Conflict of interest: The authors declare no conflict of interest.
Insulitis in type 2 diabetes
Article first published online: 2 OCT 2008
© 2008 The Authors Journal Compilation © 2008 Blackwell Publishing Ltd
Diabetes, Obesity and Metabolism
Volume 10, Issue Supplement s4, pages 201–204, November 2008
How to Cite
Böni-Schnetzler, M., Ehses, J. A., Faulenbach, M. and Donath, M. Y. (2008), Insulitis in type 2 diabetes. Diabetes, Obesity and Metabolism, 10: 201–204. doi: 10.1111/j.1463-1326.2008.00950.x
- Issue published online: 2 OCT 2008
- Article first published online: 2 OCT 2008
- Received 7 March 2008; accepted 13 May 2008
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.