Prediabetes pp 269-274 | Cite as

Prediabetes and the Pathological Lesions of the Pancreas

  • J. J. Hoet
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 246)


In the insulin dependent diabetes (Type I) a specific histological lesion has been described by W. Gepts (1). The lymphocytic infiltration in the islet of Langerhans, known as insulitis, is associated with a progressive disappearance of the Beta cells. Electron microscopy studies in men and animals indicate that an early phase consists of the invasion of the islets by macrophages and a concommitant disruption of the plasma membrane specifically of the Beta cells. At a later stage, lymphocytic infiltration is observed possibly accompanied by polinnorphonuclear leucocytes and histiocytes. The progressive destruction of Beta cells is associated in some pancreas with occasional signs of Beta cell regeneration. The impending infiltration disappears when the Beta cells have vanished. The regeneration of the Beta cells seems not to be able to cope with their destruction (2).


Beta Cell Lymphocytic Infiltration Beta Cell Mass Islet Cell Antibody Discordant Pair 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Gepts, W., 1965, Pathological anatomy of the pancreas in juvenile diabetes mellitus. Diabetes 14: 619–633.PubMedGoogle Scholar
  2. 2.
    Hoet, J.J., Reusens-Billen, B., and Remade, C., 1987, Lessons from the pathology of the diabetic pancreas. Horm Metab Res 19: 523–525.PubMedCrossRefGoogle Scholar
  3. 3.
    Betterle, C., Presotto, F., Pedini, B., Moro, L., Slack, R.S., Zanette, F., Zanchetta, R., 1987, Islet cell and insulin autoantibodies in organspecific autoimmune patients. Their behaviour and predictive value for the development of Type I (insulin dependent) diabetes mellitus. A 10- year follow-up study. Diabetologia 30: 292–297.PubMedCrossRefGoogle Scholar
  4. 4.
    Westermark, P., Wilander, E., Westermark, G.T., Johnson, K.H., 1987, Islet amyloid polypeptide-like immunoreactivity in the islet B cells of Type II (non-insulin-dependent) diabetic and non-diabetic individuals. Diabetologia 30: 887–892.PubMedGoogle Scholar
  5. 5.
    Clark, A., Copper, G.J.S., Lewis, C.E., Morris, J.F., Willis, A.C., Reid, K.B.M., Turner, R.C., 1987, Islet amyloid formed from diabetes- associated peptide may be pathogenic in Type II diabetes. The Lancet, August 1st Issue: 231–234.Google Scholar
  6. 6.
    Hoet, J. J., and Remade, C., 1987, Pancreatic Islets, Organization of the pancreatic Islets with Special References to Diabetes, Endocrinology 1987, Eds. L. J. DeGroot et al., Grune & Stratton, New York, San Francisco and London.Google Scholar

Copyright information

© Plenum Press, New York 1988

Authors and Affiliations

  • J. J. Hoet
    • 1
  1. 1.Faculty of MedicineUniversity of LouvainBrusselsBelgium

Personalised recommendations