Selective ablation of P53 in pancreatic beta cells fails to ameliorate glucose metabolism in genetic, dietary and pharmacological models of diabetes mellitus

Background Beta cell dysfunction and death are critical steps in the development of both type 1 2 diabetes (T1D T2D), but underlying mechanisms incompletely understood. Activation essential tumor suppressor transcription factor P53 was linked to beta vitro has been reported several mouse models cells humans with T2D. Therefore, we investigated specific role dysfunction, vivo.