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Physiology (Bethesda). 2009 Dec;24:325-31. doi: 10.1152/physiol.00032.2009.

Islet inflammation impairs the pancreatic beta-cell in type 2 diabetes.

Author information

1
Division of Endocrinology, Diabetes, and Nutrition, and Center for Integrated Human Physiology, University Hospital of Zürich, Zürich, Switzerland. marc.donath@usz.ch

Abstract

Onset of Type 2 diabetes occurs when the pancreatic beta-cell fails to adapt to the increased insulin demand caused by insulin resistance. Morphological and therapeutic intervention studies have uncovered an inflammatory process in islets of patients with Type 2 diabetes characterized by the presence of cytokines, immune cells, beta-cell apoptosis, amyloid deposits, and fibrosis. This insulitis is due to a pathological activation of the innate immune system by metabolic stress and governed by IL-1 signaling. We propose that this insulitis contributes to the decrease in beta-cell mass and the impaired insulin secretion observed in patients with Type 2 diabetes.

PMID:
19996363
DOI:
10.1152/physiol.00032.2009
[Indexed for MEDLINE]
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