Induction of Islet Cell Proliferation and the Proteins Associated with Islet Reorganization in the Diabetic Animal Models

초록

Although, some investigators suggested the regeneration of pancreatic tissue after partial pancreatectomy, it has been accepted that no remarkable regeneration or revitalization of the islet cells has been observed in the diabetic pancreas of the experimental animals, but also in the pancreas of the patients with diabetes. Recently, however, we reported the regeneration of islet cells following a single injection of streptozotocin to the rats with or without insulin treatment (Park et al.). The present study was designed to elucidate the changes on 1) the organization of islet during islet regeneration using the animal models for diabetes, and 2) the molecules being suggested to be associated with development or proliferation of islet cells. We induced islet cell proliferation by single injection of streptozotocin to rats and treated with insulin for 1-14 days. In addition, the pancreatic tissues showing islet proliferation were obtained from the db/db mice. In the streptozotocin treated rats, islet cell death was evident with karyolysis at 12-24 hr after treatment. At 72 hr after streptozotocin treatment, however, the number of islet cell was remarkably increased and the volume of the islets gradually increased. In those islets, the cells showing proliferation were turned out to be -cells, while - and -cells remained quiescent. The proliferating cells expressed clusterin and B/K together with glucagon in the same cells. Double immunolabeling allowed to reveal co-localization of clusterin, B/K and glucagon in the same secretory granules of these cells. Clusterin and B/K were also strongly detected in the proliferated islet cel