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Type 1 diabetes mellitus (T1DM) is a chronically progressive autoimmune disease that affects approximately 1% of the population in the developed world. This adverse immune response is induced and promoted by the interaction of both genetic and environmental factors. In contrast, in type 2 diabetes mellitus (T2DM), insulin-resistance coupled with reduced insulin output appears to be the major cause of hyperglycaemia (affecting approximately 6% of the population). Although the aetiology of diabetes may differ from T1DM to T2DM, a common feature associated with both types is the failure of pancreatic β-cells in the islets of Langerhans, thus causing a reduction in insulin secretion, cell mass and ultimately apoptotic death. However, the impact and time-course of pancreatic β-cell death, which may appear very different in T1 and T2DM, may be related through common molecular mechanisms.

The Impact of Inflammation on Pancreatic β-Cell Metabolism, Function and Failure in T1DM and T2DM: Commonalities and Differences