Abstract

Abstract A study of subjects with well-compensated cirrhosis and patients without, liver disease by means of the hepatic vein catheterization technique revealed a net splanchnic uptake of pyruvate and citrate from the blood in the basal state After intravenous glucose administration there was a net splanchnic pyruvate production in the face of continuing splanchnic citrate uptake. No significant differences were noted between the two groups of patients. Peripheral arterial-venous (A-V) differences demonstrated a release of citrate from the peripheral tissues in the fasting state. After glucose administration, the A-V citrate difference diminished. There was no difference between the arterial and peripheral venous pyruvate concentrations under the conditions of these observations. The data are consistent with the hypotheses that the plasma citrate is rapidly turned over in the organism, and that a rate limiting mechanism is present in the liver for the conversion of pyruvate to CO 2 and H 2 O via acetyl CoA and subsequent condensation of the latter compound with oxaloacetate to form citrate after glucose administration.

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