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• W2287444830 abstract "In the early 1980s we found that streptozotocin and alloxan, typical diabetogenic agents, induce pancreatic 13-cell DNA strand breaks through the formation of free radicals. The breaks induce DNA repair involving the activation of poly(ADP-ribose) polymerase (PARP), which uses NAD+as a substrate. As a result, the intracellular levels of NAD+fall dramatically. The fall in NAD+inhibits cellular functions including insulin synthesis and secretion, and thus the (3-cell ultimately dies. We subsequently proposed that maintenance of the NAD+level is essential for the synthesis and secretion of insulin, and presented a unifying model for 3-cell damage and its prevention (The Okamoto model), in which PARP activation plays an essential role. Recently, the model was reconfirmed by experiments using PARP knockout mice and has been recognized as providing the basis for necrotic death of various cells and tissues. In 1993, we found that cyclic ADP-ribose (cADPR), a metabolite of NAD+is a second messenger for intracellular Ca’ mobilization for insulin secretion by glucose, and proposed a novel mechanism of insulin secretion, the CD38-cADPR signal system. Recently, various physiological phenomena from animal to plant cells become understandable in terms of this signal system." @default.
• W2287444830 created "2016-06-24" @default.
• W2287444830 creator A5001188770 @default.
• W2287444830 date "2003-01-01" @default.
• W2287444830 modified "2023-09-27" @default.
• W2287444830 title "Recent Advances in Physiological and Pathological Significance of tryptophan-Nad+Metabolites: lessons from insulin-producing pancreatic ß-Cells" @default.
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• W2287444830 doi "https://doi.org/10.1007/978-1-4615-0135-0_28" @default.
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