Islet pathology and the pathogenesis of type 1 and type 2 diabetes mellitus revisited

Surv Synth Pathol Res. 1985;4(2):110-25. doi: 10.1159/000156969.


The present review draws attention to the diversity of islet lesions seen in human type 1 and type 2 diabetes. This heterogeneity of islet changes is best demonstrated by immunocytochemistry. In type 1 diabetes the endocrine pancreas is characterized by selective loss of B cells, which most likely results from a slowly acting autoimmune process depending on the presence of both genetic and environmental factors. The process starts years before overt diabetes develops and manifests when the B-cell volume is reduced by about 80%. In type 2 diabetes B cells are always present, regardless of the duration and severity of the disease, but lack any signs of functional activity. This reflects a secretory defect of the B cells which obviously becomes evident under the conditions of obesity, hyperinsulinism and insulin resistance. Obese but non-diabetic subjects show, in parallel to their hyperinsulinism, an increased B cell volume, suggesting that under prediabetic conditions the B cells have still the capacity to respond to increased functional demands by enhanced proliferation. In manifest diabetes the B cells have lost their proliferative potential. Whether this is due to an inherent defect or the consequence of a functional disturbance, is not clear. The development of islet amyloidosis most likely represents an associated functional abnormality of the B cell.

Publication types

  • Review

MeSH terms

  • Autoimmune Diseases / etiology
  • Autoimmune Diseases / genetics
  • Autoimmune Diseases / pathology
  • Diabetes Mellitus, Type 1 / etiology
  • Diabetes Mellitus, Type 1 / immunology
  • Diabetes Mellitus, Type 1 / pathology*
  • Diabetes Mellitus, Type 2 / etiology
  • Diabetes Mellitus, Type 2 / immunology
  • Diabetes Mellitus, Type 2 / pathology*
  • Glucagon / metabolism
  • Humans
  • Insulin / metabolism
  • Islets of Langerhans / pathology*


  • Insulin
  • Glucagon