Evidence for Residual and Partly Reparable Insulin Secretory Function and Maintained β-Cell Gene Expression in Islets From Patients With Type 1 Diabetes

摘要

It is commonly accepted that type 1 diabetes (T1D) is an autoimmune and inflammatory disease that results from the wholesale yet surprisingly selective killing of the insulin-secreting β-cells of pancreatic islets (1-4). While the relative importance of reduced β-cell function versus reduced β-cell mass is currently debated in type 2 diabetes (5), T1D has been considered the classic example where diabetes results from reduced β-cell mass secondary to autoimmune attack (1,3,4,6). However, this view has recently been challenged (2,6-9).