Type-2-Diabetes (T2D) is the most common metabolic disease in the world today. It erupts as a result of peripheral insulin resistance combined with hyperinsulinemia followed by suppression of insulin secretion from pancreatic β-cells. Mitochondria play a central role in β-cells by sensing glucose and also by mediating the suppression of insulin secretion in T2D. Here, we will summarize the evidence accumulated for the roles of β-cells mitochondria in T2D. We will present an updated view on how mitochondria in β-cells have been associated with T2D, from the genetic, bioenergetic, redox and structural points of view. The emerging picture is that mitochondrial structure and dysfunction directly contribute to β-cell function and in the pathogenesis of T2D.

2型糖尿病（T2D）是当今世界上最常见的代谢性疾病。它是由于外周胰岛素抵抗与高胰岛素血症相结合，继而抑制了胰腺β细胞分泌胰岛素而爆发的。线粒体通过感知葡萄糖以及介导T2D中胰岛素分泌的抑制，在β细胞中发挥重要作用。在这里，我们将总结积累的证据，证明β细胞线粒体在T2D中的作用。我们将从遗传，生物能，氧化还原和结构的角度，提出有关β细胞中线粒体如何与T2D相关的最新观点。新兴的现象是线粒体结构和功能障碍直接导致β细胞功能以及T2D的发病机理。