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Macrophages, cytokines and beta-cell death in Type 2 diabetes


Ehses, J A; Böni-Schnetzler, M; Faulenbach, M; Donath, M Y (2008). Macrophages, cytokines and beta-cell death in Type 2 diabetes. Biochemical Society Transactions, 36(Pt 3):340-342.

Abstract

The pathology of islets from patients with Type 2 diabetes displays an inflammatory process characterized by the presence of immune cell infiltration, cytokines, apoptotic cells, amyloid deposits and, eventually, fibrosis. Indeed, analysis of beta-cells from patients with Type 2 diabetes displays increased IL-1beta (interleukin 1beta) expression. Furthermore, increased islet-associated macrophages are observed in human Type 2 diabetic patients and in most animal models of diabetes. Importantly, increased numbers of macrophages are detectable very early in high-fat-fed mice islets, before the onset of diabetes. These immune cells are probably attracted by islet-derived chemokines, produced in response to metabolic stress, and under the control of IL-1beta. It follows that modulation of intra-islet inflammatory mediators, particularly interleukin-1beta, may prevent islet inflammation in Type 2 diabetes and therefore presents itself as a promising therapeutic approach.

The pathology of islets from patients with Type 2 diabetes displays an inflammatory process characterized by the presence of immune cell infiltration, cytokines, apoptotic cells, amyloid deposits and, eventually, fibrosis. Indeed, analysis of beta-cells from patients with Type 2 diabetes displays increased IL-1beta (interleukin 1beta) expression. Furthermore, increased islet-associated macrophages are observed in human Type 2 diabetic patients and in most animal models of diabetes. Importantly, increased numbers of macrophages are detectable very early in high-fat-fed mice islets, before the onset of diabetes. These immune cells are probably attracted by islet-derived chemokines, produced in response to metabolic stress, and under the control of IL-1beta. It follows that modulation of intra-islet inflammatory mediators, particularly interleukin-1beta, may prevent islet inflammation in Type 2 diabetes and therefore presents itself 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
04 Faculty of Medicine > Center for Integrative Human Physiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2008
Deposited On:16 Dec 2008 13:29
Last Modified:05 Apr 2016 12:42
Publisher:Biochemical Society
ISSN:0300-5127
Publisher DOI:10.1042/BST0360340
PubMed ID:18481953
Permanent URL: http://doi.org/10.5167/uzh-7995

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