Great Article On NAD+:NADH Ratio And The Randle Cycle

CLASH

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Carbs vs. Fats: Which is the Better Fuel?

Found this article that explains quite nicely the cellular mechanics behind the
NAD+: NADH ratio and how the randle cycle actually works. If you look at the krebs cycle, beta oxidation and glycolysis while you read it, the article makes a lot of sense (atleast in my experience).

Enjoy,
-CLASH
 

revenant

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Nice article and some good questions in the comments.

I can see that in theory it should be easy to lose weight on a high-carb, low-fat diet, even with reduced lipolysis, but the studies don't seem to match my own experience. I have 15kg to get rid of but nothing's happening.
 

Amazoniac

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Carbs vs. Fats: Which is the Better Fuel?

Found this article that explains quite nicely the cellular mechanics behind the
NAD+: NADH ratio and how the randle cycle actually works. If you look at the krebs cycle, beta oxidation and glycolysis while you read it, the article makes a lot of sense (atleast in my experience).

Enjoy,
-CLASH
Thanks.

"Because FADH2 donates electrons at complex II, downstream of complex I, it reduces the amount of ubiquinone available to accept electrons at complex I, leading to a buildup of electrons at complex I. This results in two major problems.

For one, this increases the electron leakage at complex I, which increases the production of ROS, specifically superoxide (9, 10, 11).

ROS are a major cause of cellular oxidative stress, and as I’ve already mentioned, damage the cell and inhibit energy production.

Second, the buildup of electrons at complex I reduces the donation of electrons by NADH, leading to a buildup of NADH and a decrease in the ratio of NAD+ to NADH (9, 10, 11, 12)."​

Is it possible for 1 kg of extra suiccidate at a time to be overwhelming?

- SDH mutations in cancer

"SDH is the only membrane-bound enzyme of the Krebs cycle and is also a functional member (complex II) of the electron transport chain (ETC). SDH is a complex of four different polypeptides (SDHA, SDHB, SDHC and SDHD) together with several prosthetic groups that include FAD, non haem iron ubiquinone and haem-b."

upload_2020-2-21_8-13-28.png

--
I had the impression from the initial tone that he was going to mention insulin and fat storage for later use.
 
Last edited:

Hans

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Is it possible for 1 kg of extra suiccidate at a time to be overwhelming?
That is a huge amount lol. There is a med (Remaxol) that contains 5.28g of succinic acid per dose that they inject that aids in liver function, but 5g is far from 1kg, so don't know.
 

yerrag

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Good article. So fatty acid oxidation competes with glucose oxidation at the ETC level, where ubiquinone is the limited resource they compete for, one in which fatty acid oxidation has first dibs at the resource. Would this explain why fatty acids impede the absorption and metabolism of glucose, thus leading to accumulation and thus the increase of blood glucose, or hyperglycemia? And if so, why would PUFAs be more prone to giving this effect than SFAs?
 

CLASH

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Nice article and some good questions in the comments.

I can see that in theory it should be easy to lose weight on a high-carb, low-fat diet, even with reduced lipolysis, but the studies don't seem to match my own experience. I have 15kg to get rid of but nothing's happening.

This is all occurring at the cellular. I think a macro view of the body and personal experience is also important to take into consideration as well. This is why, even though I understand the mechanics to some extent (still alot to learn), I still eat the way I do.
 
Last edited:

CLASH

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Thanks.

"Because FADH2 donates electrons at complex II, downstream of complex I, it reduces the amount of ubiquinone available to accept electrons at complex I, leading to a buildup of electrons at complex I. This results in two major problems.

For one, this increases the electron leakage at complex I, which increases the production of ROS, specifically superoxide (9, 10, 11).

ROS are a major cause of cellular oxidative stress, and as I’ve already mentioned, damage the cell and inhibit energy production.

Second, the buildup of electrons at complex I reduces the donation of electrons by NADH, leading to a buildup of NADH and a decrease in the ratio of NAD+ to NADH (9, 10, 11, 12)."​

Is it possible for 1 kg of extra suiccidate at a time to be overwhelming?

- SDH mutations in cancer

"SDH is the only membrane-bound enzyme of the Krebs cycle and is also a functional member (complex II) of the electron transport chain (ETC). SDH is a complex of four different polypeptides (SDHA, SDHB, SDHC and SDHD) together with several prosthetic groups that include FAD, non haem iron ubiquinone and haem-b."

View attachment 16735

--
I had the impression from the initial tone that he was going to mention insulin and fat storage for later use.

Interesting article. So essentially, If I got this right, with a breakdown of the succinate dehydrogenase enzyme, there is a build up of succinate and a stop in function of the krebs cycle and the electron transport chain. The increased amount of succinate is then transported to the cytosol, where it is a signal for the induction of Hypoxia inducible factor, signaling a hypoxic environment of the cell.
 
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