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

•  Introduction •  Insulin resistance and hyperglycaemia in burn patients •  Euglycaemic control in critically ill and burn patients •  Molecular mechanisms associated with post‐burn insulin resistance: endoplasmic reticulum stress and unfolded protein response •  Induction of the ER stress response and intracellular calcium stores •  Type 2 diabetes in animal models and links to the ER stress response •  Clinical relevance of insulin resistance and ER stress in the post‐burn response •  Targeting the ER stress response as a therapeutic for burn injury •  ConclusionsType 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.