Has Anyone Tried Sodium Acetate ? (for SIBO?)

[Amazoniac]

- Acetate Revisited: A Key Biomolecule at the Nexus of Metabolism, Epigenetics and Oncogenesis—Part 1: Acetyl-CoA, Acetogenesis and Acyl-CoA Short-Chain Synthetases
- Acetate Revisited: A Key Biomolecule at the Nexus of Metabolism, Epigenetics, and Oncogenesis – Part 2: Acetate and ACSS2 in Health and Disease

 

[Amazoniac]

- Depletion of acetate-producing bacteria from the gut microbiota facilitates cognitive impairment through the gut-brain neural mechanism in diabetic mice

- Human-derived gut microbiota modulates colonic secretion in mice by regulating 5-HT3 receptor expression via acetate production

 

[Amazoniac]

- Stimulation of Gastric Acid Secretion by Acetate

Spoiler

"Although ethyl alcohol has long been known to stimulate gastric acid secretion, there is no agreement concerning the mode of action. Dragstedt et al(2) observed that perfusion of organs with dilute alcohol solution resulted in histamine-like activity in the perfusate. They considered histamine release to be a possible mechanism. However, Irvine, Watkin and Williams(6) did not detect a rise in free histamine concentration in the urine during alcohol stimulation but a histamine infusion producing equivalent acid response raised urinary histamine levels. Woodward, Slotten and Tillmanns(12) reported that alcohol applied directly to antral mucosa was a powerful stimulant for the antral gastrin mechanism. Irvine, Watkin and William(6), although confirming the gastrin releasing effect of ethanol, did not believe that gastrin was the major factor mediating the acid response to oral or intravenous alcohol. Hirschowitz et al(5) interpreted results of experiments with human subjects to indicate a central mechanism for alcohol stimulation of gastric secretion mediated through the vagus nerve."

"The stimulatory effect of acetate, a metabolic product of ethanol, was reported by McManus(11). Gastric stimulation by acetate was used by Zawoiski, Braunschweig and Beyer(13) in experiments with asteroids. Certain similarities between acetate and ethanol stimulation were observed. In this paper are presented in more detail some of these observations."

"The gastric acid stimulants were administered intravenously by a constant velocity infusion pump at the rate of 2 ml/minute."

"Infusion of sodium acetate in doses of 2.5-5.0 uM/kg/minute had an immediate pronounced stimulatory effect on secretion of acid. Volume rose sharply and the pH dropped to about 1. Data that compare the stimulatory effect of histamine, methacholine, ethanol and sodium acetate on three dogs are summarized in Fig. 1. Each plot is the average of results for 2 separate experiments."

Spoiler

"A large number of acids were tested for similar action. Sodium propionate was approximately as potent as sodium acetate. b-Alanine and sodium hydracrylate(7,8) were moderately active in doses of 10 uM/kg/minute. The following sodium salts were inactive when infused in a dose of 50 uM/kg/minute: butyrate, pyruvate, lactate, oxalacetate, Diokine-ketoglutarate, fumarate, succinate, glutamate and acetoacetate."

"The doses of atropine required to suppress the effect of acetate were higher than those required to inhibit methacholine. Fig. 2 summarizes the results of the tests with atropine."

"Secretion stimulated by ethanol is known to be relatively low in peptic activity(9). This was also found for acetate stimulated secretion." "The peptic activity of secretion evoked by sodium acetate and by methacholine were compared. During a 1 1/2-hour period of stimulation with sodium acetate, 5.0 uM/kg/minute, the peptic activity tended to decrease slightly. Methacholine, 0.2 ug/kg/minute, produced an equivalent secretion in respect to pH and volume but with very much higher peptic power. Results of experiments with 3 dogs are summarized in Fig. 3."

Spoiler

 

[Amazoniac]

- Acetate Promotes T Cell Effector Function during Glucose Restriction

Competition for nutrients like glucose can metabolically restrict T cells and contribute to their hyporesponsiveness during cancer. Metabolic adaptation to the surrounding microenvironment is therefore key for maintaining appropriate cell function. For instance, cancer cells use acetate as a substrate alternative to glucose to fuel metabolism and growth. Here, we show that acetate rescues effector function in glucose-restricted CD8+ T cells. Mechanistically, acetate promotes histone acetylation and chromatin accessibility and enhances IFN-γ gene transcription and cytokine production in an acetyl-CoA synthetase (ACSS)-dependent manner. Ex vivo acetate treatment increases IFN-γ production by exhausted T cells, whereas reducing ACSS expression in T cells impairs IFN-γ production by tumor-infiltrating lymphocytes and tumor clearance. Thus, hyporesponsive T cells can be epigenetically remodeled and reactivated by acetate, suggesting that pathways regulating the use of substrates alternative to glucose could be therapeutically targeted to promote T cell function during cancer.

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- Dietary fructose feeds hepatic lipogenesis via microbiota-derived acetate

Fructose consumption has risen dramatically in recent decades due to use of sucrose and high fructose corn syrup in beverages and processed foods[1], contributing to rising rates of obesity and non-alcoholic fatty liver disease (NAFLD)[2–4]. Fructose intake triggers hepatic de novo lipogenesis (DNL)[4–6], which is initiated from acetyl-CoA. ATP-citrate lyase (ACLY) cleaves cytosolic citrate to generate acetyl-CoA and is upregulated upon carbohydrate consumption[7]. Ongoing clinical trials are pursuing ACLY inhibition for treatment of metabolic diseases[8]. Nevertheless, the route from dietary fructose to hepatic acetyl-CoA and lipids remains unproven. Here we show, using in vivo isotope tracing, that liver-specific deletion of Acly fails to suppress fructose-induced DNL in mice. Dietary fructose is converted by the gut microbiome into acetate[9], which supplies lipogenic acetyl-CoA independently of ACLY[10]. Depletion of the microbiome or silencing of hepatic ACSS2, which generates acetyl-CoA from acetate, potently suppresses conversion of a fructose bolus into hepatic acetyl-CoA and fatty acids, bypassing ACLY. When fructose is consumed more gradually to facilitate its absorption in the small intestine, both citrate cleavage and microbial acetate contribute to lipogenesis. The DNL transcriptional program, on the other hand, is activated in response to fructose in a manner independent of acetyl-CoA metabolism. These data reveal a two-pronged mechanism regulating hepatic DNL, in which fructolysis within hepatocytes provides a signal to promote DNL gene expression, while microbial acetate generation feeds lipogenic acetyl-CoA pools.