正常和高铜摄入量下年轻男性肠粘膜细胞中的铜滞留†

Judith R. Turnlund, Joseph M. Domek, Padmanabhan P. Nair, Sam J. Bhathena
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引用次数: 10

摘要

肠道细胞在铜稳态和储存中的作用尚未得到研究。稳态受吸收、排泄和储存的调节。铜通过胆汁排出,人们认为,当饮食中铜含量高时,胃肠道的排泄量增加是由于胆汁中的铜。一些被吸收的铜似乎被隔离在肠道细胞中。为了验证这一假设,我们测量了从8名年轻男性的粪便样本中分离的粘膜上皮细胞的铜含量,这些年轻男性在食用日常饮食时以及在补充7mg/天铜129天后。当分别食用普通日粮和补充铜的日粮时,细胞的平均铜含量(以毫克铜/克细胞蛋白表示)分别为0.78和1.65mg/g(SEM 0.19)(P<;0.02)。与血浆和尿液中的铜含量相反,当摄入量高时,肠细胞中的铜显著增加。铜很可能在吸收后被这些细胞隔离,没有进入系统循环。因此,粪便中内源性铜的含量可能是胆汁中铜排泄和脱落肠上皮细胞中铜螯合的组合。这表明,当膳食铜含量高时,肠道细胞对铜的保留会增加,并在铜稳态中发挥作用。J.Trace Elem。Exp.Med.16:105-1082003。出版于2003年,Wiley–Liss,股份有限公司。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Copper retention in intestinal mucosal cells of young men at normal and high copper intakes†
The role of intestinal cells in copper homeostasis and storage has not been studied. Homeostasis is regulated by absorption, excretion, and storage. Copper is excreted via the bile, and it has been assumed that the increased excretion into the gastrointestinal tract when diets are high in copper was due to biliary copper. It seemed possible that some of the absorbed copper is sequestered in the intestinal cells. To test this hypothesis we measured the copper content of mucosal epithelial cells isolated from stool samples of 8 young men when consuming their usual diets and after 129 days of supplementation with 7 mg/day copper. The mean copper content of the cells, expressed as mg copper per gram of cell protein, was 0.78 versus 1.65 mg/g (SEM 0.19) (P < 0.02) when the usual and copper-supplemented diets, respectively, were consumed. In contrast to the copper content of plasma and urine, copper in intestinal cells increased significantly when intake was high. It is likely that copper was sequestered by these cells following absorption and did not get into systemic circulation. Thus, the amount of endogenous copper in stools is probably a combination of biliary copper excretion and copper sequestered in exfoliated intestinal epithelial cells. This suggests that retention of copper by the intestinal cells increases when dietary copper is high and plays a role in copper homeostasis. J. Trace Elem. Exp. Med. 16:105–108, 2003. Published 2003 Wiley–Liss, Inc.
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