2型糖尿病中特异性β细胞转录银子失活

Introduction

Oxidative stress appears to contribute to pancreatic islet β cell dysfunction in both type 1 (T1DM) and type 2 (T2DM) diabetes (1–6). As a consequence, understanding how oxidative stress impacts β cells is clearly of therapeutic relevance. Compelling evidence indicates that the accumulation of ROS, such as hydroxyl radical and hydrogen peroxide (H2O2) generated by increased glucose and/or lipid metabolism, causes cell inactivation and death (7). For example, the levels of oxidative stress markers are significantly higher in human T2DM islets (e.g., 3-nitrotyrosine and 8-hydroxy-2′-deoxyguanosine) (8, 9). Notably, islet β cells have unusually low antioxidant enzyme levels