The role of gastric glucagon immunoreactivity in pancreatectomized dogs

Immunoreactive glucagon (IRG) or glucagon immunoreactivity is known to be increased in the plasma of insulin-deprived pancreatectomized dogs, most of it originating in the stomach. We attempted to clarify the extent to which gastric IRG is involved in glycogenolysis in the liver of insulin-deprived, pancreatectomized dogs. Mongrel dogs underwent total pancreatectomy. IRG levels in portal vein blood increased to 760 +/- 186 pg/ml on the 4th postoperative day while the insulin levels were negligible. On the 4th postoperative day some of the dogs underwent total gastrectomy. IRG levels in the portal vein blood of pancreatectomized dogs decreased from 760 +/- 186 pg/ml to 135 +/- 44 pg/ml one hour after gastrectomy. Glucose containing insulin was then infused into both pancreatectomized and pancreatectomized-gastrectomized grups of dogs. Glycogen synthesis in the liver during glucose and insulin infusion was much the same in both groups. However, glycogen degradation after glucose and insulin infusion was completely suppressed in pancreatectomized dogs without a stomach while pancreatectomized dogs alone showed marked glycogenolysis in the liver. No difference in portal IRI and blood sugar level was found in both groups while a marked difference in portal IRG were observed. These findings indicate that the IRG released from the stomach plays a significant role i glycogen metabolism in pancreatectomized dogs.