Role of gastrointestinal tract and liver in acetate metabolism in rat and man

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Abstract
Net acetate uptake/release by various tissues was studied in vivo in fed, starved and Paromomycin-treated rats and in patients with cirrhosis of the liver. In humans the portal vein, hepatic vein and hepatic arterial blood flow rates were determined simultaneously. In rats acetate is only intestinally produced and released into the portal vein. Intestinal production is decreased by 33% in starved and Paromomycin-treated rats compared to fed animals. Portal vein-hepatic vein acetate differences are linearly related to the portal vein acetate concentration (r = 0.92). Acetate uptake from the portal vein by the liver was found when the portal venous concentration exceeded 180 .mu.mol l-1. In humans the hepatic net acetate uptake from the portal vein/net acetate release into the hepatic vein, measured as .mu.mol min-1, is linearly related to the portal vein acetate concentration (r = 0.97). Furthermore, portal vein-hepatic vein difference are correlated to the arterial concentration (r = 0.96). The liver may homeostatically regulate the systemic acetate concentration in rat and man.

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