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Association between maternal iron deficiency and delayed neonatal auditory maturation and altered cochlear synaptic
1Department of Gynaecology and Obstetrics, First Affiliated Hospital of China Medical University, Shenyang, China.
Insights
Maternal iron deficiency (ID) during pregnancy may impact infant hearing development. This study found prenatal ID linked to delayed auditory maturation in newborns, suggesting iron supplementation could be beneficial.
Area of Science:
- Neuroscience
- Developmental Biology
- Nutritional Science
Background:
- Iron is crucial for fetal auditory system development.
- The effects of non-anemic prenatal iron deficiency (ID) on neonatal auditory function are not well understood.
- This study investigates mechanisms linking maternal ID to offspring auditory maturation.
Purpose of the Study:
- To explore how maternal iron deficiency affects fetal auditory system development.
- To identify potential cellular and molecular mechanisms involved in this process.
- To assess the association between maternal iron status and neonatal auditory function.
Main Methods:
- Analysis of population data from 696 mother-infant pairs.
- Establishment of iron deficiency mouse models during pregnancy.
- Cellular experiments and metabolomics analysis.
Main Results:
- Maternal iron status negatively correlated with auditory brainstem response (ABR) latencies and intervals in infants.
- Prenatal ID in mice led to impaired auditory function, reduced ribbon synapses, mitochondrial damage, and altered cochlear supporting cell metabolism.
- Pyruvate metabolism was downregulated in iron-deficient models, and pyruvate supplementation partially restored synaptic function.
Conclusions:
- Non-anemic maternal iron deficiency may be associated with delayed neonatal auditory maturation.
- Prenatal iron deficiency can impair cochlear development and energy metabolism.
- Iron supplementation during pregnancy may be important for optimal neonatal auditory outcomes, though further validation is needed.
Background:
Iron is a key nutrient for the development of the fetal auditory system. However, the potential impact of non-anemic prenatal iron deficiency (ID) on neonatal auditory function remains unclear. This study aimed to systematically explore the potential mechanisms by which maternal ID may affect auditory maturation of offspring.
Methods:
We analyzed population data from 696 mother-infant pairs, established ID mouse models (C57BL/6 J) during pregnancy, and conducted cellular experiments.
Results:
In the human cohort, maternal serum ferritin (SF) and hemoglobin (Hb) were significantly negatively associated with the latency (ms) of auditory brainstem response (ABR) waves I, III, and V, as well as intervals (ms) of waves I-III, III-V, and I-V and summating potential/action potential ratios (%). Neonatal SF partially mediated the association between maternal iron status and auditory function, with mediation effects ranging from 28.57 to 76.32%. In mouse models, prenatal ID was associated with decreased wave I amplitude and extended latency in offspring, along with reduced ribbon synapses in inner hair cells, mitochondrial damage, and decreased enzyme activity in supporting cells. A metabolomics analysis revealed significant downregulation of pyruvate levels in the ID group, and exogenous supplementation with sodium pyruvate partially restored ribbon synaptic function. Collectively, prenatal ID may reduce fetal iron reserves, impair energy metabolism of cochlear supporting cells, inhibit ribbon synaptic maturation, and potentially contribute to auditory dysfunction.
Conclusion:
Our findings suggest that non-anemic maternal ID may be associated with delayed neonatal auditory maturation, highlighting the potential importance of iron intervention during pregnancy for improving neonatal auditory outcomes; however, causal relationships cannot be established from the observational human data, and the animal/cellular findings should be interpreted as supportive evidence requiring further validation.
