Lönnerdal Bo
Department of Nutrition, University of California, Davis, Davis, CA
Am J Clin Nutr. 2017 Dec;106(Suppl 6):1575S-1580S. doi: 10.3945/ajcn.117.155820. Epub 2017 Oct 25.
Healthy, term, breastfed infants usually have adequate iron stores that, together with the small amount of iron that is contributed by breast milk, make them iron sufficient until ≥6 mo of age. The appropriate concentration of iron in infant formula to achieve iron sufficiency is more controversial. Infants who are fed formula with varying concentrations of iron generally achieve sufficiency with iron concentrations of 2 mg/L (i.e., with iron status that is similar to that of breastfed infants at 6 mo of age). Regardless of the feeding choice, infants' capacity to regulate iron homeostasis is important but less well understood than the regulation of iron absorption in adults, which is inverse to iron status and strongly upregulated or downregulated. Infants who were given daily iron drops compared with a placebo from 4 to 6 mo of age had similar increases in hemoglobin concentrations. In addition, isotope studies have shown no difference in iron absorption between infants with high or low hemoglobin concentrations at 6 mo of age. Together, these findings suggest a lack of homeostatic regulation of iron homeostasis in young infants. However, at 9 mo of age, homeostatic regulatory capacity has developed although, to our knowledge, its extent is not known. Studies in suckling rat pups showed similar results with no capacity to regulate iron homeostasis at 10 d of age when fully nursing, but such capacity occurred at 20 d of age when pups were partially weaned. The major iron transporters in the small intestine divalent metal-ion transporter 1 (DMT1) and ferroportin were not affected by pup iron status at 10 d of age but were strongly affected by iron status at 20 d of age. Thus, mechanisms that regulate iron homeostasis are developed at the time of weaning. Overall, studies in human infants and experimental animals suggest that iron homeostasis is absent or limited early in infancy largely because of a lack of regulation of the iron transporters DMT1 and ferroportin.
健康的足月儿，母乳喂养的婴儿通常有足够的铁储备，这些储备加上母乳中提供的少量铁，使他们在6个月龄之前铁含量充足。婴儿配方奶粉中达到铁充足的适宜铁浓度更具争议性。喂养不同铁浓度配方奶粉的婴儿，通常铁浓度为2 mg/L时可达到充足状态（即铁状态与6个月龄母乳喂养婴儿相似）。无论喂养方式如何选择，婴儿调节铁稳态的能力很重要，但与成人相比，人们对其了解较少，成人的铁吸收调节与铁状态呈负相关，且会强烈上调或下调。4至6个月龄时每天服用铁滴剂的婴儿与服用安慰剂的婴儿相比，血红蛋白浓度升高相似。此外，同位素研究表明，6个月龄时血红蛋白浓度高或低的婴儿之间铁吸收没有差异。这些研究结果共同表明，幼儿缺乏铁稳态的稳态调节。然而，据我们所知，9个月龄时稳态调节能力已经发展，但其程度尚不清楚。对乳鼠幼崽的研究也显示了类似结果，10日龄完全哺乳时没有调节铁稳态的能力，但20日龄部分断奶时出现了这种能力。小肠中的主要铁转运蛋白二价金属离子转运蛋白1（DMT1）和铁转运蛋白在10日龄时不受幼崽铁状态的影响，但在20日龄时受到铁状态的强烈影响。因此，调节铁稳态的机制在断奶时发育。总体而言，对人类婴儿和实验动物的研究表明，婴儿早期铁稳态不存在或有限，主要是因为缺乏对铁转运蛋白DMT1和铁转运蛋白的调节。
