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.

中文翻译：

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胰腺β细胞中线粒体网络、嵴和线粒体核的动态

除了外周胰岛素抵抗外，2 型糖尿病的进展还源于 β 细胞功能障碍。作为葡萄糖传感器和调节中心的线粒体在这一进程的各个阶段都受到损害。它们的生物发生和功能损伤反映在线粒体网络的形态学改变和嵴和线粒体 DNA 基因座的超形态学上，称为核素。此处回顾了所有上述变化的各个方面，并简要介绍了参与线粒体网络动力学、嵴成形和 mtDNA 类核结构和维持的蛋白质。最常见的是，病理表现为网络的碎片化、嵴膨胀或缺失以及类核蛋白数量的减少。