Islet Growth After Pancreatic Fragments Autotransplantation into the Dog’s Spleen

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 precursors^1–4. The endocrine cells, particularly the engrafted B-cells, when stressed evolve to exhaustion specially in the case of a critical islet mass engrafted^5–8. A wave of islet cell replication may go on^{9, 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 engrafted^{7, 8}. A nesidioblastic process from “precursor” ductal cells is a common finding with the cultured and engrafted fetal and neonatal pancreases^{12, 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.