Abstract
Molecular iron metabolism and its regulation are least well understood in the fetal and early postnatal periods of mammalian ontogenic development. The scope of this review is to summarize recent progress in uncovering the molecular mechanisms of fetal iron homeostasis, introduce the molecules involved in iron transfer across the placenta, and briefly explain the role of iron transporters in the absorption of this microelement during early postnatal life. These issues are discussed and parallels are drawn with the relatively well-established system for elemental and heme iron regulation in adult mammals. We conclude that detailed investigations into the regulatory mechanisms of iron metabolism at early stages of development are required in order to optimize strategies to prevent neonatal iron deficiency. We propose that newborn piglets represent a suitable animal model for studies on iron deficiency anemia in neonates.
Highlights
Molecular iron metabolism and its regulation are least well understood in the fetal and early postnatal periods of mammalian ontogenic development
Considering that the majority of iron in the body is present in the form of heme-containing proteins, it is not surprising that defects in heme synthesis and/or degradation result in perturbations of systemic iron homeostasis, such as iron overload observed in erythropoietic porphyria [54], or tissue iron redistribution associated with heme oxygenase 1 (HO-1) deficiency [55], respectively
The aim of this review was to compile and analyze the limited information available on the role of genes involved in iron metabolism during the initial stages of ontogenic mammalian development
Summary
The likely importance of hepcidin in iron homeostasis was first noted by Pigeon et al [8], who observed that levels of hepcidin mRNA are enhanced in murine hepatocytes in response to iron and after lipopolysaccharide treatment. In parallel with the regulation of organismal iron homeostasis via hepcidin, a two-component system exists that acts to maintain cellular iron availability while preventing its toxicity In mammalian cells, this system is composed of two iron regulatory proteins (IRP1 and IRP2), which posttranscriptionally regulate the expression of iron-related genes by binding to specific sequences called iron responsive elements (IREs) located within the untranslated regions (UTRs) of target mRNAs. Either of the two IRPs can inhibit translation when bound to the single 50 UTR IRE in the mRNAs encoding iron export (ferroportin— Fpn) and storage (ferritin—Ft) proteins, or they can prevent mRNA degradation when bound to the multiple IREs within the 30UTR of the mRNA encoding the transferrin receptor 1 (TfR1), an iron uptake molecule. This finding indicates that, IRPs are indispensable for the control of basal expression of iron transporters in the duodenum, they are not responsible for their regulation in response to increased body iron requirement, e.g., during erythropoiesis [45]
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