The course of alloxan diabetes during 19 months was studied in 62 duct‐ligated and 26 sham‐operated female rats. Nine additional rats were used as buffer‐injected sham‐ operated controls. Alloxan was administered 5–6 weeks after duct ligation. The mortality among the alloxan‐treated rats was high and many animals died during ether anaesthesia a t glucose tolerance tests or from late sequelae of alloxan‐induced kidney lesions. In duct‐ligated rats, both the hypoglycaemic phase 4–8 hours after alloxan administration and the subsequent hyperglycaernia during the first 4 days were distinctly marked. After these days during which signs of instability were observed, the fasting blood glucose level in the duct‐ligated rats returned within the normal range after 5 months a t which stage the only 3 surviving sham‐operated controls still were hyperglycaemic. The latter showed, how‐ ever, varying degrees of alloxan‐induced kidney lesions. The pancreas was studied by light microscopy in 29 duct‐ligated and in the 3 surviving sham‐operated alloxan‐diabetic rats. From the first week and onwards, signs of regenerative phenomena of the islet tissue, consisting of large, clear, sparsely granulated cells of the so‐called “agranular” type, were observed in the islets of the alloxan‐treated animals. Furthermore, some evidence was ob‐ tained that the large, sparsely granulated cells had the ability to differentiate into β‐cells. Despite this normalization of the fasting blood glucose level of the alloxan‐diabetic duct‐ligated rats and despite these morphological signs of β‐cell regeneration, no alloxan‐ treated animals showed a complete recovery from their diabetes, as glucose tolerance tests, performed 8 months after alloxan administration, were still of diabetic type. However, histological examination of the pancreas in 2 rats 19 months after alloxan administration were by light microscopy found to present mainly normal islet cells in both the atrophied and the intact parts of the pare