Zinc (Zn2+) appears to be intimately involved in insulin metabolism since insulin secretion is correlated with zinc secretion in\nresponse to glucose stimulation, but little is known about the regulation of zinc homeostasis in pancreatic beta-cells. This study set\nout to identify the intracellular zinc transient by imaging free cytosolic zinc in HIT-T15 beta-cells with fluorescent zinc indicators.\nWe observed that membrane depolarization by KCl (30ââ?¬â??60mM) was able to induce a rapid increase in cytosolic concentration of\nzinc. Multiple zinc transients of similar magnitude were elicited during repeated stimulations. The amplitude of zinc responses\nwas not affected by the removal of extracellular calcium or zinc. However, the half-time of the rising slope was significantly slower\nafter removing extracellular zinc with zinc chelator CaEDTA, suggesting that extracellular zinc affect the initial rising phase of zinc\nresponse. Glucose (10mM) induced substantial and progressive increases in intracellular zinc concentration in a similar way as\nKCl, with variation in the onset and the duration of zinc mobilization. It is known that the depolarization of beta-cell membrane\nis coupled with the secretion of insulin. Rising intracellular zinc concentration may act as a critical signaling factor in insulin\nmetabolism of pancreatic beta-cells.
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