Can vinegar/acetate counteract the negative effects of sugar consumption?

In several older posts, I have shown that about 5% sodium acetate in the diet of laboratory mice or rats can suppress or even correct metabolic changes caused by a high-fat diet. Could vinegar/acetate also counteract the negative changes in metabolism caused by fructose, i.e. sugar? Given that the essence of both metabolic changes is identical, namely the initiation of de novo lipogenesis (DNL), i.e. the activation of the ACC1 enzyme and the reversal of the direction of mitochondrial isocitrate dehydrogenase, accompanied by the production of ammonia and urea and the slowing down of metabolism. So it can be assumed that vinegar/acetate will also work against fructose.

First, let's review what we already know about what fructose causes. The results of studies are not always unequivocally negative. Fructose alone manifests itself differently than when combined with glucose, such as in regular sugar. Fructose, specifically fructose-1-phosphate (F1P), affects glycolysis without being further metabolized. It redirects pyruvate towards lactate formation. However, this pyruvate comes from glucose. Without glucose, the formation of lactate and the triggering of pseudohypoxia by the transcription factor HIF1 do not occur. The negative effect of fructose is therefore reduced without additional glucose, for example mice do not become fat.

However, fructose can manifest itself through another mechanism, fructose-1-phosphate activates the enzyme AMP deaminase (AMPD2). When fructose is activated (phosphorylated to F1P) in the cell, ATP is depleted and AMP is increased, this should normally have a positive effect on metabolism, activating AMPK and suppressing fat formation via ACC1 phosphorylation. This is how vinegar/acetate does it. But it doesn't work with fructose. Why? The study tells us that in the presence of fructose, AMP will be broken down by the AMPD2 enzyme and deamination, increased ammonia formation and activation of xanthine oxidase, the main source of hydrogen peroxide, oxidative stress and obesity, will occur. Genetic or pharmacological (Metformin) suppression of the AMPD2 enzyme can prevent this. We already recognized the effect of xanthine oxidase on obesity in another study with a fatty diet. What a coincidence!

Two pathways of AMP processing, AMPK accelerates metabolism and suppresses fat formation, AMPD2 slows metabolism and increases fat formation.


Fructose activates the formation of uric acid, this process can be suppressed by turning off the AMPD2 enzyme or turning off xanthine oxidase by adding Allopurinol to the diet.
Uric acid (UA) suppresses AMPK phosphorylation and thus slows metabolism and increases fat formation. Stv = starvation.


So what about the acetate?

It works! A study on pregnant female rats confirms this. It is enough to add 200 mg/kg of sodium acetate to their diet, and the negative effect of fructose is almost completely suppressed.

Effect of dietary sodium acetate supplementation on fructose-induced metabolic changes of pregnant rats, glucose levels, insulin and insulin resistance.

Effect of adding sodium acetate to the diet of pregnant female rats on metabolism. FRU fructose, ACE sodium acetate, ADA adenosine deaminase, XO xanthine oxidase.


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References:

Counteracting Roles of AMP Deaminase and AMP Kinase in the Development of Fatty Liver

Role of AMPD2 in impaired glucose tolerance induced by high fructose diet

Novel role of xanthine oxidase-dependent H2O2 production in 12/15-lipoxygenase-mediated de novo lipogenesis, triglyceride biosynthesis and weight gain

Suppression of uric acid and lactate production by sodium acetate ameliorates hepatic triglyceride accumulation in fructose-insulin resistant pregnant rats

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