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lüll Pdx1 and other factors that regulate pancreatic beta-cell survival Fujimoto K; Polonsky KSDiabetes Obes Metab 2009[Nov]; 11 Suppl 4 (Suppl 4): 30-7A progressive reduction in beta-cell mass occurs in the evolution of diabetes. Thus understanding the mechanisms responsible for this reduction in beta-cell mass is important for understanding the pathogenesis of diabetes and in developing novel approaches to prevention and treatment. Pancreatic duodenal homeobox 1 (Pdx1) is a transcription factor that plays a central role in pancreatic beta-cell function and survival. Complete deficiency of Pdx1 is associated with pancreatic agenesis, and partial deficiency leads to severe beta-cell dysfunction, and increases beta-cell death and diabetes both in rodent and human. Chronic hyperglycaemia and dyslipidaemia, which are major features of type 2 diabetes, cause beta-cell dysfunction via reduced Pdx1 expression. Inhibition of insulin/insulin-like growth factor (Igf) signalling followed by reduced Pdx1 expression is a common pathway induced by the majority of the mechanisms in apoptotic beta-cells. Although the report so far paid little attention to non-apoptotic beta-cell death (autophagy and necrosis), we expect these are also involved in the pathogenesis of diabetes. The potential role of Pdx1 in non-apoptotic beta-cell death should also be considered in future studies in diabetes, and in attempts to develop novel agents that target this process for prevention and treatment of the disorder.|Animals[MESH]|Apoptosis Regulatory Proteins/deficiency/*metabolism[MESH]|Autophagy[MESH]|Cell Count[MESH]|Cell Survival/physiology[MESH]|Gene Expression Regulation[MESH]|Homeodomain Proteins/*physiology[MESH]|Humans[MESH]|Insulin-Secreting Cells/metabolism/*physiology[MESH]|Mice[MESH]|Trans-Activators/deficiency/*physiology[MESH] |