Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Department of Pediatrics, Division of Endocrinology & Diabetes, Department of Genetics, Stanford Diabetes Research Center, Stanford University School of Medicine, Stanford, CA, USA.
Cell. 2024 Jul 25;187(15):3789-3820. doi: 10.1016/j.cell.2024.06.029.
Diabetes, a complex multisystem metabolic disorder characterized by hyperglycemia, leads to complications that reduce quality of life and increase mortality. Diabetes pathophysiology includes dysfunction of beta cells, adipose tissue, skeletal muscle, and liver. Type 1 diabetes (T1D) results from immune-mediated beta cell destruction. The more prevalent type 2 diabetes (T2D) is a heterogeneous disorder characterized by varying degrees of beta cell dysfunction in concert with insulin resistance. The strong association between obesity and T2D involves pathways regulated by the central nervous system governing food intake and energy expenditure, integrating inputs from peripheral organs and the environment. The risk of developing diabetes or its complications represents interactions between genetic susceptibility and environmental factors, including the availability of nutritious food and other social determinants of health. This perspective reviews recent advances in understanding the pathophysiology and treatment of diabetes and its complications, which could alter the course of this prevalent disorder.
糖尿病是一种以高血糖为特征的复杂多系统代谢紊乱，会导致生活质量下降和死亡率增加的并发症。糖尿病的病理生理学包括β细胞、脂肪组织、骨骼肌和肝脏的功能障碍。1 型糖尿病（T1D）是由免疫介导的β细胞破坏引起的。更为常见的 2 型糖尿病（T2D）是一种异质性疾病，其特征是β细胞功能障碍的程度不同，同时伴有胰岛素抵抗。肥胖与 T2D 之间的强烈关联涉及由中枢神经系统调节的途径，该途径控制食物摄入和能量消耗，整合来自外周器官和环境的输入。发生糖尿病或其并发症的风险代表了遗传易感性与环境因素（包括营养食品的可获得性和其他健康的社会决定因素）之间的相互作用。本观点综述了理解糖尿病及其并发症的病理生理学和治疗的最新进展，这些进展可能改变这种普遍疾病的进程。
