The effect of feeding a low iron diet prior to and during gestation on fetal and maternal iron homeostasis in two strains of rat.
The effect of feeding a low iron diet prior to and during gestation on fetal and maternal iron homeostasis in two strains of rat.
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DOI：
10.1186/1477-7827-11-32
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发表时间：
2013-05-01
期刊：
影响因子：
--
通讯作者：
McMullen S
中科院分区：
文献类型：
--
作者：
Cornock R;Gambling L;Langley-Evans SC;McArdle HJ;McMullen S
怀孕期间缺铁性贫血是一个全球性问题，对孕产妇和儿童健康造成短期和长期影响。动物模型已经证明，发育中的胎儿容易受到母体铁限制的影响，影响出生后的代谢和血压调节。虽然不同模型的长期结局相似，但不同模型之间的机制事件的共性尚不清楚。本研究探讨了铁缺乏对母体和胎儿铁稳态的影响，在两个品系的大鼠。Wistar（n=20）和Rowett Hooded Lister（RHL，n=19）大鼠在妊娠前和妊娠期间喂食对照或低铁饮食4周。在妊娠第21天收集组织用于分析铁含量以及调节蛋白和转运蛋白的mRNA/蛋白表达。响应于低铁饮食的母体肝脏铁含量的减少与运铁蛋白受体表达的上调和两种菌株的肝脏中铁调素表达的减少相关，这将预期促进通过肠道的铁吸收增加和肝脏中铁的周转增加。转铁蛋白和DMT 1 +IRE的胎盘表达也上调，表明适应性反应，以确保胎儿铁的可用性。不同品系间肝脏母胎铁含量差异较大。从Wistar大鼠肝脏中存在的铁的量较高，不能解释的肠铁转运蛋白的表达差异，而可能反映了更大的母胎转移RHL大鼠胎盘铁转运蛋白的表达增加，在这个菌株。我们的研究结果表明，两种品系的大鼠在怀孕期间的铁稳态存在实质性差异，铁缺乏对胎儿的影响各不相同。虽然在怀孕期间不同的营养限制模型中观察到了共同的发育过程和途径，但这项研究表明了母体适应的差异，这可能会影响程序化反应的轨迹。
Iron deficiency anaemia during pregnancy is a global problem, with short and long term consequences for maternal and child health. Animal models have demonstrated that the developing fetus is vulnerable to maternal iron restriction, impacting on postnatal metabolic and blood pressure regulation. Whilst long-term outcomes are similar across different models, the commonality in mechanistic events across models is unknown. This study examined the impact of iron deficiency on maternal and fetal iron homeostasis in two strains of rat. Wistar (n=20) and Rowett Hooded Lister (RHL, n=19) rats were fed a control or low iron diet for 4 weeks prior to and during pregnancy. Tissues were collected at day 21 of gestation for analysis of iron content and mRNA/protein expression of regulatory proteins and transporters. A reduction in maternal liver iron content in response to the low iron diet was associated with upregulation of transferrin receptor expression and a reduction in hepcidin expression in the liver of both strains, which would be expected to promote increased iron absorption across the gut and increased turnover of iron in the liver. Placental expression of transferrin and DMT1+IRE were also upregulated, indicating adaptive responses to ensure availability of iron to the fetus. There were considerable differences in hepatic maternal and fetal iron content between strains. The higher quantity of iron present in livers from Wistar rats was not explained by differences in expression of intestinal iron transporters, and may instead reflect greater materno-fetal transfer in RHL rats as indicated by increased expression of placental iron transporters in this strain. Our findings demonstrate substantial differences in iron homeostasis between two strains of rat during pregnancy, with variable impact of iron deficiency on the fetus. Whilst common developmental processes and pathways have been observed across different models of nutrient restriction during pregnancy, this study demonstrates differences in maternal adaptation which may impact on the trajectory of the programmed response.
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