Effect of Glucagon on the Acinar Portion of the Pancreas1

Abstract

An attempt has been made to determine the mechanism by which glucagon produces degranulation of the acinar cells of the pancreas. By histologic examination, a progressive decrease in zymogen granules was found in sections of pancreas of rats treated with repeated injections of glucagon suspended in corn oil, reaching 75% degranulation at 12 hours, and 90 % at 18 hours. Fasting neither caused degranulation nor prevented degranulation after glucagon injection. Five hours after sc injection of glucagon in alkaline solution, a 33 % degranulation was found, and there was a 32% decrease in amylase concentration in the homogenates of these pancreases. Adrenalectomy, hypophysectomy or atropinization did not alter the degranulation after glucagon injection. In contrast, there was a 19% increase in the zymogen granules of pancreases of cortisone acetate- treated rats compared with the controls. The pancreatic ducts of rabbits were cannulated and the pancreatic juice was collected. No apparent difference was found between the amylase concentration, the rate of flow and the rate of amylase secretion between glucagon-treated and control rabbits over a 4-hr period. In the same time interval the serum amylase values of these animals coincided; nor was any difference found between serum amylase values of glucagontreated and control rabbits whose pancreatic ducts were not cannulated. However, there was a 31 % decrease in amylase concentration in the homogenates of the pancreases of the glucagon-treated rabbits 5 hours after injection, in comparison with the controls. It was concluded that the action of glucagon on the acinar portion of the pancreas is not mediated through the vagus nerve or the adrenal or pituitary gland. Fasting had no effect on the hormone’s action on the pancreas. The most likely mechanism of action of glucagon on the exocrine portion of the pancreas is an inhibition of zymogen granule synthesis, with normal release occurring. No conclusion could be drawn as to whether this was a direct inhibition of zymogen granule synthesis by glucagon or was secondary to the lowering of blood amino acid levels.