Li Xiudan, Wan Tingting, Li Yanbo
Department of Endocrinology, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Exp Ther Med. 2021 Jul;22(1):707. doi: 10.3892/etm.2021.10139. Epub 2021 May 2.
Type 2 diabetes mellitus (T2DM) is a major chronic disease that is characterized by pancreatic β-cell dysfunction and insulin resistance. Autophagy is a highly conserved intracellular recycling pathway and is involved in regulating intracellular homeostasis. Transcription factor Forkhead box O1 (FoxO1) also regulates fundamental cellular processes, including cell differentiation, metabolism and apoptosis, and proliferation to cellular stress. Increasing evidence suggest that autophagy and FoxO1 are involved in the pathogenesis of T2DM, including β-cell viability, apoptosis, insulin secretion and peripheral insulin resistance. Recent studies have demonstrated that FoxO1 improves insulin resistance by regulating target tissue autophagy. The present review summarizes current literature on the role of autophagy and FoxO1 in T2DM. The participation of FoxO1 in the development and occurrence of T2DM via autophagy is also discussed.
2型糖尿病(T2DM)是一种主要的慢性疾病,其特征为胰腺β细胞功能障碍和胰岛素抵抗。自噬是一种高度保守的细胞内循环途径,参与调节细胞内稳态。转录因子叉头框O1(FoxO1)也调节包括细胞分化、代谢、凋亡以及细胞对压力的增殖反应等基本细胞过程。越来越多的证据表明,自噬和FoxO1参与了T2DM的发病机制,包括β细胞活力、凋亡、胰岛素分泌和外周胰岛素抵抗。最近的研究表明,FoxO1通过调节靶组织自噬来改善胰岛素抵抗。本综述总结了关于自噬和FoxO1在T2DM中作用的当前文献。还讨论了FoxO1通过自噬参与T2DM的发生和发展。