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The liver exerts a strong influence on the level of bile acids in the blood, since its bile acids are taken up by the hepatocytes. Therefore, in portal systemic encephalopathy (PSE) there is hypoaminoacidemia, and therefore the liver cannot synthesize the bile acids which are necessary to compensate the hypoaminoacidemia. In order to determine the regulatory mechanism of bile acid synthesis in PSE, we measured the activity of enzymes required for the synthesis of bile acids in both normal and PSE rats. The activity of the total bilirubin UDPglucuronyl transferase (tBGT) was lower in PSE rats (129 +/- 11 nmol 4-h-5-cholesten-3 beta-ol, 5-7% of control, n = 4) than in the controls (373 +/- 32 nmol 4-h-5-cholesten-3 beta-ol, n = 5). This is because in PSE there is a decrease in the bile acid synthesis. Moreover, the activity of tBGT was specifically low in rats with PSE in which there was a gastric resection (182 +/- 26 nmol 4-h-5-cholesten-3 beta-ol, n = 4). We could not find any enzymatic alteration in the hepatic stellate cells of PSE rats compared with control rats. It is likely that the liver’s regulatory mechanisms involved in bile acid synthesis have been altered in PSE. These results indicate that a liver-specific regulation has been altered in PSE. The hepatic regulatory mechanism of bile acid synthesis is not yet known.?” ” No.” “You?” “No.” ” I’ve been quiet for hours.” ” Oh, well.” “Don’t worry.” “We’ll save you!” ” Just one touch… and we
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