Effects of Acetate

The role of acetate in alcohol-induced pathology is not well understood. The uptake and utilization of acetate by tissues depend on the activity of acetyl-CoA synthetase. Acetyl-CoA and adenosine are produced from the metabolism of acetate. Acetate crosses the blood-brain barrier easily and is actively metabolized in the brain. Many of the central nervous system depressant effects of etha-nol may be blocked by adenosine receptor blockers. Thus, acetate and adenosine may be important in the intoxicating effects of ethanol.

Ethanol increases portal blood flow, mainly by increasing GI tract blood flow. This effect is reproduced by acetate. Acetate also increases coronary blood flow, myocardial contractility, and cardiac output. Acetate inhibits lipolysis in adipose tissue and promotes steatosis in the liver. The reduced circulating free fatty acids (a source of energy for many tissues) may have significant metabolic consequences. Thus, many of the effects of alcohol may be due to acetate.

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