Abstract
The secretory mechanism of extrapancreatic glucagon (considered mainly as being of gastrointestinal origin) was investigated in depancreatized dogs and a totally depancreatized patient. The basal level of glucagon immunoreactivity (GI, as measured with pancreatic glucagon specific antisera) and of gut glucagon-like immunoreactive materials (gut GLI: calculated as the difference between the values with crossreacting anti serum and GI) were elevated in systemic blood of depancreatized dogs and were reduced by insulin therapy. The secretion of GI was stimulated following arginine infusion but was not by insulin-induced hypoglycemia in depancreatized dogs. The paradoxycal rise of GI was observed during oral glucose tolerance test in a totally depancreatized patient. These findings are similar to the glucagon abnormalities observed in insulin deficient diabetics. Thus, gastrointestinal glucagon may contribute to the overall glucagon abnormalities characteristic of insulin deficient diabetes. However, suppression of GI is not effective for the reduction of blood glucose once an extreme hyperglycemia is brought about by insulin deficiency because blood glucose did not change during somatostatin infusion in depancreatized dogs.
