Is β‐cell aging involved in the pathogenesis of diabetes?

Background β‐Cells at different stages have different functions and capacity for proliferation, regenerative and apoptosis. The aim of the present study was to investigate whether there are changes in β‐cell phonotype in the development of diabetes to identify potential β‐cell targets to prevent the progression of diabetes. Methods A cross‐sectional study was performed on pancreatic tissues obtained from 80 patients classified into three groups: 25 with type 2 diabetes ( T2D ), 25 with impaired fasting glucose ( IFG ), and 30 non‐diabetics ( ND ). The ratio of the insulin‐positive area to pancreatic area was used as an indirect marker of β‐cell mass. Insulin‐positive duct cells and scattered β‐cells were defined as newly generated β‐cells, whereas insulin/neurogenin 3 (Ngn3), insulin/v‐maf musculoaponeurotic fibrosarcoma oncogene family, protein A ( MafA ) and insulin/ P16 double‐positive cells were defined as immature, mature, and senescent β‐cells, respectively; Ki67 was used as a marker of cell proliferation, and terminal deoxyribonucleotidyl transferase‐mediated dUTP –digoxigenin nick end‐labeling ( TUNEL ) was used as a marker of cell apoptosis. Data were analyzed using the Kruskal–Wallis test. Results There were no significant differences in β‐cell mass, the prevalence of insulin‐positive duct cells, scattered β‐cells, or insulin/Ngn3, insulin/ MafA , and Insulin/Ki67 double‐positive cells among groups. The incidence of insulin/ P16 double‐positive cells was significantly higher in T2D than ND . β‐Cell apoptosis was significantly higher in T2D and IFG than ND . Conclusion The senescence and apoptosis of β‐cells may be involved in the course of diabetes.