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Abstract: Several studies have shown that β cell possesses a limited potential for regeneration upon cellular toxicity and tissue injury. One of the difficulties in studying β-cell regeneration has been the lack of an animal model system that allow β-cell loss and subsequent proliferation. Here we examined the regenerative and/or proliferative capacity of β cells by severely destroying β cells and by restoring hyperglycemia in streptozotocin (STZ)-induced diabetic model. Animals were made diabetic by a single intraperitoneally injection of high dose of STZ, and blood glucose level was kept in normal range with twice-daily insulin detemir (long-acting human insulin analog) or islet transplantation for 10 weeks. In insulin detemir-treated mice, hyperglycemia was reversed and glycemic control was successful, but no β-cell increase or new formation was detected. In contrast, in islet transplanted mice, β cells and islets increased, and islet structure was greatly recovered. This recover involved both increased neogenesis and replication. Our results suggest that the effect of insulin detemir on the pancreatic β cell was very different from islet transplantation, and that islet transplantation could be a trigger for the induction of new formation and replication.
Key words: Islet transplantation, islet regeneration, insulin detemir
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