作者: Xianglan Quan , Ranjan Das , Shanhua Xu , Gary W. Cline , Andreas Wiederkehr
DOI: 10.1016/J.MCE.2013.08.003
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摘要: Here, we have investigated the role of inorganic phosphate (Pi) transport in mitochondria rat clonal β-cells. In α-toxin-permeabilized INS-1E cells, succinate and glycerol-3-phosphate increased mitochondrial ATP release which depends on exogenous ADP Pi. presence substrates, addition Pi caused matrix acidification hyperpolarisation promoted export. Dissipation pH gradient or pharmacological inhibition blocked effects electrochemical Knock-down transporter PiC, however, neither prevented Pi-induced activation nor glucose-induced insulin secretion. Using (31)P NMR observed reduction pools during nutrient stimulation cells. Interestingly, loss was less pronounced than cytosol. We conclude that alkalinisation is necessary to maintain a pool, at levels sufficient stimulate energy metabolism insulin-secreting cells beyond its as substrate for synthesis.