Fibrotic pancreas was caused by ligation of the pancreatic ducts in mongrel dogs. Four weeks later, reconstruction of the pancreatic duct and major pancreatic resection were performed. Changes of carbohydrate metabolism and functional and morphological changes of islet cells in the remnant pancreas were investigated. 1) Immediately after resection of more than 84% of the fibrotic pancreas, diabetes developed, and insulin and glucagon secretion decreased, accompanied with marked degeneration of B, A and D cells in the islets. 2) During the early periods after 63 to 84% pancreatectomy, secretion of both insulin and glucagon decreased, and then showed a tendency to recover, but later the secretion gradually decreased again and so-called Sandmeyer's diabetes developed. The size of the islets and the number of B cells decreased, but the rate of A and D cells in the islets increased relatively in the remnant pancreas. 3) After resection of less than 63% of the fibrotic pancreas, secretion of both insulin and glucagon decreased temporarily with subsequent recovery. Diabetes did not develop. There were no marked morphological changes in the islets, nor significant changes in the distribution of B, A and D cells of the islets in the remnant pancreas. Diabetes developed after resection of more than 63% of the fibrotic pancreas 4 weeks after ligation of the pancreatic duct, while it developed after resection of more than 74% of the normal pancreas in dogs. Therefore, with regard to carbohydrate metabolism, resectability of the fibrotic pancreas was about 10% less than that of the normal pancreas in dogs.