Abstract
Using the method of gastrin bioassay and its modified technique, the inactivation of gastrin-like synthetic peptide was found to exist both in the liver and serum. The experimental liver damage induced by carbon tetrachloride (CCl4) reduced the gastrin-like peptideinactivation in the liver. These findings may indicate that the high incidence of peptic ulcer among the patients with liver diseases is due in part to hypergastrinemia caused by a disturbed inactivation of endogenous gastrin in the liver.