Header

UZH-Logo

Maintenance Infos

Insulitis in type 2 diabetes


Böni-Schnetzler, M; Ehses, J A; Faulenbach, M; Donath, M Y (2008). Insulitis in type 2 diabetes. Diabetes, Obesity and Metabolism, 10(Suppl.):201-204.

Abstract

Islets of patients with type 2 diabetes have the feature of an inflammatory process reflected by the presence of cytokines, immune cells, beta-cell apoptosis, amyloid deposits and fibrosis. Indeed, beta-cells from patients with type 2 diabetes display inflammatory markers, including increased interleukin (IL)-1 beta 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 most likely attracted by islet-derived chemokines, produced in response to metabolic stress, and under the control of IL-1 beta. It follows that modulation of intra-islet inflammatory mediators, in particular IL-1 beta, may prevent insulitis in type 2 diabetes and therefore presents itself as a possible causal therapy with disease-modifying potential.

Abstract

Islets of patients with type 2 diabetes have the feature of an inflammatory process reflected by the presence of cytokines, immune cells, beta-cell apoptosis, amyloid deposits and fibrosis. Indeed, beta-cells from patients with type 2 diabetes display inflammatory markers, including increased interleukin (IL)-1 beta 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 most likely attracted by islet-derived chemokines, produced in response to metabolic stress, and under the control of IL-1 beta. It follows that modulation of intra-islet inflammatory mediators, in particular IL-1 beta, may prevent insulitis in type 2 diabetes and therefore presents itself as a possible causal therapy with disease-modifying potential.

Statistics

Citations

24 citations in Web of Science®
24 citations in Scopus®
Google Scholar™

Altmetrics

Downloads

5 downloads since deposited on 16 Dec 2008
0 downloads since 12 months
Detailed statistics

Additional indexing

Item Type:Journal Article, refereed, original work
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:10 November 2008
Deposited On:16 Dec 2008 11:26
Last Modified:05 Apr 2016 12:40
Publisher:Wiley-Blackwell
ISSN:1462-8902
Additional Information:The definitive version is available at www.blackwell-synergy.com
Publisher DOI:https://doi.org/10.1111/j.1463-1326.2008.00950.x
PubMed ID:18834448

Download

Preview Icon on Download
Filetype: PDF - Registered users only
Size: 1MB
View at publisher

TrendTerms

TrendTerms displays relevant terms of the abstract of this publication and related documents on a map. The terms and their relations were extracted from ZORA using word statistics. Their timelines are taken from ZORA as well. The bubble size of a term is proportional to the number of documents where the term occurs. Red, orange, yellow and green colors are used for terms that occur in the current document; red indicates high interlinkedness of a term with other terms, orange, yellow and green decreasing interlinkedness. Blue is used for terms that have a relation with the terms in this document, but occur in other documents.
You can navigate and zoom the map. Mouse-hovering a term displays its timeline, clicking it yields the associated documents.

Author Collaborations