1. Quantitative study of insular tissue has revealed that the number of B cells is greatly diminished in Patients with acute juvenile diabetes from the time of clinical onset of the disease. The number of these cells is as a rule less than 10 per cent of normal. Such B cells as are still present show the cytological signs of marked activity.

2. The normal or supranormal insular activity that is usually found in juvenile diabetics in this stage of the disease cannot therefore be due to the presence of a normal insular tissue, but is produced by a small number of hyperactive B cells.

3. On the basis of histological findings (presence of islets of large size, signs of new islet formation), it may be assumed that during the preclinical phase of juvenile diabetes, an extrapancreatic factor has exerted a strong stimulant action on the insular tissue. In the long run this must lead to exhaustion of the islet-forming capacity on the pancreatic parenchyma and to a decrease in the number of the B cells. By the time the disease becomes clinically manifest only the latter stage of this process can be observed and the majority of islets consist of A cells or of atrophic tissue devoid of B cells.

4. Peri- and intra-insular inflaminatory infiltrates have been found in 68 per cent of those patients with juvenile diabetes who died soon after the clinical onset of their disease. In other words, and contrary to the generally held view, this lesion is not uncommon. It is specific for diabetes and has never been observed in the chronic cases

5. In patients with chronic juvenile diabetes, the B cells are completely absent, except in occasional cases. The islets consist of small, atrophic cells.

6. A valid assessment of the functional capacity of insular tissue can only be achieved if as much use as pos sible is made of quantitative technics and of cytological examination