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
Abstract
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.
Footnotes
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M.Y.D. is listed as the inventor on a patent (WO6709) filed in 2003 for the use of an interleukin-1 receptor antagonist for the treatment of or prophylaxis against type 2 diabetes. The patent is owned by the University of Zurich, and M.Y.D. has no financial interest in the patent. No other potential conflict of interest relevant to this article was reported.
This article is based on a presentation at the 1st World Congress of Controversies in Diabetes, Obesity and Hypertension (CODHy). The Congress and the publication of this article were made possible by unrestricted educational grants from MSD, Roche, sanofi-aventis, Novo Nordisk, Medtronic, LifeScan, World Wide, Eli Lilly, Keryx, Abbott, Novartis, Pfizer, Generx Biotechnology, Schering, and Johnson & Johnson.
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