Clinic for Endocrinology, Diabetes and Metabolic Diseases, University Clinical Centre of Serbia, Faculty of Medicine, University of Belgrade, Dr Subotica 13, 11000 Belgrade, Serbia.
Institute of Histology and Embryology, Faculty of Medicine, University of Belgrade, Visegradska 26, 11000 Belgrade, Serbia.
Mitochondrion. 2021 Nov;61:165-173. doi: 10.1016/j.mito.2021.10.001. Epub 2021 Oct 8.
Mitochondrial dysfunction in diabetes is a widely studied topic, but inconsistency in literature data suggests a need for valid and reproducible models that will help to clarify this interaction. We aimed to establish insulin resistance models using chronic high insulin treatment in two cell types: myocytes and hepatocytes, characterise them in terms of mitochondrial function and compare them to the widely used palmitate-induced model of insulin resistance. We found that insulin lowered phosphorylation of Akt while not affecting cell viability, ROS production, mitochondrial morphology or respiration, and caused decrease in mitochondrial coupling only in muscle but not in liver cells.
糖尿病中的线粒体功能障碍是一个广泛研究的课题，但文献数据的不一致表明需要有效的、可重复的模型来帮助阐明这种相互作用。我们的目的是使用两种细胞类型（心肌细胞和肝细胞）中的慢性高胰岛素处理来建立胰岛素抵抗模型，从线粒体功能的角度对其进行特征描述，并将其与广泛使用的棕榈酸诱导的胰岛素抵抗模型进行比较。我们发现，胰岛素降低了 Akt 的磷酸化，但不影响细胞活力、ROS 产生、线粒体形态或呼吸，并且仅在肌肉细胞中而不是在肝细胞中引起线粒体偶联的下降。
