• inflammation;
  • insulin;
  • interleukin;
  • apoptosis

Islets of patients with type 2 diabetes have the feature of an inflammatory process reflected by the presence of cytokines, immune cells, β-cell apoptosis, amyloid deposits and fibrosis. Indeed, β-cells from patients with type 2 diabetes display inflammatory markers, including increased interleukin (IL)-1β expression. Furthermore, increased islet-associated macrophages are observed in human type 2 diabetic patients and in most animal models of diabetes. Importantly, increased numbers of macrophages are detectable very early in high fat–fed mice islets, before the onset of diabetes. These immune cells are most likely attracted by islet-derived chemokines, produced in response to metabolic stress, and under the control of IL-1β. It follows that modulation of intra-islet inflammatory mediators, in particular IL-1β, may prevent insulitis in type 2 diabetes and therefore presents itself as a possible causal therapy with disease-modifying potential.