LAUSR

The classical definition of type 1 diabetes, of which the pathogenesis lies in the autoimmune destruction of beta cells that eventually leads to complete loss of insulin secretion capacity, is recently being revisited with the emerging concept of endotype to address the heterogeneity of the disease1 . In the Diabetes Control and Complications Trial (DCCT), it was observed that some individuals retained a clinically meaningful C-peptide persistence years after diagnosis of type 1 diabetes; post-mortem studies of pancreas specimens of long-standing type 1 diabetes also revealed insulin-containing beta cells2 .