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REVIEW

Islet Inflammation Impairs the Pancreatic β-Cell in Type 2 Diabetes

Marc Y. Donath, Marianne Böni-Schnetzler, Helga Ellingsgaard and Jan A. Ehses

Division of Endocrinology, Diabetes, and Nutrition, and Center for Integrated Human Physiology, University Hospital of Zürich, Zürich, Switzerland marc.donath{at}usz.ch

Onset of Type 2 diabetes occurs when the pancreatic β-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, β-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 β-cell mass and the impaired insulin secretion observed in patients with Type 2 diabetes.