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Islet inflammation in type 2 diabetes: from metabolic stress to therapy


Donath, M Y; Schumann, D M; Faulenbach, M; Ellingsgaard, H; Perren, A; Ehses, J A (2008). Islet inflammation in type 2 diabetes: from metabolic stress to therapy. Diabetes Care, 31 Sup:S161-S164.

Abstract

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.

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.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Endocrinology and Diabetology
Dewey Decimal Classification:610 Medicine & health
Date:2008
Deposited On:05 Jan 2009 11:07
Last Modified:05 Apr 2016 12:40
Publisher:American Diabetes Association
ISSN:0149-5992
Publisher DOI:10.2337/dc08-s243
PubMed ID:18227479
Permanent URL: http://doi.org/10.5167/uzh-7325

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