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Updated: Jul 23, 2025
Quantitating Iron Transport Across the Mouse Placenta In Vivo Using Nonradioactive Iron Isotopes
Published on: May 10, 2022
Perinatal iron restriction is associated with changes in neonatal cardiac function and structure in a sex-dependent
Ronan M N Noble1,2, Claudia D Holody1,2, Andrew G Woodman3
1Department of Pediatrics, University of Alberta, Edmonton, Canada.
Insights
Iron deficiency in pregnant rats impacts offspring heart development, causing distinct systolic and diastolic dysfunctions in males and females, respectively. These findings highlight critical risks for neonatal cardiac health.
Area of Science:
- Developmental Biology
- Cardiovascular Physiology
- Nutritional Science
Background:
- Iron deficiency (ID) and anemia are prevalent in pregnancy and infancy, potentially affecting long-term cardiovascular health.
- Limited understanding exists regarding the specific impacts of perinatal iron deficiency on neonatal cardiac development and function.
Purpose of the Study:
- To investigate the effects of maternal iron deficiency on the cardiac development and function of offspring during the neonatal period.
- To identify sex-specific cardiac functional impairments and underlying molecular mechanisms in neonates exposed to iron deficiency in utero.
Main Methods:
- Female Sprague-Dawley rats received either an iron-restricted or iron-replete diet before and during gestation.
- Offspring cardiac function was evaluated using echocardiography on postnatal days 4, 14, and 28.
- Quantitative shotgun proteomics was performed on heart tissues from a separate cohort of offspring.
Main Results:
- Iron deficiency led to reduced body weight and increased relative heart weights in offspring across all assessed time points.
- Echocardiography revealed sex-specific cardiac dysfunction: males exhibited greater systolic impairment, while females showed greater diastolic impairment.
- Proteomic analysis indicated downregulation of structural proteins and enriched cellular stress responses in iron-deficient offspring, with more pronounced effects in males.
Conclusions:
- Perinatal iron deficiency induces functional cardiac changes in neonates, potentially representing maladaptive compensation to anemia.
- Systolic and diastolic dysfunctions are identified as comorbidities of perinatal iron deficiency anemia, with implications for neonatal cardiac health.
- Therapeutic strategies aimed at improving cardiac output may offer a means to mitigate the adverse effects of iron deficiency on neonatal organ development.
Abstract:
Iron deficiency (ID) is common during gestation and in early infancy and can alter developmental trajectories with lasting consequences on cardiovascular health. While the effects of ID and anemia on the mature heart are well documented, comparatively little is known about their effects and mechanisms on offspring cardiac development and function in the neonatal period. Female Sprague-Dawley rats were fed an iron-restricted or iron-replete diet before and during pregnancy. Cardiac function was assessed in a cohort of offspring on postnatal days (PD) 4, 14, and 28 by echocardiography; a separate cohort was euthanized for tissue collection and hearts underwent quantitative shotgun proteomic analysis. ID reduced body weight and increased relative heart weights at all time points assessed, despite recovering from anemia by PD28. Echocardiographic studies revealed unique functional impairments in ID male and female offspring, characterized by greater systolic dysfunction in the former and greater diastolic dysfunction in the latter. Proteomic analysis revealed down-regulation of structural components by ID, as well as enriched cellular responses to stress; in general, these effects were more pronounced in males. ID causes functional changes in the neonatal heart, which may reflect an inadequate or maladaptive compensation to anemia. This identifies systolic and diastolic dysfunction as comorbidities to perinatal ID anemia which may have important implications for both the short- and long-term cardiac health of newborn babies. Furthermore, therapies which improve cardiac output may mitigate the effects of ID on organ development.
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