Recovery of pancreatic beta cells in response to long-term normoglycemia after pancreas or islet transplantation in severely streptozotocin diabetic adult rats

A Jörns, J Klempnauer, M Tiedge, S Lenzen
Pancreas 2001, 23 (2): 186-96
In the well-established, high-dose streptozotocin diabetic rat model, it is unknown whether normoglycemia after pancreas or islet transplantation may induce the expression of the glucose recognition structures and stimulate the replication of the few surviving pancreatic beta cells. Therefore, the endocrine pancreatic tissue was examined immunocytochemically in streptozotocin-treated major histocompatibility complex congenic Lewis rats at 10 and 100 days after transplantation of whole pancreata or isolated islets implanted under the kidney capsule. In the diabetic state the pancreatic beta cells displayed a weak immunostaining for insulin and glucokinase together with a lack of GLUT2 glucose transporter immunoreactivity in the plasma membrane. Ten days after transplantation, the surviving beta cells had regained their normal immunostaining for insulin and for the glucose recognition structures glucokinase and the A single high dose of streptozotocin causes severe experimental insulin-dependent diabetes mellitus in adult rats due to a selective destruction of the pancreatic beta cells in the islets of Langerhans. At doses between 50 and 60 mg/kg of body weight, only very few beta cells survive in the pancreas (1-3). The diabetic state is irreversible and insulin-dependent, thus representing an experimental animal model for type I diabetes (2). Because of the prevailing hyperglycemia, even the few residual beta cells in the pancreas do not function properly and therefore cannot contribute even to a basal supply of insulin to the organism (4). Pancreatic beta cells can function properly in a diabetic organism apparently only after restitution of normoglycemia (5). GLUT2 glucose transporter. One hundred days after transplantation, both of whole pancreas or isolated islets, the number of surviving beta cells in islets of the pancreata of the recipient animals had increased by two- to threefold. The regenerated beta cells were surrounded by a rim of other endocrine cells. The increase in the number of beta cells was not accompanied by signs of neogenesis from ductal structures in the pancreata. The authors' observations support the concept that strict long-term maintenance of normoglycemia through adequate supply of insulin from endocrine grafts is the ideal prerequisite for beta-cell recovery and restitution of the glucose recognition structures, as well as replication of beta cells in pancreata with end-stage diabetic beta-cell destruction after high-dose streptozotocin treatment.

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