FURTHER STUDIES ON THE BLOOD GLUCOSE AND PANCREATIC ISLETS OF LIZARDS1

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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. The production of a blood glucose maintaining and elevating factor by the pancreas of lizards is indicated by the observations that these animals are very glucagon sensitive and that in the absence of the pancreas, they become severely hypoglycemic. The latter fact would tend to indicate that lizards, like certain birds are more dependent on a pancreatic factor for the maintenance of the blood sugar level than are other vertebrates which so far have been investigated. We interpret the marked hyperglycemia evoked by insulin in the pancreatectomized animal as a response to the hyperglycemic-glycogenolytic factor present in certain mammalian insulin preparations acting in an unapposed situation (no lizard beta cells or insulin). In addition, it may be that the lizard is more responsive to the blood sugar raising substance (glucagon) of mammalian preparations than it is to the blood sugar lowering material (insulin). Thus, the hypoglycemic action of insulin may be masked and the animal made to appear "insulin resistant". Although lizards become hypoglycemic after administration of Synthalin A, the failure to destroy selectively the alpha cells leaves undecided the question of the source of the hyperglycemic factor. However, indirect evidence, such as the stimulation of the alpha cell after chronic insulin administration and by starvation would implicate it as a likely source of such a material.