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Using Multi-fluorinated Bile Acids and In Vivo Magnetic Resonance Imaging to Measure Bile Acid Transport
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Using Multi-fluorinated Bile Acids and In Vivo Magnetic Resonance Imaging to Measure Bile Acid Transport

Published on: November 27, 2016

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Maternal bile acid transporter deficiency promotes neonatal demise

Yuanyuan Zhang1, Fei Li2, Yao Wang1

  • 1Department of Pharmaceutical Sciences, St Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, Tennessee 38105, USA.

Nature Communications
|September 30, 2015
PubMed

Insights

Maternal cholestasis during pregnancy causes neonatal death by affecting lung development. Targeting pulmonary bile acids may improve neonatal survival in cases of intrahepatic cholestasis of pregnancy (ICP).

Area of Science:

  • Reproductive biology
  • Neonatal physiology
  • Hepatology

Background:

  • Intrahepatic cholestasis of pregnancy (ICP) affects 0.4-5% of pregnancies globally, leading to adverse neonatal outcomes.
  • Neonatal mortality is a significant concern in ICP, necessitating research into underlying mechanisms.

Purpose of the Study:

  • To investigate the mechanisms by which maternal cholestasis leads to neonatal death.
  • To identify potential therapeutic targets for improving neonatal survival in ICP.

Main Methods:

  • Utilized a mouse model with Abcb11 deficiency to induce maternal cholestasis.
  • Analyzed pulmonary bile acid levels and surfactant structure in neonates.
  • Investigated the effect of Nr1i2 deficiency in combination with Abcb11 deficiency.

Main Results:

  • Maternal cholestasis (Abcb11 deficiency) caused neonatal death within 24 hours due to pulmonary hypoxia and atelectasis.
  • Neonates exhibited elevated pulmonary bile acids and disrupted pulmonary surfactant structure.
  • Co-deficiency of Abcb11 and Nr1i2 reduced maternal bile acids and improved neonatal survival.

Conclusions:

  • Pulmonary bile acids are identified as a key factor disrupting pulmonary surfactant structure in neonates of ICP.
  • Findings suggest therapeutic interventions targeting pulmonary bile acids could ameliorate neonatal respiratory failure in ICP.
  • This study provides critical insights into the pathophysiology of neonatal respiratory distress associated with elevated maternal bile acids.

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