Zaidalkilani Ayah Talal, Al-Kuraishy Hayder M, Fahad Esraa H, Al-Gareeb Ali I, Elewa Yaser Hosny Ali, Zahran Mahmoud Hosny, Alexiou Athanasios, Papadakis Marios, Al-Farga Ammar, Batiha Gaber El-Saber
Department of Nutrition, Faculty of Pharmacy and Medical Sciences, University of Petra, Amman, Jordan.
Department of Clinical Pharmacology and Medicine, College of Medicine, Al-Mustansiriyah University, Baghdad, Iraq.
J Diabetes. 2024 Dec;16(12):e70010. doi: 10.1111/1753-0407.70010.
Type 2 diabetes (T2D) is a chronic metabolic disorder caused by defective insulin signaling, insulin resistance, and impairment of insulin secretion. Autophagy is a conserved lysosomal-dependent catabolic cellular pathway involved in the pathogenesis of T2D and its complications. Basal autophagy regulates pancreatic β-cell function by enhancing insulin release and peripheral insulin sensitivity. Therefore, defective autophagy is associated with impairment of pancreatic β-cell function and the development of insulin rersistance (IR). However, over-activated autophagy increases apoptosis of pancreatic β-cells leading to pancreatic β-cell dysfunction. Hence, autophagy plays a double-edged sword role in T2D. Therefore, the use of autophagy modulators including inhibitors and activators may affect the pathogenesis of T2D. Hence, this review aims to clarify the potential role of autophagy inhibitors and activators in T2D.
2型糖尿病（T2D）是一种由胰岛素信号缺陷、胰岛素抵抗和胰岛素分泌受损引起的慢性代谢紊乱。自噬是一种保守的、依赖溶酶体的分解代谢细胞途径，参与T2D及其并发症的发病机制。基础自噬通过增强胰岛素释放和外周胰岛素敏感性来调节胰腺β细胞功能。因此，自噬缺陷与胰腺β细胞功能受损和胰岛素抵抗（IR）的发展有关。然而，过度激活的自噬会增加胰腺β细胞的凋亡，导致胰腺β细胞功能障碍。因此，自噬在T2D中起着双刃剑的作用。因此，使用包括抑制剂和激活剂在内的自噬调节剂可能会影响T2D的发病机制。因此，本综述旨在阐明自噬抑制剂和激活剂在T2D中的潜在作用。
