title: Endoplasmic reticulum stress and insulin resistance post-trauma: similarities to type 2 diabetes.
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.
authors.affiliation: Ross Tilley Burn Center, Sunnybrook Health Science Centre and University of Toronto, ON, Canada. marc.jeschke@sunnybrook.ca
authors.forename: Marc G
authors.initials: MG
authors.lastname: Jeschke
authors.forename: Darren
authors.initials: D
authors.lastname: Boehning
mesh_terms: D000818:Animals; D002056:Burns / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D002118:Calcium / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D004721:Endoplasmic Reticulum / Q000378:metabolism / Q000473:pathology; D059865:Endoplasmic Reticulum Stress; D006801:Humans; D006943:Hyperglycemia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D007333:Insulin Resistance; D015398:Signal Transduction; D013312:Stress, Physiological; D056811:Unfolded Protein Response
chemical_list: D002118:Calcium