Diabetes Care
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Diabetes Care 31:S161-S164, 2008
DOI: 10.2337/dc08-s243
© 2008 by the American Diabetes Association
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Section I: Diabetes-What Is New in the Management and Understanding of the Disease?
Original Article

Islet Inflammation in Type 2 Diabetes

From metabolic stress to therapy

Marc Y. Donath, MD, Desiree M. Schumann, PHD, Mirjam Faulenbach, MD, Helga Ellingsgaard, PHD, Aurel Perren, MD and Jan A. Ehses, PHD

From the Clinic of Endocrinology and Diabetes, Department of Pathology, University Hospital Zurich, Zurich, Switzerland

Address correspondence and reprint requests to Marc Y. Donath, MD, Clinic of Endocrinology and Diabetes, Department of Medicine, University Hospital, CH-8091 Zurich, Switzerland. E-mail: marc.donath{at}usz.ch

Decreases in both mass and secretory function of insulin-producing β-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-1β, appears as a promising therapeutic approach.

Abbreviations: IL, interleukin • KATP channel, ATP-sensitive K+ channel


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