Endoplasmic reticulum stress and insulin resistance post-trauma: similarities to type 2 diabetes

J Cell Mol Med. 2012 Mar;16(3):437-44. doi: 10.1111/j.1582-4934.2011.01405.x.

Abstract

Type 2 diabetes, a rapidly growing disease of modern aetiology, has a profound impact on morbidity and mortality. Explosions in the understanding of the underlying cellular mechanisms which lead to type 2 diabetes have recently been elucidated. In particular, the central role of endoplasmic reticulum stress (ER stress) and the unfolding protein response (UPR) in insulin resistance in type 2 diabetes has recently been discovered. We hypothesize that ER stress and UPR are not only central for type 2 diabetes but also for stress-induced diabetes. We review here the evidence that post-burn insulin resistance and hyperglycaemia have pathophysiologic mechanisms in common with type 2 diabetes. These recent discoveries not only highlight the importance of ER stress in the post-burn patient recovery, but furthermore enable new models to study fundamental and interventional aspects of type 2 diabetes.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Burns / metabolism
  • Burns / pathology
  • Burns / physiopathology*
  • Calcium / metabolism
  • Diabetes Mellitus, Type 2 / metabolism
  • Diabetes Mellitus, Type 2 / pathology
  • Diabetes Mellitus, Type 2 / physiopathology*
  • Endoplasmic Reticulum / metabolism
  • Endoplasmic Reticulum / pathology
  • Endoplasmic Reticulum Stress*
  • Humans
  • Hyperglycemia / metabolism
  • Hyperglycemia / pathology
  • Hyperglycemia / physiopathology*
  • Insulin Resistance*
  • Signal Transduction
  • Stress, Physiological
  • Unfolded Protein Response

Substances

  • Calcium