IT HAS long been known that the liver plays a major role in the metabolism of amino acids.* It is not surprising, therefore, that abnormally high concentrations of amino acids have been found in the blood of patients with acute yellow atrophy of the liver.2 The fasting blood amino acid concentration is rarely altered by liver injury less severe than acute or subacute yellow atrophy or some comparable catastrophe.† Individual amino acids, however, may be elevated in less severe hepatic disease.3 In normal persons, after a high-protein meal the blood amino acid level rises,4 as does the blood sugar in a glucose-tolerance test, and one might expect that this postprandial amino acid curve would be higher and more prolonged in patients with liver disease. But data bearing upon this hypothesis are scanty. Kinsell and his co-workers have demonstrated an abnormally high blood methionine level in patients with