Effects of Zn2+ on glucose-induced electrical activity and insulin release from mouse pancreatic islets

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Abstract
The effects of Zn2+ and Co2+ on glucose-induced .beta.-cell electrical activity and on insulin release from microdissected mouse pancreatic islets were studied. In 11 mM glucose the electrical activity is characterized by a burst pattern with a bimodal distribution of spike amplitudes along the plateau phase. Zn2+ at 0.05 mM induced a reduction in the number of spikes during the burst and preferentially blocked the large action potentials. Zn2+ at 0.1 mM and Co2+ at 1.0 mM completely inhibited the electrical activity in response to glucose. Zn2+ inhibition of electrical activity was poorly reversible, whereas Co2+ inhibition was rapidly and completely reversible. Zn2+ and Co2+ inhibited the glucose-stimulated insulin release from microdissected perifused islets. Half-maximal inhibition occurred at about 0.3 mM for both metals. Zn2+ also inhibited K+-induced insulin release in the absence of glucose, indicating that Zn2+ inhibition does not involve glucose metabolism. It is proposed that Zn2+ blocks the voltage-gated Ca2+ channels in pancreatic .beta.-cells.