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Regulation of the zinc transporter ZnT-1 by dietary zinc

机译:膳食锌对锌转运蛋白ZnT-1的调节

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摘要

Using animal models, this study examined the pattern of expression of the Zn transporter, ZnT-1, in the intestine and the regulation of ZnT-1 by dietary Zn in the intestine and liver. Immunofluorescence demonstrated that intestinal ZnT-1 was most abundant at the basolateral surface of enterocytes lining the villi of the duodenum and jejunum. By Western blot analysis, intestinal and liver ZnT-1 protein migrated as a 42- and 36-kDa protein, respectively. Dietary Zn supplementation elevated the levelof intestinal ZnT-1 mRNA and protein approximately 50 and 10%, respectively, but had no effect in the liver. In response to an acute oral Zn dose, the level of intestinal ZnT-1 mRNA was up-regulated 8-fold, without a corresponding increase in ZnT-1 protein. Conversely, the acute oral dose did not affect liver ZnT-1 mRNA, but resulted in a 5-fold increase in liver ZnT-1 protein. The data suggest that ZnT-1 is at least part of the mechanism by which dietary Zn is absorbed and that, despite the Zn responsiveness of the ZnT-1 gene, additional factors may be regulating the steady-state level of ZnT-1 transporter protein.
机译:使用动物模型,本研究检查了肠道中锌转运蛋白ZnT-1的表达模式以及肠道和肝脏中膳食锌对ZnT-1的调节。免疫荧光显示,肠道ZnT-1在十二指肠和空肠绒毛内衬的肠上皮细胞的基底外侧表面最丰富。通过蛋白质印迹分析,肠道和肝脏ZnT-1蛋白分别迁移为42-kDa和36-kDa蛋白。膳食锌补充剂分别使肠道ZnT-1 mRNA和蛋白质的水平分别升高约50%和10%,但对肝脏无影响。响应急性口服锌剂量,肠道ZnT-1 mRNA的水平上调了8倍,而ZnT-1蛋白却没有相应增加。相反,急性口服剂量不会影响肝脏ZnT-1 mRNA,但会导致肝脏ZnT-1蛋白增加5倍。数据表明ZnT-1至少是膳食锌吸收的机制的一部分,尽管ZnT-1基因具有Zn反应性,但其他因素可能调节ZnT-1转运蛋白的稳态水平。

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