Figure 3.

Pancreatic islets are protected from STZ-induced B cell loss in PARP −/− mice. In wild-type and PARP +/− mice, pancreatic islets were small and distorted 6 weeks after a single i.p. injection of 200 mg/kg of STZ, as judged by staining with hematoxylin/eosin staining. Immunohistochemistry for insulin demonstrated that the majority of islet atrophy was caused by a marked loss of B cells. Glucagon immunoreactive cells appeared relatively spared but were no longer arranged peripherally in the islet. In contrast, islets from PARP −/− mice showed no evidence of atrophy (as judged by hematoxylin/eosin staining), B cell loss (as judged by insulin staining), or altered cellular arrangement (as judged by normal glucagon staining), and were histologically similar to vehicle treated PARP +/+ mice. The number and distribution of insulin and glucagon immunoreactive cells were also similar to those from islets from untreated controls. Results are representative of two trials with at least 5 mice per group.