Electron microscopic studies on the secretory mechanism of pancreatic islet cells, with particular reference to beta cells. I. Normal secretion in mice, rats, rabbits and chickens, and secretion stimulated by a single intravenous injection of glucose or chlorpropamide in rats.

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The secretory cycle of pancreatic islet cells of mice (C3H), Wistar rats, white rabbits and chickens has been indicated by ultrastructural changes of the roughsurfaced endoplasmic reticulum and Golgi body, both of which represent cellular activity, ranging from the granular to hypogranular appearance of the cytoplasm of pancreatic islet cells. The ergastoplasm seems to be a primary synthetic site of insulin or glucagon molecules and appears to be carried by numerous microvesicles in moderate electron density toward the Golgi zone. These microcarriers then, constitute the lamellar component of the Golgi apparatus. Irregular swelling and shortening of the above lamellae occur and the vacuoles with amorphous raw substance seem to be formed by pinching off at their terminal dilated portions. At the Golgi zone of beta cells of the animals, microfibrils measuring approximately 60A in width attach on the outer surface of some of the above vacuoles, and occur both inside and through it, whereas in rats, microvesicles may be frequently engulfed into sacs via their incomplete or partially interrupted surrounding membrance. Thereafter, immature granules may develop and gain electron density gradually, followed by a molding of the storage form of characteristic crystallization of mature granules. Moreover, even after leaving the Golgi area the microfilamentous structures also may fall into the sacs of secretory granules in beta cells, although less frequently. The developed granules are released by an emiocytotic process into the perisinusoidal space. A single intravenous injection of glucose or chlorpropamide in the rat was performed and the ultrastructural alterations of beta cell organelles were observed. The primary effect of these two beta cell stimulants were assumed to be different. The granule synthesis, storage and discharge in the stimulated conditions of beta cells were almost the same process as found in the non-stimulated beta cells, except in the maximally effected state of glucose administration.