Metabolism of short chain fatty acid in rat liver in biliary obstruction.
In an attempt to clarify the hepatic insufficiency in obstructive jaundice, hepatic metabolic rate of n-butyric acid, ketogenesis and CO2 formation from butyric acid were investigated using liver slices obtained from rats subjected to choledochal ligation or carbon tetrachloride (CCl4) injection. The hepatic metabolic rate of n-butyric acid was reduced with the prolongation of biliary obstruction, and the reduction was presumed to be caused for the most part by the reduced ketogenesis and in part by the impairment of the citric acid cycle (TCA-cycle). In 3approximately4 weeks after biliary obstruction, the metabolic rate reduced to a level comparable to liver necrosis produced by CCl4. This reduction of the metabolic rate of n-butyric acid is postulated as one of the pathogenic factors for fatal liver insufficiency in many cases of obstructive jaundice. While the reduction is mild and mobile in the early stage of jaundice, it may be of significance for preventing fatal liver insufficiency to relieve the obstruction as early as possible.
D000818:Animals; D002087:Butyrates / Q000378:metabolism*; D002245:Carbon Dioxide / Q000378:metabolism; D002779:Cholestasis / Q000378:metabolism* / Q000473:pathology; D007657:Ketone Bodies / Q000096:biosynthesis; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008111:Liver Function Tests; D051381:Rats
D002087:Butyrates; D007657:Ketone Bodies; D002245:Carbon Dioxide