论文部分内容阅读
胰腺β细胞功能障碍导致糖尿病发生，在糖尿病早期，胰腺β细胞通过自身调节代偿高血糖和外周胰岛素抵抗，涉及的信号通路之一称为未折叠蛋白反应（ UPR）。 UPR不但可以维持内质网（ER）动态平衡和β细胞完整性，而且在ER 折叠中起重要作用，UPR 可以加快错误折叠蛋白降解，还可以抑制信使RNA（ mRNA）转录，从而减少内质网腔内未折叠蛋白的堆积。该文着重阐述 UPR在糖尿病期间的β细胞代偿和衰竭中的主要作用。“,”The dysfunction of pancreatic βcells leads to diabetes.In the early stage of diabetes,the βcells compensate hyperglycemia and the peripheral insulin resistance through their own regulation ,and one of the signaling pathways involved is called the unfolded protein response ( UPR) .UPR not only can maintain the dynamic balance of the endoplasmic reticulum(ER) and the integrity of the beta cells,but also plays an important role in ER folding,increasing the degradation of misfolded proteins,inhibiting the messenger RNA ( mRNA) transcription,thereby reducing the unfolded protein accumulation in endoplasmic reticulum lumen . Here is to make a review of the role of UPR in the compensatory and depletion of βcells during diabetes.