Chronic Kidney Disease Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Weill Cornell Medicine Qatar, Doha, Qatar.
J Cell Physiol. 2019 Jun;234(6):8402-8410. doi: 10.1002/jcp.27754. Epub 2018 Nov 11.
The prevalence of type 2 diabetes mellitus (T2DM) is increasing rapidly with its associated morbidity and mortality. Many pathophysiological pathways such as oxidative stress, inflammatory responses, adipokines, obesity-induced insulin resistance, improper insulin signaling, and beta cell apoptosis are associated with the development of T2DM. There is increasing evidence of the role of mitochondrial dysfunction in the onset of T2DM, particularly in relation to the development of diabetic complications. Here, the role of mitochondrial dysfunction in T2DM is reviewed together with its modulation by antidiabetic therapeutic agents, an effect that may be independent of their hypoglycemic effect.
2 型糖尿病(T2DM)的患病率迅速增加,其相关的发病率和死亡率也随之增加。许多病理生理途径,如氧化应激、炎症反应、脂肪因子、肥胖引起的胰岛素抵抗、胰岛素信号异常和β细胞凋亡,都与 T2DM 的发生有关。越来越多的证据表明线粒体功能障碍在 T2DM 的发病中起作用,特别是与糖尿病并发症的发生有关。本文综述了线粒体功能障碍在 T2DM 中的作用,以及其与抗糖尿病治疗药物的调节作用,这种作用可能与其降血糖作用无关。