Abstract
The prospective mechanisms by which the transplanted islet mass may satisfy an increased demand for its specific products must be, as in the pancreas in situ the hypertrophy or the increase of the synthetic and secretion mechanisms of the islet cells, their replication or their eventual regeneration from ductal precursors1–4. The endocrine cells, particularly the engrafted B-cells, when stressed evolve to exhaustion specially in the case of a critical islet mass engrafted5–8. A wave of islet cell replication may go on9, 10 and we know that the engrafted islet cell mass can duplicate in two weeks11, but the potential of that mechanism is obviously limited1, so its efficacy for the stabilization of the metabolic state is largely dependent on the islet mass engrafted7, 8. A nesidioblastic process from “precursor” ductal cells is a common finding with the cultured and engrafted fetal and neonatal pancreases12, 13 and the neogenesis of B-cells from adult ductal cells has been recently reported14 Culture experiments, histochemical and ultrastructural studies conjugated with the molecular biology15 may be the best methods for the study of the global characteristics of the morphogenetic mechanisms of the pancreatic regenerative process, of its promoters, for identifying the nature of the “precursor cells” and for the characterization of transition cells of the acinar and islet differentiation. The purpose of this work is to present preliminar evidence that the neogenesis of islet cells is a complementary mechanism for the growth of the engrafted adult islet tissue.
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Madureira, M.L.C. (1997). Islet Growth After Pancreatic Fragments Autotransplantation into the Dog’s Spleen. In: Soria, B. (eds) Physiology and Pathophysiology of the Islets of Langerhans. Advances in Experimental Medicine and Biology, vol 426. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1819-2_56
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DOI: https://doi.org/10.1007/978-1-4899-1819-2_56
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