Article

Pancreatic islet inflammation in type 2 diabetes: from alpha and beta cell compensation to dysfunction.

Division of Endocrinology, Diabetes and Nutrition, Center for Integrated Human Physiology, University Hospital of Zürich, 8091 Zürich, Switzerland.
Archives of Physiology and Biochemistry 09/2009; 115(4):240-7. DOI:10.1080/13813450903025879 pp.240-7
Source: PubMed

ABSTRACT Evidence in support of the concept of local pancreatic islet inflammation as a mechanism of beta cell failure in type 2 diabetes is accumulating. Observations in human islets from type 2 diabetic patients and rodent models of the disease indicate the increased presence of IL-1 driven cytokines and chemokines in pancreatic islets, concomitant with immune cell infiltration. Inflammation is the body's protective response to harmful stimuli and tissue damage. However, under chronic stress (e.g. metabolic stress in obesity and type 2 diabetes) the body's own defensive response may become deleterious to tissue function. Here, we summarize the current evidence that islet inflammation is a feature of type 2 diabetes, and discuss its role with respect to alpha and beta cell compensation and eventual beta cell failure.

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Keywords

body's own defensive response
 
body's protective response
 
deleterious
 
harmful stimuli
 
IL-1
 
immune cell infiltration
 
local pancreatic islet inflammation
 
metabolic stress
 
Observations
 
pancreatic islets
 
rodent models
 
tissue damage
 
tissue function
 
type 2 diabetes
 
type 2 diabetic patients