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lüll Pancreatic beta-cell death, regeneration and insulin secretion: roles of poly(ADP-ribose) polymerase and cyclic ADP-ribose Takasawa S; Okamoto HInt J Exp Diabetes Res 2002[Apr]; 3 (2): 79-96In the early 1980s, we proposed a unifying model for beta-cell damage (The OKAMOTO model), in which poly(ADP-ribose) synthetase/polymerase (PARP) activation plays an essential role in the consumption of NAD+, which leads to energy depletion and necrotic cell death. In 1984, we demonstrated that the administration of PARP inhibitors to 90% depancreatized rats induces islet regeneration. From the regenerating islet-derived cDNA library we isolated Reg (Regenerating Gene) and demonstrated that Reg protein induces beta-cell replication via the Reg receptor and ameliorates experimental diabetes. More recently, we showed that the combined addition of IL-6 and dexamethasone induces the Reg gene expression in beta-cells and that PARP inhibitors enhance the expression. In 1993, we found that cyclic ADP-ribose (cADPR), a product synthesized from NAD+, is a second messenger for intracellular Ca2+ mobilization for insulin secretion by glucose, and proposed a novel mechanism of insulin secretion, the CD38-cADPR signal system. Therefore, PARP inhibitors prevent beta-cell necrosis, induce beta-cell replication and maintain insulin secretion.|Animals[MESH]|Cell Death[MESH]|Cyclic ADP-Ribose/*metabolism[MESH]|Humans[MESH]|Insulin Secretion[MESH]|Insulin/*metabolism[MESH]|Islets of Langerhans/*cytology/enzymology/*physiology[MESH]|Poly(ADP-ribose) Polymerases/*metabolism[MESH]|Regeneration/*physiology[MESH] |