ADULT PANCREATIC TISSUE FATE AFTER PANCREATIC FRAGMENT AUTOTRANSPLANTATION INTO THE SPLEEN OF THE PANCREATECTOMIZED DOG

As far as we know, after adult enzyme-digested pancreatic fragment autotransplantation, the fate of the inoculated pancreatic tissue has never been reported and the hypothetic engrafted islet mass growth by mitotic division or by a true islet neogenesis from ductular precursor cells has never been demonstrated. In dogs with total or near-total (90%) pancreatectomy that preserves the duodenum and the common bile duct, morphologic study of the pancreatic tissue inoculated into the spleen has demonstrated an exuberant ductular-acinar-islet regenerative process, with progressive cystic degeneration of the newly formed ductular-acinar structures occurring simultaneously with the selective survival and growing predominance of extraductal tissue scattered as distinct islets, clusters of islet cells, or single islet cells. In addition to the B, A(2), and D cell types of the normal adult dog islet, we have also seen a peculiar ultrastructural pleomorphism of the insular B cells, frequently combined with their ductular or glandular arrangement in maturing islets. Rare or never before reported islet cell types in the adult dog's islets (G cells, mixed endocrine cells of the A(2)-D, D-B, and A(2)-B types, and mixed acinar-islet cells of the D-acinar type) were also putatively identified. Using light microscopy we have identified many mitotic figures on ductular and centroacinar cells in ductules and ductular-acinar structures. Moreover, we have ultrastructurally characterized a pluriendocrine nesidioblastic process identified in the most common islet cell types (B, A(2), D) and in G cells and mixed acinar islet cells of the B-ac, A(2)-ac, D-ac, F-ac, and G-ac types as well as ''intermediary'' or ''transitional'' cells of incipient ductular-acinar, ductular-islet, and ductular-acinar-islet differentiation. The characteristics of the extraductal islet tissue and the exuberant nesidioblastic process have demonstrated neogenesis of islets and islet cells from precursor ductular cells at several points after the autotransplant, and we suggest that this mechanism may be of fundamental importance for the engrafted islet mass growth-keeping in mind the age of the pancreatic tissue donors and the life-span of the juvenile diabetic recipient receiving the transplant. This evolution has taken place simultaneously with the progressive rarefaction of the regenerated ductular-acinar structures definitively deprived of an intestinal drainage route by virtue of their heterotopic location.