Ross Tilley Burn Center, Sunnybrook Health Science Centre and University of Toronto, ON, Canada.
J Cell Mol Med. 2012 Mar;16(3):437-44. doi: 10.1111/j.1582-4934.2011.01405.x.
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.
2 型糖尿病是一种现代病因学中迅速增长的疾病，对发病率和死亡率有深远影响。最近，人们对导致 2 型糖尿病的潜在细胞机制有了更深入的理解。特别是，内质网应激（ER 应激）和未折叠蛋白反应（UPR）在 2 型糖尿病胰岛素抵抗中的核心作用最近被发现。我们假设 ER 应激和 UPR 不仅对 2 型糖尿病，而且对应激诱导性糖尿病都很重要。我们在这里回顾了烧伤后胰岛素抵抗和高血糖与 2 型糖尿病具有共同的病理生理机制的证据。这些新发现不仅突出了 ER 应激在烧伤患者康复中的重要性，而且还为研究 2 型糖尿病的基础和干预方面提供了新的模型。
