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An islet in distress: β cell failure in type 2 diabetes

Authors :
Raghavendra G. Mirmira
Takeshi Ogihara
Source :
Journal of Diabetes Investigation
Publication Year :
2010
Publisher :
Wiley, 2010.

Abstract

Over 200 million people worldwide suffer from diabetes, a disorder of glucose homeostasis. The majority of these individuals are diagnosed with type 2 diabetes. It has traditionally been thought that tissue resistance to the action of insulin is the primary defect in type 2 diabetes. However, recent longitudinal and genome‐wide association studies have shown that insulin resistance is more likely to be a precondition, and that the failure of the pancreatic β cell to meet the increased insulin requirements is the triggering factor in the development of type 2 diabetes. A major emphasis in diabetes research has therefore shifted to understanding the causes of β cell failure. Collectively, these studies have implicated a complex network of triggers, which activate intersecting execution pathways leading to β cell dysfunction and death. In the present review, we discuss these triggers (glucotoxicity, lipotoxicity, amyloid and cytokines) with respect to the pathways they activate (oxidative stress, inflammation and endoplasmic reticulum stress) and propose a model for understanding β cell failure in type 2 diabetes. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.00021.x, 2010)

Details

ISSN :
20401124 and 20401116
Database :
OpenAIRE
Journal :
Journal of Diabetes Investigation
Accession number :
edsair.doi.dedup.....92a4df139a1a059c076ec2cc9461db7e
Full Text :
https://doi.org/10.1111/j.2040-1124.2010.00021.x