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Diabetes Care. 2008 Feb;31 Suppl 2:S161-4. doi: 10.2337/dc08-s243.

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

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  • 1Clinic of Endocrinology and Diabetes, Department of Medicine, University Hospital, CH-8091 Zurich, Switzerland. marc.donath@usz.ch

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.

PMID:
18227479
DOI:
10.2337/dc08-s243
[PubMed - indexed for MEDLINE]
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