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缺铁饮食喂养大鼠十二指肠铁吸收的结构和细胞适应性

Structural and cellular adaptation of duodenal iron uptake in rats maintained on an iron-deficient diet.

作者信息

Smith M W, Debnam E S, Dashwood M R, Srai S K

机构信息

Department of Physiology, Royal Free and University College Medical School, London, UK.

出版信息

Pflugers Arch. 2000 Feb;439(4):449-54. doi: 10.1007/s004249900193.

DOI:10.1007/s004249900193
PMID:10678741
Abstract

Iron deficiency induced in rats maintained on a commercial diet with a low iron content has been used to investigate adaptive mechanisms that enhance duodenal iron uptake. These adaptive changes have been divided into those that result from changes in villus surface area (structural adaptation) and those that reflect changes in the way individual enterocytes express iron transport function (cellular adaptation). Cellular adaptation was assessed by carrying out microdensitometry of autoradiographs prepared from duodenal tissue previously incubated for 5 min in 200 micromol/l 59Fe2+-ascorbate. Structural adaptation was studied by performing image analysis of microdissected and sectioned villi. Cellular adaptation involved increased iron uptake by enterocytes present in the lower villus. Thus iron deficiency resulted in a threefold enhanced expression of uptake in the lower 100 microm villus (3.9+/-2.4 versus 12.6+/-1.5 arbitrary units, P<0.001). Maximal uptake was reached in the upper region of both control and iron-deficient villi, but iron deficiency had no effect on cellular uptake at this part of the villus. Structural adaptation involved the lengthening (+16%, P<0.05) and broadening (+14%) of villi in the duodenum of iron-deficient rats. The resultant expansion in villus area caused a further increase in uptake that was mostly expressed in the upper villus. Maximal uptake corrected for structure occurred in the middle third of villi from control and iron-deficient rats. Cellular plus structural adaptation produced a twofold increase in iron uptake. More than half of this effect was caused by changes in villus structure. [3H]Thymidine labelling experiments revealed a slightly earlier expression of enterocyte iron uptake in iron deficiency.

摘要

以低铁含量的商业饲料喂养大鼠诱导缺铁,已被用于研究增强十二指肠铁摄取的适应性机制。这些适应性变化可分为由绒毛表面积变化引起的(结构适应性)和反映单个肠上皮细胞表达铁转运功能方式变化的(细胞适应性)。通过对十二指肠组织制备的放射自显影片进行显微密度测定来评估细胞适应性,该十二指肠组织先前在200微摩尔/升的59Fe2 + -抗坏血酸盐中孵育5分钟。通过对显微解剖和切片的绒毛进行图像分析来研究结构适应性。细胞适应性涉及绒毛下部存在的肠上皮细胞铁摄取增加。因此,缺铁导致下部100微米绒毛摄取的表达增强了三倍(3.9±2.4对12.6±1.5任意单位,P <0.001)。对照和缺铁绒毛的上部区域均达到最大摄取,但缺铁对绒毛该部分的细胞摄取没有影响。结构适应性涉及缺铁大鼠十二指肠绒毛的延长(+ 16%,P <0.05)和变宽(+ 14%)。绒毛面积的扩大导致摄取进一步增加,这主要表现在绒毛上部。校正结构后的最大摄取发生在对照和缺铁大鼠绒毛的中间三分之一处。细胞适应性加结构适应性使铁摄取增加了两倍。这种效应的一半以上是由绒毛结构的变化引起的。[3H]胸腺嘧啶标记实验显示缺铁时肠上皮细胞铁摄取的表达略早。

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