Feb 18, 2013
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Coming straight from Khan Academy. "Fatty-acid oxidation fuels gluconeogenesis."

How does fatty-acid oxidation fuel gluconeogenesis? I thought fatty-acid oxidation makes acetyl-CoA and gluconeogenesis uses other starting materials to make glucose.
 
Aug 27, 2012
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Acetyl-CoA is converted to pyruvate and lactate via ketogenesis - which can "fuel" gluconeogenesis.
Acetyl-CoA formation is irreversible. You cannot generate pyruvate from Acetyl-CoA.

The glycerol backbone of TAGs can be converted to glycerol-3-phosphate and then Dihydroxyacetone (DHAP) for gluconeogenesis. Since you mentioned FAs directly, if you have an odd numbered FA then during beta-oxidation you will generate a 3-carbon fragment termed propionyl-CoA which can be used as a precursor for gluconeogenesis.
 
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Acetyl-CoA formation is irreversible. You cannot generate pyruvate from Acetyl-CoA.

The glycerol backbone of TAGs can be converted to glycerol-3-phosphate and then Dihydroxyacetone (DHAP) for gluconeogenesis. Since you mentioned FAs directly, if you have an odd numbered FA then during beta-oxidation you will generate a 3-carbon fragment termed propionyl-CoA which can be used as a precursor for gluconeogenesis.
Cool story friend, but you are wrong. Acetyl-CoA enters the ketogenic pathway to form acetone, which can later be used to generate pyruvate via this enzyme: https://en.wikipedia.org/wiki/CYP2E1. Fatty-acid oxidation fuels gluconeogenesis in conditions when the levels of Acetyl-CoA are too high to feed the citric acid cycle (because of low levels of intermediates like oxaloacetate) and thus enter the ketogenesis pathway to form ketone bodies. Acetone is a ketone synthesized from Acetyl-CoA and used in a sort of roundabout pathway to form pyruvate and fuel gluconeogenesis as mentioned earlier.

The DHAP thing has nothing to do with what the OP was asking in regards to the connection between fatty acid oxidation and gluconeogenesis. The statement about propionyl-CoA is correct, but acetyl-CoA is also involved.
 
Aug 27, 2012
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Cool story friend, but you are wrong. Acetyl-CoA enters the ketogenic pathway to form acetone, which can later be used to generate pyruvate via this enzyme: https://en.wikipedia.org/wiki/CYP2E1. Fatty-acid oxidation fuels gluconeogenesis in conditions when the levels of Acetyl-CoA are too high to feed the citric acid cycle (because of low levels of intermediates like oxaloacetate) and thus enter the ketogenesis pathway to form ketone bodies. Acetone is a ketone synthesized from Acetyl-CoA and used in a sort of roundabout pathway to form pyruvate and fuel gluconeogenesis as mentioned earlier.

The DHAP thing has nothing to do with what the OP was asking in regards to the connection between fatty acid oxidation and gluconeogenesis. The statement about propionyl-CoA is correct, but acetyl-CoA is also involved.
That is without a doubt completely out of the scope of the MCAT. Kaplan doesn't mention a thing about converting Acetyl-CoA to ketones via that or any enzyme, and neither does TBR. Here's a direct quote from TBR Bio II "It turns out that animals cannot get a net conversion of a two carbon (C2) compound like acetyl CoA into glucose."

There's exceptions to a lot of things, and many concepts are definitely simplified. Take for example neurotransmitter release at the synaptic cleft - TPR states that only 1 neurotransmitter is released per synapse, but if you look in the literature that is certainly not the case.

I mentioned the DHAP just for a little bit of extra information. You don't need to get so uptight buddy. Relax.
 
Jul 21, 2015
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That is without a doubt completely out of the scope of the MCAT. Kaplan doesn't mention a thing about converting Acetyl-CoA to ketones via that or any enzyme, and neither does TBR. Here's a direct quote from TBR Bio II "It turns out that animals cannot get a net conversion of a two carbon (C2) compound like acetyl CoA into glucose."

There's exceptions to a lot of things, and many concepts are definitely simplified. Take for example neurotransmitter release at the synaptic cleft - TPR states that only 1 neurotransmitter is released per synapse, but if you look in the literature that is certainly not the case.

I mentioned the DHAP just for a little bit of extra information. You don't need to get so uptight buddy. Relax.
Sorry, I am really passionate about acetyl-coa.
 

DingoPingo

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Jan 8, 2013
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Fatty-acid oxidation doesn't necessarily fuel gluconeogenesis as in acetyl-CoA doesn't become glucose, but acetyl-CoA produced by fatty-acid oxidation activates pyruvate carboxylase, which adds a CO2 group with ATP to pyruvate, forming OAA, which can be shuttled out into the cytoplasm for conversion into phosphoenolpyruvate, which can be used in gluconeogenesis. In other words, fatty-acid oxidation doesn't make glucose but it activates the gluconeogenesis pathway, which is important when you run out of ingested glucose.
 
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