It has been suggested, since many years, that endocrine function of the pancreas may be related to the peptic ulceration of the stomach. There has been, however, no unanimous opinion on this item. To clarify this problem, the author investigated, from several points of view, the changes in gastric mucosa following administration of NPH-Insulin to the rat. By the intramuscular administration of NPH-Insulin hemorrhagic erosion of the gastric mucosa, instead of ulceration, was observed especially on the corpus of the glandular stomach. The occurrence of erosion was related to the severity of hypoglycemia produced by the Insulin and the rats showing erosion of the gastric mucosa were always associated with hypoglycemic shock. In the rats with gastric erosion weight of their adrenal glands was increased, concentration of K in sera was decreased, and concentration of Na in sera was increased. The occurrence of erosion in the gastric mucosa following administration of NPH-Insulin was completely hindered by vagotomy and was slightly depressed by administration of Chlorpromazin and of Dietazin. In the adrenaletomized rat, the erosion was more marked even after administration of small dosis of NPH-Insulin, and was not hindered by vagotomy. Gastric secretory function in rat with erosion of the gastric mucosa was depressed by administration of the Insulin. In the histological study of the stomach, contraction of the arteries in the submucosa, dilatation and stagnation of the veins in the submucosa and the mucosa were observed. The erosion did not develop to chronic ulcer even after repeated administration of the Insulin. It was, therefore, confirmed that circulatory disturbance in the gabtric mucosa caused by vascular change which was produced by means of vagal stimulation played a main role on the occurrence of erosion in the administration of the Insulin, and was also surmized that the reduced resistance of the gastric mucosa caused by hypoglycemia promoted formation of erosion.