Department of Cell Physiology and Metabolism, University of Geneva Medical Centre, CH-1211 Geneva 4, Switzerland.
Adv Exp Med Biol. 2010;654:193-216. doi: 10.1007/978-90-481-3271-3_9.
Pancreatic beta-cells are poised to sense glucose and other nutrient secretagogues to regulate insulin exocytosis, thereby maintaining glucose homeostasis. This process requires translation of metabolic substrates into intracellular messengers recognized by the exocytotic machinery. Central to this metabolism-secretion coupling, mitochondria integrate and generate metabolic signals, thereby connecting glucose recognition to insulin exocytosis. In response to a glucose rise, nucleotides and metabolites are generated by mitochondria and participate, together with cytosolic calcium, to the stimulation of insulin release. This review describes the mitochondrion-dependent pathways of regulated insulin secretion. Mitochondrial defects, such as mutations and reactive oxygen species production, are discussed in the context of beta-cell failure that may participate to the etiology of diabetes.
胰岛β细胞能够感知葡萄糖和其他营养物分泌刺激物，从而调节胰岛素的胞吐作用，维持血糖稳态。这一过程需要将代谢底物转化为胞吐机制识别的细胞内信使。在这个代谢-分泌偶联中，线粒体整合并产生代谢信号，从而将葡萄糖识别与胰岛素胞吐作用联系起来。当葡萄糖上升时，线粒体产生核苷酸和代谢物，并与细胞质钙一起参与胰岛素释放的刺激。本文综述了受调控的胰岛素分泌的线粒体依赖性途径。还讨论了β细胞功能衰竭时线粒体缺陷（如突变和活性氧产生）的情况，这可能与糖尿病的病因有关。
