ISLETS OF LANGERHANS IN JUVENILE DIABETES MELLITUS

Abstract

SUMMARY The number of islets per square centimetre section of post‐mortem pancreas was counted and the intensity of β‐cell granulation (Gomori's aldehyde‐fuchsin stain) assessed in thirteen cases of untreated juvenile diabetes and thirteen matched controls, and in thirteen cases of treated juvenile onset diabetes and thirteen matched controls. The morphology of the islets was studied. In two cases of untreated diabetics the number of islets overlapped with those of the control series. In the remaining eleven, the number was reduced to an average of about one seventh of the controls. β‐Cell granulation was normal in five cases and markedly reduced in the remainder. Eleven of the thirteen treated diabetics showed a similarly marked reduction in number of islets and loss of β‐granulation. In one case the islets showed marked β‐cell hyperplasia with margination of granules. The remaining case showed marked loss of exocrine parenchyma, diffuse fibrosis and crowded surviving islets rich in β‐cells. Nuclear pleomorphism and hypertrophy of some islets was slightly more marked in untreated juveniles, dying within a few weeks of onset of the disease, than in matched controls. There were no examples of lymphocytic infiltration of islets. Pancreatic fibrosis was seen much more commonly and was more marked in the diabetics than in the controls. The average weight of pancreas was reduced to 32 g in the treated diabetics, the expected weight being 68 g. It is suggested that the findings support the hypothesis that juvenile diabetes results from failure of islet cell regeneration in response to injury rather than exhaustion atrophy of overstimulated normal β‐cells, and that this is associated with retardation of growth of the exocrine pancreas.