Effects of iron supplementation on growth, gut microbiota, metabolomics and cognitive development of rat pups.
Effects of iron supplementation on growth, gut microbiota, metabolomics and cognitive development of rat pups.
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DOI：
10.1371/journal.pone.0179713
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发表时间：
2017
期刊：
影响因子：
3.7
通讯作者：
Lönnerdal B
中科院分区：
文献类型：
--
作者：
Alexeev EE;He X;Slupsky CM;Lönnerdal B
铁缺乏在婴儿期很常见，因此建议补充铁。最近的报告表明，在已经充满铁的婴儿中补充铁可能会对生长、认知发育和发病率产生不利影响。正常和生长受限的大鼠幼仔从出生到出生后第20天（PD）每天给予铁（30或150 μg/d），并随访至PD 56。在PD 20时，测量血液学、组织铁和肝脏代谢组。在PD 20和PD 56评估血浆代谢组和结肠微生物生态学。T-迷宫（PD 35）和被动回避（PD 40）测试用于评估认知发育。铁补充剂以剂量依赖性方式增加两组的铁状态，但没有观察到铁对生长的显着影响。被动回避显着降低，只有在正常大鼠给予高铁与对照组相比。在正常和生长受限大鼠的血浆和肝脏中，过量的铁增加了3-羟基丁酸，减少了几种氨基酸，尿素和肌醇。虽然观察到正常和生长受限大鼠的肠道微生物群存在显著差异，但在补铁的情况下，观察到严格厌氧菌丰度的差异。过量的铁会对认知发育产生不利影响，这可能是代谢改变和/或肠道微生物群变化的结果。
Iron deficiency is common during infancy and therefore iron supplementation is recommended. Recent reports suggest that iron supplementation in already iron replete infants may adversely affect growth, cognitive development, and morbidity. Normal and growth restricted rat pups were given iron daily (30 or 150 μg/d) from birth to postnatal day (PD) 20, and followed to PD56. At PD20, hematology, tissue iron, and the hepatic metabolome were measured. The plasma metabolome and colonic microbial ecology were assessed at PD20 and PD56. T-maze (PD35) and passive avoidance (PD40) tests were used to evaluate cognitive development. Iron supplementation increased iron status in a dose-dependent manner in both groups, but no significant effect of iron on growth was observed. Passive avoidance was significantly lower only in normal rats given high iron compared with controls. In plasma and liver of normal and growth-restricted rats, excess iron increased 3-hydroxybutyrate and decreased several amino acids, urea and myo-inositol. While a profound difference in gut microbiota of normal and growth-restricted rats was observed, with iron supplementation differences in the abundance of strict anaerobes were observed. Excess iron adversely affects cognitive development, which may be a consequence of altered metabolism and/or shifts in gut microbiota.