Abstract
The first successful transplants of islet cells in diabetic patients have been reported recently1–4. However, restoration of normoglycemia is often not achieved or has limited duration. Failure of islets autotransplanted in large animals5 suggests that nonimmunological factors, such as limited growth capacity could play a role in the limited survival of islet transplants in diabetic patients. One of the major problems in human islet transplantation is that a greater quantity of islet tissue is required than had been predicted on the basis of beta cell measurements in diabetes6. The reasons for the need of such a large amount of islet tissue are not known. In addition, a critical islet mass must be transplanted to achieve normoglycemia with continued success being dependent upon the number of initially transplanted islets7–9. An unknown factor in these considerations is the growth capacity of transplanted islets. A limitation in the growth capacity of transplanted islets compared to endogenous pancreatic islets could lead to continuous loss of beta cell mass and failure of the graft. We studied the beta cell replication and mass in short term successful islet tranplants and the capacity of transplanted beta cells to modify their replication and mass in response to changes in metabolic demand.
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© 1997 Springer Science+Business Media New York
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Montaña, E., Bonner-Weir, S., Weir, G.C. (1997). Beta Cell Replication and Mass in Islet Transplantation. 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_55
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DOI: https://doi.org/10.1007/978-1-4899-1819-2_55
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