Streptozotocin, which produces diabetes mellitus in experimental animals, has been reported to reduce the level of NAD in pancreatic isletsand to inhibit islet synthesis of proinsulin.Streptozotocin can induce pancreatic insulitis, which is a new model of diabetes mellitus.
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Streptozotocin and alloxan induce DNA strand breaks and poly(ADP-ribose) synthetase in pancreatic islets.[Pubmed: 6272129
Streptozotocin, which produces diabetes mellitus in experimental animals, has been reported to reduce the level of NAD in pancreatic isletsand to inhibit islet synthesis of proinsulin. The decrease in NAD is due to increased NAD degradation mediated by islet nuclear poly(ADP-ribose) synthetase. Evidence suggests that poly(ADP-ribose) synthetase is activated when DNA is fragmented.
METHODS AND RESULTS:
Here we describe that both Streptozotocin and alloxan, which also produces experimental diabetes mellitus, cause DNA strand breaks which stimulate nuclear poly(ADP-ribose) synthetase, thereby depleting intracellular NAD and inhibiting proinsulin synthesis in isolated pancreatic islets of rats.
Science, 1976, 193(4251):415-7.
Streptozotocin-induced pancreatic insulitis: new model of diabetes mellitus.[Pubmed: 180605
METHODS AND RESULTS:
Multiple small injections of Streptozotocin in mice produce pancreatic insulitis, with progression to nearly complete beta cell destruction and diabetes mellitus.
The timing and appearance of the inflammatory islet lesions suggest but do not prove that Streptozotocin acts by initiating a cell-mediated immune reaction.
Ultrastructural evidence of abundant type C viruses within beta cells of treated mice suggests that Streptozotocin may activate murine leukemia virus in vivo in susceptible hosts.