Islet inflammation in type 2 diabetes: from metabolic stress to therapy

Diabetes Care. 2008 Feb:31 Suppl 2:S161-4. doi: 10.2337/dc08-s243.

Abstract

Decreases in both mass and secretory function of insulin-producing beta-cells contribute to the pathophysiology of type 2 diabetes. The histology of islets from patients with type 2 diabetes displays an inflammatory process characterized by the presence of cytokines, apoptotic cells, immune cell infiltration, amyloid deposits, and eventually fibrosis. This inflammatory process is probably the combined consequence of dyslipidemia, hyperglycemia, and increased circulating adipokines. Therefore, modulation of intra-islet inflammatory mediators, in particular interleukin-1 beta, appears as a promising therapeutic approach.

Publication types

  • Review

MeSH terms

  • Cytokines / physiology
  • Diabetes Mellitus, Type 2 / complications*
  • Diabetes Mellitus, Type 2 / drug therapy
  • Diabetes Mellitus, Type 2 / metabolism
  • Diabetes Mellitus, Type 2 / physiopathology*
  • Dyslipidemias / etiology
  • Glucose / pharmacology
  • Humans
  • Hypoglycemic Agents / therapeutic use
  • Inflammation / chemically induced
  • Inflammation / epidemiology
  • Inflammation / physiopathology*
  • Insulin-Secreting Cells / drug effects
  • Insulin-Secreting Cells / pathology
  • Insulin-Secreting Cells / physiology
  • Interleukin-1beta / physiology
  • Islets of Langerhans / immunology
  • Leptin / blood
  • Obesity / epidemiology
  • Pancreatic Diseases / physiopathology*

Substances

  • Cytokines
  • Hypoglycemic Agents
  • Interleukin-1beta
  • Leptin
  • Glucose