Wdr13 and streptozotocin-induced diabetes

Type I diabetes, though contributes to only 5-10% of total diabetes cases, is a rising concern in today's world. Our previous studies have shown that the absence of WDR13 in mouse results in pancreatic beta-cell hyper-proliferation. Also, amelioration of the diabetic phenotype on introgression of Wdr13-null (Wdr13(-/0)) mutation in genetically diabetic mice (Lepr(db/db)) [type II diabetes] was observed. It was thus, interesting to see the role of WDR13 in streptozotocin-mediated diabetes in mice, a model for type I diabetes. Wdr13(-/0) mice along with its wild type (Wdr13(+/0) mice) littermates were administered streptozotocin intraperitoneally for 5 consecutive days. Blood glucose levels and body weights of these mice were monitored for subsequent 5 weeks and then they were sacrificed for physiological and histological analyses. Results showed that Wdr13(-/0) mice exhibited higher serum insulin levels, better glucose clearance and significantly higher number of proliferating beta-cells; reiterating the finding that absence of WDR13 helps in beta-cell hyper-proliferation and recovery from diabetes; further underscoring WDR13 as a key target molecule for diabetes treatment/amelioration.

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