Hyperglucagonemia in hepatic cirrhosis: its relation to hepatocellular dysfunction and normalization on recovery.

Plasma glucagon, insulin and glucose concentrations, and liver function tests were determined after an overnight fast in 24 normal subjects and 50 male cirrhotic patients. In cirrhotic patients with normal liver profiles, plasma glucagon remained within normal limits, irrespective of the presence of portasystemic anastomoses either pathological or surgical. Hyperglucagonemia was documented in presence of advanced liver dysfunction alone. Significant correlations were established between plasma glucagon and several liver function tests, i.e., serum bilirubin, albumin/globulin ratio, and prothrombin time. Moreover, hyperglucagonemia normalized on recovery from clinical manifestations and improvement in liver profile. Plasma insulin was raised primarily in the presence of a significant portasystemic shunting and maximum levels were observed in patients manifesting advanced liver dysfunction as well. However, no correlation was evident between plasma insulin and any of the liver function tests. Fasting plasma glucose was not altered in cirrhotic patients. Therefore, it is concluded that in hepatic cirrhosis, glucagon secretion by pancreatic alpha-cell may be dependent on the severity of the hepatocellular damage whereas portasystemic shunting may be responsible for hyperinsulinemia which may be further exaggerated in presence of advanced liver dysfunction.