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The portal vein was catheterized via the umbilical vein under local anaesthesia in 10 non-diabetic subjects about to undergo exploratory laparotomy and in 8 patients with liver cirrhosis. Immunoreactive insulin (IRI) and glucagon (IRG) were assayed in portal and peripheral blood before and during IV infusion of glucose (0.33 g/kg) or arginine (25 g). Basal peripheral plasma (IRI) levels were raised in cirrhotic patients (19±2 versus 10±1 μU/ml; P<0.001). Basal portal insulin values, however, did not differ in the two groups. After glucose cirrhotic patients had higher peripheral insulin concentrations, compared to controls, significant at 45 and 60 minutes. In contrast portal insulin levels were higher in controls than in cirrhotics by 1 minute (403±43 versus 158±38 μU/ml; P<0.001) and remained so for the 60 minutes of study. Similarly, after arginine cirrhotics had significantly higher peripheral insulin concentrations and lower portal concentrations than controls. Peak portal vein insulin levels were delayed in cirrhotics (168±16 μU/ml at 3 min) compared with controls (413±25 μU/ml at 1 min). In the basal state both portal and peripheral glucagon levels were higher in cirrhotics than control subjects. Unlike in controls, IV glucose did not suppress glucagon secretion in cirrhotic patients. Peripheral plasma glucagon concentrations after arginine were also consistently higher in cirrhotics than controls, but unlike insulin portal venous glucagon levels were also raised (1800±360 pg/ml, cirrhotics; 960±87 pg/ml, controls; P<0.001; 1 min after arginine infusion). We conclude that insulin secretion is decreased in liver cirrhosis and that the peripheral hyperinsulinaemia observed reflects diminished hormone metabolism. The high plasma glucagon levels observed in cirrhotic patients are the result of pancreatic hypersecretion of glucagon.

Insulin and glucagon concentrations in portal and peripheral veins in patients with hepatic cirrhosis