As has been reported in the author's previous paper (KANO 1961), apparent hydropic degeneration based upon glycogen infiltration appears in beta cells of the pancreatic islets of the tortoise (
Clemmys japonica) during hibernation (from December to February). In order to know whether it is possible or not to bring about the hydropic degeneration in pancreatic beta cells by certain experimental procedures, the following experiments were carried out. Experiment 1. Tortoises (
Clemmys japonica) having no hydropic beta cells in islets (in September and October) were given intraperitoneal injections of 12g of glucose per kg of body weight daily for 20 days. Experiment 2. Hibernating tortoises having hydropic beta cells in islets (in January and February) were given intraperitoneal injections of 0.3 unit of insulin and 0.2-0.3g of glucose per kg of body weight daily for 33 days. Experiment 3. Hibernating tortoises having hydropic beta cells in islets were given intraperitoneal injections of 2.4 unit of insulin per kg of body weight daily for 21 days. Experiment 4. Hibernating tortoises having hydropic beta cells in islets (in January) were kept in an incubator at 25°C to awake from the hibernation and fed ad libitum on some fish meat for 30 days.
Tissues from pancreas were fixed in LEVI's solution and in ZENKER formol. Paraffin sections were cut 4μ thick and stained with hematoxylin eosin or HEIDENHAIN's azan. Glycogen was demonstrated by the periodic acid-SCHIFF method (PAS) and identified by saliva-digestion test.
Experiment 1. By the prolonged intraperitoneal administrations of glucose there appeared degranulation and hydropic degeneration in beta cells of islets, alpha cells showed, however, almost no signs of hydropic change, packed by fairly large amount of alpha granules. By PAS-method much glycogen was demonstrated in islets cells, proving that the hydropic degeneration is nothing other than the glycogen infiltration of the islet cells. Besides in the islet cells the glycogen was observed abundantly in duct epithelium and centroacinous cells of the exocrine pancreatic tissue. These findings well correspond to the results of observation on control specimens taken from the hibernating animals. The hydropic degeneration of the beta cells found in this experiment may be regarded as a partial phenomenon of the widespread increase of glycogen in tissue cells caused by the hyperfunction of the beta cells and hyperinsulinemia which had been resulted by the glucose administration.
Experiment 2. The prolonged intraperitoneal administration of small doses of insulin and glucose to the hibernating tortoises was not able to diminish or to take away the hydropic change from beta cells.
Experiment 3. In the hibernating tortoises received large doses of insulin, the hydropic degeneration of beta cells was somewhat diminished, but never disappeared. This fact may suggest that in the cold-blooded animal like the tortoise the hydropic degeneration of islet cells found in the hibernation season should not be brought about merely by the hypoinsulinemia. It must be, however, taken into consideration that in the cold climate the hypofunction of tissue cells induced by low temperature of animals may probably inhibit the effect of insulin.
Experiment 4. The beta cells were found generally packed by considerable amounts of granules and without any signs of hydropic degeneration. Alpha granules were seen in moderate amount in general. Glycogen disappeared almost completely from islet cells. This finding may indicate that accelerating suppressed function of cells during the hibernation by means of keeping the animals warm is more effective to vanish the hydropic degeneration than the administration of large doses of insulin. The low temperatur of animals induced by cold climate may presumably play an important roll in producing the so-called hydropic degeneration in islet cells during hibernation.
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