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1. Glucose tolerance and metabolic changes after intravenous glucose were studied in fifteen patients with acute viral hepatitis and in eight patients after recovery. In the acute stage glucose tolerance was significantly impaired compared with control subjects or with patients after recovery from hepatitis. 2. Serum insulin concentrations were significantly higher in fasting acute hepatitis patients than in control subjects and the time-integrated serum insulin concentration in the first 5 min after glucose was inappropriately high for the observed glucose disappearance rate, indicating insulin resistance. Serum growth hormone concentrations in male acute hepatitis patients were significantly higher than controls and suppressed poorly. 3. Fasting blood lactate concentrations were significantly elevated and after intravenous glucose there was a variable response. 2-Oxoglutarate, glutamate and glutamine concentrations from blood of fasting subjects, were significantly higher in acute hepatitis patients than controls. 4. There were no significant differences in blood ketones, glycerol and plasma free fatty acid concentrations from fasting subjects, but plasma triglycerides were significantly increased in the acute hepatitis patients. 5. The results indicate that viral hepatitis is associated with glucose intolerance and insulin resistance. After recovery the lactate response after glucose is diminished compared with controls.

1. Intravenous glucose tolerance tests were performed in fourteen patients with mild or moderate liver damage due to paracetamol overdose. 2. In patients managed conservatively there was glucose intolerance associated with a diminished early insulin response to glucose, suggesting inadequate nutrition in the period between the overdose and the glucose tolerance test. 3. Patients given intravenous glucose supplements to maintain nutrition were also glucose intolerant and, in these, insulin responses to glucose were normal. The decreased fractional disappearance rate was partly due to an increase in glucose distribution space and partly due to a decrease in absolute glucose disappearance rate. 4. Impaired gluconeogenesis was suggested by mild fasting hypoglycaemia in four patients and raised fasting blood lactate concentrations. Serum growth hormone concentrations showed a paradoxical increase after glucose. 5. All these variables had returned to normal in four patients re-tested after recovery.