综述：胰腺β细胞中的自噬及其在糖尿病中的意义。
Minireview: Autophagy in pancreatic β-cells and its implication in diabetes.
作者信息
Watada Hirotaka, Fujitani Yoshio
机构信息
Department of Metabolism and Endocrinology (H.W., Y.F.), Centers for Molecular Diabetology (H.W., Y.F.) and Therapeutic Innovations in Diabetes (H.W.), and Japan Science and Technology Agency (JST)-CREST Program (Y.F.), Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
出版信息
Mol Endocrinol. 2015 Mar;29(3):338-48. doi: 10.1210/me.2014-1367. Epub 2015 Jan 29.
Autophagy is a conserved system for the degradation of cytoplasmic proteins and organelles. During insulin resistance, in which insulin secretion is enhanced and β-cell mass is increased owing to changes in the expression and function of various proteins in pancreatic β-cells, autophagic activity appears to also be enhanced to adapt to the dynamic changes occurring in β-cells. Indeed, defective autophagy in β-cells recapitulates several features that are observed in islets during the development of type 2 diabetes mellitus. In addition, the dyregulation of autophagic activity appears to occur in the β-cells of type 2 diabetic model mice and type 2 diabetes mellitus patients. These lines of evidence suggest that autophagic failure may be implicated in the pathophysiology of type 2 diabetes mellitus. In this review, we summarized the recent findings regarding how autophagy in β-cells is regulated and how dysfunction of the autophagic machinery may lead to the dysfunction of β-cells.
自噬是一种保守的系统，用于降解细胞质蛋白和细胞器。在胰岛素抵抗期间，由于胰腺β细胞中各种蛋白质的表达和功能发生变化，胰岛素分泌增强且β细胞量增加，自噬活性似乎也会增强，以适应β细胞中发生的动态变化。事实上，β细胞中的自噬缺陷概括了2型糖尿病发展过程中在胰岛中观察到的几个特征。此外，自噬活性的失调似乎发生在2型糖尿病模型小鼠和2型糖尿病患者的β细胞中。这些证据表明，自噬功能障碍可能与2型糖尿病的病理生理学有关。在这篇综述中，我们总结了关于β细胞中的自噬如何被调节以及自噬机制功能障碍如何导致β细胞功能障碍的最新发现。
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