there is a huge energy requirement for gluconeogenesis. Could this by why it's inhibited by amp? Someone else should explain this better. Sorry OP

a source stating fructose 1,6 bisphosphatase is inhibited by AMP would be nice. can't find it in my first aid...

i could be ******ed though.

 

[GTP]

a source stating fructose 1,6 bisphosphatase is inhibited by AMP would be nice. can't find it in my first aid...

i could be ******ed though.

I randomly googled it and found several sources. Even when you begin to type "f 1,6 bisphosphatase inhibition by ...", it finishes it off by adding AMP for you.

Maybe this concept is low yield. I didn't find it in gunner training either. Also, if you think about it, amp is the product of the reaction in question. Maybe that's also why it's inhibited? Lol someone else should chime in on this.

 

[JackShephard MD]

In gluconeogenesis, it seems that the enzymatic steps are induced via high energy molecules such as Acetyl CoA (pyruvate carboxylase) and ATP/Citrate (fructose 1,6 bphosphatase). Fructose 1,6 BPhosphatase is also inhibited by AMP and fructose 1,6 bp.

Why is this the case? Shouldn't you want to ramp up gluconeogenesis in low energy state where AMP is high?

a source stating fructose 1,6 bisphosphatase is inhibited by AMP would be nice. can't find it in my first aid...

i could be ******ed though.

I randomly googled it and found several sources. Even when you begin to type "f 1,6 bisphosphatase inhibition by ...", it finishes it off by adding AMP for you.

Maybe this concept is low yield. I didn't find it in gunner training either. Also, if you think about it, amp is the product of the reaction in question. Maybe that's also why it's inhibited? Lol someone else should chime in on this.

Acetyl CoA inducing gluconeogenesis: in the liver, pyruvate carboxylase is activated by acetyl CoA during fasting. Think about what happens during fasting? Excessive lipolysis creates a flood of acetyl CoA (also NADH + ATP) which will happen in a state with high glucagon or low insulin. Notice that acetyl CoA also inhibits pyruvate dehydrogenase (shunting towards gluconeogenesis).

Citrate: If you notice, citrate not only stimulates gluconeogenesis, it also inactivates the glycolytic pathway (via inhibition of PFK-1). Again, like the previous scenario, hepatic oxidation of fatty acids will lead to increased ATP, acetyl CoA, and citrate.

AMP: In a situation with high AMP, you want to stimulate glycolysis for quick energy while NOT making glucose which requires energy (ATP). AMP inhibits fructose 1,6 bisphosphatase. Think about gluconeogenesis, it requires ATP and NADH to make the glucose (which is brilliant because they are produced in large quantities during fasting state via beta oxidation of FA). Having lots of AMP means you don't have lots of ATP, so AMP should inhibit gluconeogenesis.

sources: RR biochem + lipincott biochem

 

[GTP]

Acetyl CoA inducing gluconeogenesis: in the liver, pyruvate carboxylase is activated by acetyl CoA during fasting. Think about what happens during fasting? Excessive lipolysis creates a flood of acetyl CoA (also NADH + ATP) which will happen in a state with high glucagon or low insulin. Notice that acetyl CoA also inhibits pyruvate dehydrogenase (shunting towards gluconeogenesis).

Citrate: If you notice, citrate not only stimulates gluconeogenesis, it also inactivates the glycolytic pathway (via inhibition of PFK-1). Again, like the previous scenario, hepatic oxidation of fatty acids will lead to increased ATP, acetyl CoA, and citrate.

AMP: In a situation with high AMP, you want to stimulate glycolysis for quick energy while NOT making glucose which requires energy (ATP). AMP inhibits fructose 1,6 bisphosphatase. Think about gluconeogenesis, it requires ATP and NADH to make the glucose (which is brilliant because they are produced in large quantities during fasting state via beta oxidation of FA). Having lots of AMP means you don't have lots of ATP, so AMP should inhibit gluconeogenesis.

sources: RR biochem + lipincott biochem

This is also wha I was taught in ms1. I was only 90% sure and didn't want to come across as all knowing. Lol. Thanks jack shepard