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Background <p>Exogenous corticosteroid exposure is common in premature infants and can interfere with normal developmental processes. It remains unknown if there are long-term alterations to cardiometabolic health following antenatal corticosteroid (ANCS) plus postnatal corticosteroid (PNCS) exposure.</p> Methods <p>Pregnant mice received intraperitoneal (IP) injections of dexamethasone 0.5 mg/kg on gestational days 15–16. Pups delivered naturally. On postnatal days (PD) 1–3, offspring received IP injections of dexamethasone 1.2 mg/kg or saline control. On PD 90, offspring were euthanized and organs harvested for study.</p> Results <p>Compared to ANCS alone, offspring exposed to ANCS + PNCS had decreased body weights, and lungs had alveolar simplification with increased mean linear intercept and decreased radial alveolar count. Exposure to ANCS + PNCS increased cardiomyocyte diameter compared to ANCS alone. Mice exposed to ANCS + PNCS had attenuation in liver mRNA levels in genes responsible for energy homeostasis including adiponectin, peroxisome proliferator-activated receptor gamma coactivator 1-alpha, and sirtuin 1, and alterations in free fatty acids.</p> Conclusions <p>Young adult mice exposed to ANCS + PNCS compared to ANCS alone have evidence of lung simplification, cardiomyocyte hypertrophy, and metabolism-related gene alterations in liver. This study is limited by the lack of a control group with no exposure to corticosteroids.</p> Impact <p><UnorderedList Mark="Bullet"> <ItemContent> <p>Antenatal + short course of postnatal corticosteroid exposure (3 days) results in long-term multi-organ system changes in adult mice.</p> </ItemContent> <ItemContent> <p>Mice exposed to antenatal + postnatal corticosteroids exhibit impaired alveolarization, cardiomyocyte hypertrophy, and metabolic alterations in young adulthood.</p> </ItemContent> <ItemContent> <p>Corticosteroids are a common exposure in premature infants and may contribute to long-term morbidities in this population.</p> </ItemContent> </UnorderedList></p>

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Long-term multi-organ system abnormalities in mice exposed to antenatal and postnatal corticosteroids

  • 期刊论文

  • 发表日期：

    2025年9月27日

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  • Julie A. Dillard,
  • Emily X. Royse,
  • Noah H. Hillman

摘要

Background

Exogenous corticosteroid exposure is common in premature infants and can interfere with normal developmental processes. It remains unknown if there are long-term alterations to cardiometabolic health following antenatal corticosteroid (ANCS) plus postnatal corticosteroid (PNCS) exposure.

Methods

Pregnant mice received intraperitoneal (IP) injections of dexamethasone 0.5 mg/kg on gestational days 15–16. Pups delivered naturally. On postnatal days (PD) 1–3, offspring received IP injections of dexamethasone 1.2 mg/kg or saline control. On PD 90, offspring were euthanized and organs harvested for study.

Results

Compared to ANCS alone, offspring exposed to ANCS + PNCS had decreased body weights, and lungs had alveolar simplification with increased mean linear intercept and decreased radial alveolar count. Exposure to ANCS + PNCS increased cardiomyocyte diameter compared to ANCS alone. Mice exposed to ANCS + PNCS had attenuation in liver mRNA levels in genes responsible for energy homeostasis including adiponectin, peroxisome proliferator-activated receptor gamma coactivator 1-alpha, and sirtuin 1, and alterations in free fatty acids.

Conclusions

Young adult mice exposed to ANCS + PNCS compared to ANCS alone have evidence of lung simplification, cardiomyocyte hypertrophy, and metabolism-related gene alterations in liver. This study is limited by the lack of a control group with no exposure to corticosteroids.

Impact

Antenatal + short course of postnatal corticosteroid exposure (3 days) results in long-term multi-organ system changes in adult mice.

Mice exposed to antenatal + postnatal corticosteroids exhibit impaired alveolarization, cardiomyocyte hypertrophy, and metabolic alterations in young adulthood.

Corticosteroids are a common exposure in premature infants and may contribute to long-term morbidities in this population.