Department of Mitochondrial Physiology, Institute of Physiology of the Czech Academy of Sciences, Czech Republic.
Mitochondrion. 2019 Nov;49:245-258. doi: 10.1016/j.mito.2019.06.007. Epub 2019 Jun 25.
Type 2 diabetes progression stems from dysfunction of β-cells, besides the peripheral insulin resistance. Mitochondria as glucose sensor and regulation center are impaired at various stages of this progression. Their biogenesis and functional impairment is reflected by altered morphology of the mitochondrial network and ultramorphology of cristae and mitochondrial DNA loci, termed nucleoids. Aspects of all above changes are reviewed here together with a brief introduction to proteins involved in mitochondrial network dynamics, cristae shaping, and mtDNA nucleoid structure and maintenance. Most frequently, pathology is reflected by the fragmentation of network, cristae inflation or absence and declining number of nucleoids.
2 型糖尿病的进展源于β细胞功能障碍，除了外周胰岛素抵抗。线粒体作为葡萄糖感受器和调节中心，在该进展的各个阶段都会受到损伤。它们的生物发生和功能障碍反映在改变线粒体网络的形态和嵴的超微结构以及线粒体 DNA 位置，称为核区。本文综述了这些变化的各个方面，并简要介绍了参与线粒体网络动力学、嵴形成以及 mtDNA 核区结构和维持的蛋白质。最常见的是，病理变化反映在网络的碎片化、嵴的膨胀或缺失以及核区数量的减少。
