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大鼠胎儿的铁平衡

Fetal iron balance in the rat.

作者信息

Finch C A, Huebers H A, Miller L R, Josephson B M, Shepard T H, Mackler B

出版信息

Am J Clin Nutr. 1983 Jun;37(6):910-7. doi: 10.1093/ajcn/37.6.910.

Abstract

Maternal and fetal iron balance through pregnancy was examined in the rat. The 20th day was selected for detailed study because of the peak iron requirements at that time. The standard diet provided a borderline iron supply to the fetus due to the limited availability of its iron for absorption. When a more available form of iron was used, normal fetal development occurred over a range of dietary iron content from 16 to 2500 mg/kg. At a level of 5 to 8 mg/kg, there was attrition of placental tissues with frequent fetal death and resorption. When the iron-deficient pregnancy was sustained, both maternal and fetal iron deficiency were present. At progressively higher levels of dietary iron, feto-placental iron content was constant despite a progressive increase in maternal iron stores. Fetal iron supply appeared to be determined primarily by plasma iron concentration, and, at normal levels, about 25% of transferrin iron passing through the uterine vasculature, was removed by the intact placentas. Low levels of plasma iron resulted in damage to fetal tissues and reduced the capacity of placental tissues to take up iron. At high levels of plasma iron, plasma iron turnover initially increased 5-fold over basal levels in nonpregnant animals due to increased placental uptake. However, with continued hyperferremia, uptake was regulated so as to maintain fetal iron at a normal level. A comparison of these data with human iron requirements explained the occurrence of both maternal and fetal iron deficiency in the rat, but only maternal iron deficiency in the human.

摘要

对大鼠孕期母胎铁平衡进行了研究。由于第20天铁需求量达到峰值,故选择该时间点进行详细研究。标准饮食因铁的可吸收性有限,为胎儿提供的铁供应处于临界水平。当使用更易吸收的铁形式时,在饮食铁含量为16至2500毫克/千克的范围内,胎儿发育正常。当铁含量为5至8毫克/千克时,胎盘组织出现损耗,胎儿频繁死亡和吸收。当维持缺铁妊娠时,母体和胎儿均出现缺铁。随着饮食中铁含量逐渐升高,尽管母体铁储备逐渐增加,但胎儿-胎盘铁含量保持恒定。胎儿的铁供应似乎主要由血浆铁浓度决定,在正常水平下,通过子宫血管的转铁蛋白铁约25%被完整的胎盘摄取。血浆铁水平低会导致胎儿组织受损,并降低胎盘组织摄取铁的能力。在血浆铁水平高时,由于胎盘摄取增加,血浆铁周转率最初比未怀孕动物的基础水平增加了5倍。然而,随着持续高铁血症,摄取量受到调节,以维持胎儿铁处于正常水平。将这些数据与人类铁需求量进行比较,解释了大鼠中母体和胎儿缺铁的发生情况,但人类中仅出现母体缺铁。

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