Islet inflammation in type 2 diabetes: from metabolic stress to therapy.
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.
Donath
Marc Y
MY
Clinic of Endocrinology and Diabetes, Department of Medicine, University Hospital, CH-8091 Zurich, Switzerland. marc.donath@usz.ch
Schumann
Desiree M
DM
Faulenbach
Mirjam
M
Ellingsgaard
Helga
H
Perren
Aurel
A
Ehses
Jan A
JA
D016207:Cytokines / Q000502:physiology; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D050171:Dyslipidemias / Q000209:etiology; D005947:Glucose / Q000494:pharmacology; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007249:Inflammation / Q000139:chemically induced / Q000453:epidemiology / Q000503:physiopathology*; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D053583:Interleukin-1beta / Q000502:physiology; D007515:Islets of Langerhans / Q000276:immunology; D020738:Leptin / Q000097:blood; D009765:Obesity / Q000453:epidemiology; D010182:Pancreatic Diseases / Q000503:physiopathology*
D016207:Cytokines; D007004:Hypoglycemic Agents; D053583:Interleukin-1beta; D020738:Leptin; D005947:Glucose