Mackenzie Bryan, Garrick Michael D
Dept. of Molecular and Cellular Physiology, University of Cincinnati College of Medicine, OH 45267-0576, USA.
Am J Physiol Gastrointest Liver Physiol. 2005 Dec;289(6):G981-6. doi: 10.1152/ajpgi.00363.2005.
How does iron enter enterocytes? Ablating SLC11A2, the gene for the divalent metal ion transporter DMT1, supports evidence from the Belgrade rat and mk mouse models establishing DMT1 as the primary mechanism serving apical uptake of nonheme iron. DMT1 harnesses the energy from the proton electrochemical potential gradient to drive active transport of Fe(2+) (and perhaps Mn(2+) and other metal ions) into enterocytes. Fe(III) must first be reduced by ascorbic acid and surface ferrireductases. Among these is duodenal cytochrome B (DcytB), but lack of an obvious phenotype in DcytB (Cybrd1) knockout mice suggests ferrireductase redundancy. Our understanding of heme absorption has lagged, but the time is ripe for gains.
铁是如何进入肠上皮细胞的?敲除二价金属离子转运体DMT1的基因SLC11A2,为来自贝尔格莱德大鼠和mk小鼠模型的证据提供了支持,这些证据确立了DMT1作为非血红素铁顶端摄取的主要机制。DMT1利用质子电化学势梯度的能量来驱动Fe(2+)(可能还有Mn(2+)和其他金属离子)主动转运进入肠上皮细胞。Fe(III)必须首先被抗坏血酸和表面铁还原酶还原。其中包括十二指肠细胞色素B(DcytB),但DcytB(Cybrd1)基因敲除小鼠缺乏明显的表型,这表明铁还原酶存在冗余。我们对血红素吸收的理解一直滞后,但现在取得进展的时机已经成熟。