Laboratory of Experimental Medicine, Université Libre de Bruxelles (ULB), CP-618, Route de Lennik 808, 1070 Brussels, Belgium.
Trends Mol Med. 2012 Jan;18(1):59-68. doi: 10.1016/j.molmed.2011.07.010. Epub 2011 Aug 31.
The endoplasmic reticulum (ER) stress response, also commonly known as the unfolded protein response (UPR), is an adaptive response used to align ER functional capacity with demand. It is activated in various tissues under conditions related to obesity and type 2 diabetes. Hypothalamic ER stress contributes to inflammation and leptin/insulin resistance. Hepatic ER stress contributes to the development of steatosis and insulin resistance, and components of the UPR regulate liver lipid metabolism. ER stress in enlarged fat tissues induces inflammation and modifies adipokine secretion, and saturated fats cause ER stress in muscle. Finally, prolonged ER stress impairs insulin synthesis and causes pancreatic β cell apoptosis. In this review, we discuss ways in which ER stress operates as a common molecular pathway in the pathogenesis of obesity and diabetes.
内质网（ER）应激反应，也通常称为未折叠蛋白反应（UPR），是一种适应性反应，用于使 ER 功能能力与需求保持一致。在与肥胖和 2 型糖尿病相关的各种情况下，它会在各种组织中被激活。下丘脑 ER 应激会导致炎症和瘦素/胰岛素抵抗。肝 ER 应激会导致脂肪变性和胰岛素抵抗，并且 UPR 的成分调节肝脏脂质代谢。肥大脂肪组织中的 ER 应激会引发炎症并改变脂肪因子的分泌，而饱和脂肪会导致肌肉中的 ER 应激。最后，长期的 ER 应激会损害胰岛素的合成并导致胰岛β细胞凋亡。在这篇综述中，我们讨论了 ER 应激作为肥胖和糖尿病发病机制中的共同分子途径的作用方式。
