Impaired function of pancreatic islets from rats with portal hypertension resulting from cirrhosis and partial portal vein ligation

✍ Scribed by Ramon Gomis; Josefa Fernández-Alvarez; Pilar Pizcueta; Mercedes Fernández; Roser Casamitjana; Jaume Bosch; Joan Rodés

• Publisher: John Wiley and Sons
• Year: 1994
• Tongue: English
• Weight: 524 KB
• Volume: 19
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840190526

✦ Synopsis

Increased circulating insulin and glucagon levels are a common observation in patients with cirrhosis, as well as in portal hypertensive models. Hyperinsulinemia and hyperglucagonemia may be caused either by increased beta-and alpha-cell secretion or by defective hepatic clearance of these hormones. To elucidate whether an abnormal endocrine pancreatic function might contribute to the hyperinsulinism or to the hyperglucagonism observed in chronic portal hypertension, insulin and gllucagon secretion were measured in uitro in isolated pancreatic islets from rats with partial portal vein ligated and rats with cirrhosis caused by carbon tetrachloride poisoning. Both rats with partial portal vein ligation and rats with cirrhosis caused by carbon tetrachloride poisoning exhibited hype-* m and hyperglucagonism as compared with control rats. Isolated pancreatic islets from both experimental portal hypertensive models showed an impaired insulin Secretion after glucose stimulation. On the contrary, glucagon secretion was significantly increased, and there was a markedly enhanced response to arginine. This increased in uitro glucagon production could not be corrected, even in the presence of high glucose concentrations in the incubation medium. Therefore our data show that although hyperglucagonism in rats with partial portal vein ligation and in rats with cirrhosis caused by carbon tetrachloride poisoning is promoted by an enhanced alpha-cell secretion, hyperinsulinism is associated with impaired beta-cell secretion.