FURTHER STUDIES ON THE BLOOD GLUCOSE AND PANCREATIC ISLETS OF LIZARDS¹

Abstract

In this investigation, the changes in the blood sugar and the pancreatic islet cells of a lizard, Eumeces obsoletus, were studied after the administration of adrenaline, glucagon, hydrocortisone, cobaltous chloride, and Synthalin A and after hypophysectomy and pancreatectomy. Adrenaline, glucagon, and hydrocortisone all produced hyperglycemia and beta cell degranulation. The blood sugar response was the greatest with glucagon while the beta cells were the most stimulated as a result of hydrocortisone hyperglycemia. Cobaltous chloride produced a hyperglycemia but no observable histological changes. Synthalin A evoked a severe hypoglycemia accompanied by alpha cell degranulation together with a small degree of alpha cell necrosis. Hypophysectomy produced a moderate hypoglycemia while total pancreatectomy resulted in a severe hypoglycemia. Insulin given to pancreatectomized animals resulted in a moderately high hyperglycemia. From these and previous studies on the lizard, the pancreatic beta cell, as evidenced by its destruction with alloxan and subsequent hyperglycemia and its stimulation and degranulation by glucose, adrenaline, and hydrocortisone, is undoubtedly the site of origin of insulin.