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Introduction <p>Due to the global obesity crisis, increasing numbers of women enter pregnancy with overweight or obesity. Their offspring are at greater risk of respiratory complications at birth due to metabolic changes that impact lung development that may reduce capacity for surfactant production. We hypothesize that a high-fat-high-energy diet (HF-HED) negatively impacts late gestation fetal lung development.</p> Methods <p>Female baboons were randomly assigned to Control (metabolizable energy content, MEC = 3.07 kcal/g, 12% from fat; <i>n</i> = 5 M, 3 F fetuses) or high-fat high-energy diet (MEC = 4.03 kcal/g, 45% energy from fat; <i>n</i> = 6 M, 6 F fetuses) before and throughout pregnancy. Fetal lung tissue was collected at 0.9 gestation (term, 184 d). qRT-PCR and immunohistochemistry were utilized to measure expression of key molecules involved in surfactant maturation, the transition to air breathing.</p> Results <p>HF-HED decreased fetal type-II alveolar epithelial cells and reduced lung surfactant protein expression (<i>SFTPB, SFTPC</i>, and <i>SFTPD</i>). The rate-limiting genes involved in surfactant phospholipid production <i>PCY1TA</i> and <i>ABCA3</i> was reduced. Genes involved in water (<i>AQP1</i>) and sodium (<i>ATP1A1</i> and <i>SCNN1B</i>) transport were also downregulated, indicating impaired lung liquid reabsorption.</p> Conclusion <p>These data indicate that a maternal obesogenic diet impairs surfactant maturation and reduces the capacity for lung liquid reabsorption, increasing the risk of neonatal respiratory complications.</p> <p></p>

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Maternal high-fat high-energy diet impairs surfactant maturation in the non-human primate fetal lung

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月27日

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  • Mitchell C. Lock,
  • Hillary F. Huber,
  • Cun Li,
  • Sandra Orgeig,
  • Peter W. Nathanielsz,
  • Janna L. Morrison

摘要

Introduction

Due to the global obesity crisis, increasing numbers of women enter pregnancy with overweight or obesity. Their offspring are at greater risk of respiratory complications at birth due to metabolic changes that impact lung development that may reduce capacity for surfactant production. We hypothesize that a high-fat-high-energy diet (HF-HED) negatively impacts late gestation fetal lung development.

Methods

Female baboons were randomly assigned to Control (metabolizable energy content, MEC = 3.07 kcal/g, 12% from fat; n = 5 M, 3 F fetuses) or high-fat high-energy diet (MEC = 4.03 kcal/g, 45% energy from fat; n = 6 M, 6 F fetuses) before and throughout pregnancy. Fetal lung tissue was collected at 0.9 gestation (term, 184 d). qRT-PCR and immunohistochemistry were utilized to measure expression of key molecules involved in surfactant maturation, the transition to air breathing.

Results

HF-HED decreased fetal type-II alveolar epithelial cells and reduced lung surfactant protein expression (SFTPB, SFTPC, and SFTPD). The rate-limiting genes involved in surfactant phospholipid production PCY1TA and ABCA3 was reduced. Genes involved in water (AQP1) and sodium (ATP1A1 and SCNN1B) transport were also downregulated, indicating impaired lung liquid reabsorption.

Conclusion

These data indicate that a maternal obesogenic diet impairs surfactant maturation and reduces the capacity for lung liquid reabsorption, increasing the risk of neonatal respiratory complications.