5 replies to this topic

[Primal]

SAM-e is the global methyl donor, what is the global acetyl donor? Acetyl phosphate (or is it as more a phospho donor)? acetyl-coenzyme A ? What about a global acetyl acceptor? 

 

B9 and B12 are the main cofactors for methylation, what are the cofactors for acetylation/deacetylation? anything is rate-limiting ?

 

calorie restriction has much effect on acetylation/deacetylation? Other epigenetics factors? 

 

An acetyl group is an acyl, so Sirtuin deacylases cause deacetylation. Would this imply that taking Apple cider vinagar, ALCAR and other acetyl donors could accelerate aging?

 

HDAC (except class III) contain zinc and are known as Zn-dependent histone deacetylases.

The Class III group is considered an atypical category of its own, which are NAD⁺-dependent, whereas other groups require Zn²⁺ as a cofactor.^[6]

 

Edited by Primal, 10 July 2014 - 12:38 AM.

[Primal]

There is a claim that B1 and B5 would be to acetylation what B9 and B12 are to methylation. http://www.longecity...ar/#entry673603

 

Not sure about deacetylation (or, more generally, deacylation).

[Ultravioletbllc]

I think you might be on too something here however I must say the evidence / peer generated reviews and bio assays for something like Acetyl-L-Carnitine Arginate speak against this idea especially in someone supplementing sulbutiamine thiamine , bentofiamine or other de acetylation modulators

[Primal]

For reference some of the questions are being discussed in another thread http://www.longecity...ad/#entry676248

 

I think you might be on too something here however I must say the evidence / peer generated reviews and bio assays for something like Acetyl-L-Carnitine Arginate speak against this idea especially in someone supplementing sulbutiamine thiamine , bentofiamine or other de acetylation modulators

 

You're saying ALCAR arginate together with B1 in various forms make people feel better, or improve some characteristics of the cells (which?) or was shown to extend lifespan in some species? If you could explain what you're saying or give some references we could understand what your point is

[Raza]

Acetyl-CoA is the primary activated carrier (donor) for acetyl groups, according to Albert's Molecular Biology of the Cell. Not sure about a global deacetylator.

 

But let me copypaste my response from the other thread:

Acetylation is am incredibly diverse mechanism for reversibly modifying target molecules to change their function on the fly as needed by the body/cell. A deficit in the acetyl acceptors needed for deacetylation might play a role in aging because this keeps important molecules in the wrong setting in spite of a signal to deacetylate them, and resolving this deficit might then help against aging by fixing this broad problem, but I'm pretty sure you don't want to be globally reducing acetylation or activating deacetylation by other mechanisms. The idea is that these groups are added and removed at exactly the right time and place to suit the needs of the cell, not that molecules are bad for you when they're modified with an acetyl group and good for you when they aren't.

Edited by Raza, 23 July 2014 - 01:39 PM.

[Primal]

There is a claim that B1 and B5 would be to acetylation what B9 and B12 are to methylation. http://www.longecity...ar/#entry673603

 

I looked it up and it seems like B1 (TPP), B2 (FAD), B3 (NAD+), R-Lipoic Acid and Magnesium are the main cofactors to produce acetyl groups from glucose, while Zinc and NAD+ are the ones to produce them from ethanol (alcohol).

Edited by Primal, 12 August 2014 - 06:23 PM.