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.