Insulitis in type 2 diabetes

Diabetes Obes Metab. 2008 Nov;10 Suppl 4:201-4. doi: 10.1111/j.1463-1326.2008.00950.x.

Abstract

Islets of patients with type 2 diabetes have the feature of an inflammatory process reflected by the presence of cytokines, immune cells, beta-cell apoptosis, amyloid deposits and fibrosis. Indeed, beta-cells from patients with type 2 diabetes display inflammatory markers, including increased interleukin (IL)-1 beta 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-1 beta. It follows that modulation of intra-islet inflammatory mediators, in particular IL-1 beta, may prevent insulitis in type 2 diabetes and therefore presents itself as a possible causal therapy with disease-modifying potential.

MeSH terms

  • Animals
  • Apoptosis / physiology
  • Diabetes Mellitus, Type 2 / immunology*
  • Diabetes Mellitus, Type 2 / metabolism
  • Female
  • Glucagon / biosynthesis
  • Humans
  • Immunohistochemistry
  • Insulin / biosynthesis
  • Insulin / immunology*
  • Interleukin-1beta / immunology*
  • Interleukin-1beta / metabolism
  • Islets of Langerhans / immunology*
  • Islets of Langerhans / metabolism
  • Male
  • Mice
  • Rats

Substances

  • Insulin
  • Interleukin-1beta
  • Glucagon