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

Takeshi Ogihara, Raghavendra G. Mirmira

Research output: Contribution to journalReview article

18 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)123-133
Number of pages11
JournalJournal of Diabetes Investigation
Volume1
Issue number4
DOIs
StatePublished - Aug 1 2010

Keywords

  • Diabetes
  • Insulin resistance
  • Islet

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Internal Medicine

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