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 ß-cell hyper-proliferation. Also, amelioration of the diabetic phenotype on introgression of Wdr13-null (Wdr13-/0) mutation in genetically diabetic mice (Leprdb/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 ß-cells; reiterating the finding that absence of WDR13 helps in ß-cell hyper-proliferation and recovery from diabetes; further underscoring WDR13 as a key target molecule for diabetes treatment/amelioration.