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Exp Clin Endocrinol Diabetes 1987; 89(3): 242-250
DOI: 10.1055/s-0029-1210646
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© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Neuroendocrine Background of the Pathology of the Islets of Langerhans

A Minireview with Particular Reference to Synaptophysin and Chromogranin A as Neuroendocrine Markers and to the Ontogeny of Argyrophil Insulin Immunoreactive Cells in the RabbitM. Titlbach, G. Chejfec, L. Grimelius, S. Falkmer
  • Institute of Experimental Medicine, Czechoslovak Academy of Sciences, Prague/Czechoslovakia; Division of Endocrine Pathology at the Department of Pathologyof the University of Uppsala, Uppsala, and Department of Tumour Pathology, Karolinska Institute, Karolinska Hospital, Stockholm/Sweden
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Publication History

1986

Publication Date:
16 July 2009 (online)

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Summary

As in diseases of other (neuro)endocrine glands, the pathology of the islets of Langerhans comprises both states of hypofunction, notably hypoinsulinism, — diabetes mellitus — and those of hyperfunction, such as hyperinsulinism from either nesidiodysplasia (“nesidioblastosis”) or genuine islet-cell neoplasms. The pathogenesis of some characteristic structural lesions of these diseases of the islet parenchymal cells is reviewed against their neuroendocrine background, both phylogenetically and ontogenetically. A preliminary report is given of the appearance of argyrophil insulin cells during the normal foetal development of the islet parenchyma of the rabbit. In addition, the distribution of the newly discovered neuroendocrine markers synaptophysin and chromogranin A has been reviewed immunohistochemically in normal and neoplastic islet parenchyma cells; the insulin cells do not seem to contain chromogranin A.

Key words

Islet of Langerhans - Phylogeny - Ontogeny - Argyrophilia - B-cell - Synaptophysin - Chromogranin A - Nesidioblastosis - Neuro-endocrine system

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