Secretion and degradation of insulin and glucagon in carbon tetrachloride-induced liver injury rats.

To elucidate the mechanism of hyperinsulinemia and hyperglucagonemia in liver diseases, secretion of insulin and glucagon from perfused pancreas and extraction of insulin and glucagon by perfused liver were investigated in carbon tetrachloride inhalated liver injury rats. Fasting plasma insulin and glucagon levels and insulin and glucagon levels after arginine injection (0.25 g/kg) in liver injury rats were significantly higher than those in control rats. Glucagon levels after glucose injection (0.5 g/kg) were slightly increased in the liver injury group. Insulin responses to 16.7 mM glucose and 10 mM arginine from perfused pancreas were similar in liver injury rats and control rats. Glucagon response to 10 mM arginine from perfused pancreas was also similar in liver injury rats and control rats. Insulin extraction by perfused liver in liver injury rats (45 +/- 9%) was significantly (P less than 0.05) lower than that (64 +/- 11%) in control rats, and glucagon extraction by perfused liver was also significantly (P less than 0.05) decreased in liver injury rats (57 +/- 8%) compared with controls (73 +/- 9%). It is concluded that in carbon tetrachloride-induced liver injury rats, hyperinsulinemia and hyperglucagonemia may be dependent on decreased insulin and glucagon extraction by the liver.