Islet inflammation impairs the pancreatic beta-cell in type 2 diabetes.
Onset of Type 2 diabetes occurs when the pancreatic beta-cell fails to adapt to the increased insulin demand caused by insulin resistance. Morphological and therapeutic intervention studies have uncovered an inflammatory process in islets of patients with Type 2 diabetes characterized by the presence of cytokines, immune cells, beta-cell apoptosis, amyloid deposits, and fibrosis. This insulitis is due to a pathological activation of the innate immune system by metabolic stress and governed by IL-1 signaling. We propose that this insulitis contributes to the decrease in beta-cell mass and the impaired insulin secretion observed in patients with Type 2 diabetes.
Donath
Marc Y
MY
Division of Endocrinology, Diabetes, and Nutrition, and Center for Integrated Human Physiology, University Hospital of Zürich, Zürich, Switzerland. marc.donath@usz.ch
Böni-Schnetzler
Marianne
M
Ellingsgaard
Helga
H
Ehses
Jan A
JA
D000818:Animals; D016207:Cytokines / Q000276:immunology; D003924:Diabetes Mellitus, Type 2 / Q000276:immunology / Q000473:pathology*; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D007333:Insulin Resistance / Q000276:immunology; D050417:Insulin-Secreting Cells / Q000276:immunology / Q000473:pathology*
D016207:Cytokines