In recent years, the incidence rate of type 2 diabetes (T2D) has risen rapidly and has become a global health crisis. Recent experimental and clinical studies have shown that islet β-cell dysfunction is an important cause of T2D and its related complications. β-cells undergo dynamic compensation and decompensation in the course of T2D. In this process, metabolic stress responses, such as ER stress, oxidative stress and inflammation, are key regulators of β-cell functional alternations. In this review, we summarize the research progress on the β-cell functional dynamics in the course of T2D, in order to deepen the understanding of the molecular mechanism of T2D, and provide reference for its precise diagnosis and clinical intervention.
近年来,2型糖尿病(type 2 diabetes,T2D)发病率迅速上升,已成为全球性的健康危机。最近的临床和基础研究表明,胰岛β细胞功能障碍是导致T2D及其相关并发症的重要原因。在2型糖尿病的自然病程中,胰岛β细胞经历从代偿到失代偿的动态变化;其中,代谢应激反应,如内质网应激(endoplasmic reticulum stress,ER stress)、氧化应激(oxidative stress)和炎症(inflammation)是β细胞功能变化的关键调控机制。本文总结了β细胞功能在2型糖尿病病程中动态变化的研究进展,以期深化对2型糖尿病分子机制的理解,为精准诊断和临床干预2型糖尿病提供参考。.
Keywords: molecular mechanism; type 2 diabetes; β-cell.