Role of spontaneous portal-systemic shunting in hyperinsulinism of cirrhosis

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Abstract
The possible contribution of hepatocellular damage and portal-systemic shunting to hyperinsulinism in cirrhosis was studied in 23 cirrhotics, 8 of whom had a surgical portacaval shunt, and 16 controls by measuring insulin and the connecting peptide (C-peptide) concentrations in simultaneous samples of peripheral arterial and hepatic venous blood. The fractional hepatic insulin extraction (0.48 .+-. 0.06, mean .+-. SE) was normal in cirrhosis. The hepatic insulin elimination rate was directly related to arterial insulin levels (r = 0.91, P < 0.001) even at very high circulating levels. Extrahepatic insulin metabolism was measured across the kidney and lower limb. There were no significant differences between cirrhotics and; control subjects in relation to renal (0.25 .+-. 0.05 vs. 0.23 .+-. 0.04) and lower limb insulin extraction (0.14 .+-. 0.07 vs. 0.19 .+-. 0.04). While in the control group hepatic venous insulin (0.143 .+-. 0.018 pmol/ml) markedly exceeded the peripheral insulin concentration (0.083 .+-. 0.009 pmol/ml, P < 0.01), the contrary was found in cirrhotics with end-to-side portacaval shunt in whom all the pancreactic venous effluent is shunted to the systemic circulation (hepatic venous insulin, 0.130 .+-. 0.028 pmol/ml; peripheral, 0.234 .+-. 0.037 pmol/ml; P < 0.01). Portal-hypertensive cirrhotics without a surgical portocaval shunt also had hepatic venous insulin levels (0.132 .+-. 0.029 pmol/ml) below peripheral arterial insulin concentrations (0.205 .+-. 0.041 pmol/ml, P < 0.01). Hyperinsulinism in cirrhosis apparently is not the result of an intrinsic defect of hepatic insulin metabolism but of the spontaneous shunting of portal blood to the systemic circulation.