Gluconeogenesis question

[pkrpkrpkr]

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Fats cannot be transformed into sugars because the enzyme
pyruvate dehydrogenase transforming pyruvate into
acetyl-CoA is irreversible. Hence, acetylCoA from fat cannot be tranformed
into pyruvate, which is needed in the beginning of glyconeogenesis.
I understand this.

But in my notes it is also said that "without the burning of fat
there can be no glyconeogenesis" and some vague reference to an
enzyme called pyruvate carboxylase that transforms pyruvate into
oxaloacetate.

I know that Oxaloacetate is one of the last products in the Kreb's.
So maybe (?) in order to get this you need to run the Kreb's first and starting
it with the use of fats. Is this the reason why glyconeogenesis needs
the burning of fat? But if that is the case, why cannot the Krebs be
run by amino acids instead, creating oxaloacetate - thereby bypassing
the need to use the burning of fat?

I don't know if you understand me. My English is not the best.
What I wonder about is in bold. Thanks! : - )

 

[I'm No Superman]

Seriously? isn't it obvious? Wow, if you don't even know why there can be no glyconeogenesis without the burning of fat, you'll never make it as a doctor.

 

[pkrpkrpkr]

Seriously? isn't it obvious? Wow, if you don't even know why there can be no glyconeogenesis without the burning of fat, you'll never make it as a doctor.

If it is obvious please write why.

I'm already in med school (I hope you get in to : ) ) and "if you don't even know why there can be no glyconeogenesis without the burning of fat, you'll never make it as a doctor" is probably true, and that's why I'm trying to learn it. I wanna become a forensic psychiatrist, and I have no interest in these things.

 

[pkrpkrpkr]

This picture is what I don't get. AA:s Alanin, Glycine, Threonine etc. can be converted into pyruvate and fed into the glyconeogenesis. So why then is it not possible to run the g-neo-g without B-oxidation? I understand that it may be smarter for the body to use fats instead of amino acids, but I don't understand why in principle it is not possible. Probably very simple, yes.

http://en.wikipedia.org/wiki/File:Amino_acid_catabolism.png

 

[I'm No Superman]

If it is obvious please write why.

I'm already in med school (I hope you get in to : ) ) and "if you don't even know why there can be no glyconeogenesis without the burning of fat, you'll never make it as a doctor" is probably true, and that's why I'm trying to learn it. I wanna become a forensic psychiatrist, and I have no interest in these things.

I was actually wondering why then you are posting these questions in the high school section instead of the med school section. I guess it's hard to convey sarcasm over the Internet.

I actually have no clue what the answer is, but if I had to guess, it would be that the first cycle of cellular respiration requires ATP to facilitate the process, and that ATP would need to come from somewhere, possibly through the process of burning fat.

 

[pkrpkrpkr]

Alright then, I hold nu grudge. Sarcasm is said to be the last thing you learn in a new language, so alright then ;d I found this explanation. http://wiki.answers.com/Q/Why_can't_fatty_acids_be_converted_directly_to_glucose

I'll post my simplest questions here and in the med forums when they I've worked my way up a little in difficulty =)

 

[I'm No Superman]

I'll post my simplest questions here and in the med forums when they I've worked my way up a little in difficulty =)

this is the high school section though. I guarantee that I've taken more biology and chemistry than any other high schooler here and I had no clue what you were talking about. All I'm saying is that you'll get better answers from the med school sections.

 

[TheBigCat]

But in my notes it is also said that "without the burning of fat there can be no glyconeogenesis" and some vague reference to an enzyme called pyruvate carboxylase that transforms pyruvate into oxaloacetate.

I think what your professor was getting at was control of gluconeogenesis. Acetyl CoA is the end product of fatty acid catabolism. It inhibits pyruvate dehydrogenase, thus inhibiting the formation of more acetyl CoA from pyruvate, and it stimulates pyruvate carboxylase which like you said is the first step of gluconeogenesis. This makes sense from a physiologic standpoint: if you're in a starvation state you're burning your fat stores. You need to get glucose to your brain and red cells and this is how you do it.

Hope this helps. Next time it would probably be better to post questions like this in Allo or Step I.