2024-03-29T12:31:29Zhttps://eprints.lib.hokudai.ac.jp/dspace-oai/requestoai:eprints.lib.hokudai.ac.jp:2115/853842022-11-17T02:08:08Zhdl_2115_20046hdl_2115_138Zinc directly stimulates cholecystokinin secretion from enteroendocrine cells and reduces gastric emptying in ratsNakajima, Shingo1000010396301Hira, TohruIwaya, Hitoshi1000070198894Hara, Hiroshiopen access© 2016. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 InternationalCholecystokininZincGastric emptyingTransient receptor potential ankyrin 1 (TRPA1)610Zinc, an essential mineral element, regulates various physiological functions such as immune responses and hormone secretion. Cholecystokinin (CCK), a gut hormone, has a role in protective immunity through the regulation of gastrointestinal motility, appetite, and inflammatory response. Here, we examined the effect of zinc on CCK secretion in STC-1 cells, an enteroendocrine cell line derived from murine duodenum, and in rats. Extracellular zinc triggered CCK secretion accompanied with increased intracellular Ca2+ and Zn2+ mobilization in STC-1 cells. Zinc-induced CCK secretion was abolished in the absence of intracellular Zn2+ or extracellular calcium. Upon inhibition of transient receptor potential ankyrin 1 (TRPA1), extracellular zinc failed to increase intracellular Ca2+ and subsequent CCK secretion. In rats, oral zinc administration decreased gastric emptying through the activation of CCK signaling. These results suggest that zinc is a novel stimulant for CCK secretion through the activation of TRPA1 related to intracellular Zn2+ and Ca2+ mobilization.2016-07-15engjournal articleAMhttp://hdl.handle.net/2115/85384https://doi.org/10.1016/j.mce.2016.04.0100303-7207Molecular and Cellular Endocrinology430108114https://eprints.lib.hokudai.ac.jp/dspace/bitstream/2115/85384/1/MCE-D-16-00011R1.pdfapplication/pdf732.02 KB2016-07-15