Insulin, C-peptide and glucagon levels during OGTT in hepatic cirrhosis and in patients with prehepatic block.
In order to investigate pancreatic B-cell function in hepatic cirrhosis and to elucidate the role of porto-caval shunt-circulation in the development of hyperinsulinism and hyperglucagonemia in cirrhotic patients, blood glucose, plasma insulin and glucagon, and serum C-peptide concentrations were measured during OGTT in 11 control and 16 cirrhotic subjects as well as in 7 patients with prehepatic block secondary to thrombosis of the portal vein. Insulin and glucagon levels were significantly higher in the cirrhotic than in the control group (for insulin: p less than 0.01, less than 0.001, less than 0.01 and less than 0.05 at 0, 60, 90 and 120 min, respectively; for glucagon: p less than 0.01, less than 0.01, and less than 0.05 at 0, 30 and 60 min, respectively). Serum C-peptide levels were, however, similar in the two groups with the exception of the 30-min value, which was significantly lower in the cirrhotic group (p less than 0.05). Plasma insulin and glucagon concentrations in patients with prehepatic block were similar to those of the controls but significantly lower than the values found in cirrhotic patients (for insulin: p less than 0.05 at 0, 30, 60 min, respectively). Serum C-peptide levels of these patients were not significantly different either from the control values or from those obtained in the cirrhotic group. Accordingly, pancreatic B-cell secretion is not increased in hepatic cirrhosis. Hence, the hyperinsulinism is due to decreased heptic degradation of the hormone. Decreased degradation of both insulin and glucagon should be attributed mainly to parenchymal liver damage, rather than porto-systemic shunting.