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Fetal Echocardiography and Pulsed-wave Doppler Ultrasound in a Rabbit Model of Intrauterine Growth Restriction
Published on: June 29, 2013
Uteroplacental insufficiency decreases leptin expression and impairs lung development in growth-restricted newborn
Merryl Esther Yuliana1, Hsiu-Chu Chou2, Emily Chia-Yu Su3,4
1International PhD Program in Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Insights
Uteroplacental insufficiency (UPI) in rats caused intrauterine growth restriction (IUGR), leading to reduced leptin and impaired lung development. Leptin supplementation may aid lung development in IUGR neonates.
Area of Science:
- Reproductive Biology
- Neonatal Physiology
- Developmental Biology
Background:
- Uteroplacental insufficiency (UPI) is a primary cause of intrauterine growth restriction (IUGR) in neonates.
- Leptin plays a crucial role in fetal development and lung maturation.
- The impact of UPI-induced IUGR on leptin expression and lung development requires further investigation.
Purpose of the Study:
- To investigate the effects of UPI-induced IUGR on leptin expression and lung development in neonatal rats.
- To determine the relationship between leptin levels and lung development parameters in IUGR offspring.
Main Methods:
- Time-dated Sprague-Dawley rats underwent either UPI surgery (IUGR group) or sham surgery (control group).
- Offspring were assessed on postnatal days 0 and 7 for serum leptin, lung leptin, and leptin receptor levels.
- Lung tissue underwent immunohistochemistry, PCNA, western blot, and metabolomic analyses to evaluate development.
Main Results:
- UPI-induced IUGR significantly decreased serum leptin, lung leptin, and leptin receptor levels.
- IUGR offspring exhibited impaired lung development, characterized by reduced surface area, volume, and alveolarization.
- Significant correlations were observed between serum leptin, lung development markers, and specific metabolites in the IUGR group.
Conclusions:
- Leptin expression is reduced in neonatal rats with UPI-induced IUGR, correlating with impaired lung development.
- Leptin may play a critical role in promoting lung development during the postnatal period in IUGR neonates.
- Leptin supplementation presents a potential therapeutic strategy for improving lung development in IUGR infants.
Background:
The study aimed to analyze the effect of uteroplacental insufficiency (UPI) on leptin expression and lung development of intrauterine growth restriction (IUGR) rats.
Methods:
On day 17 of pregnancy, time-dated Sprague-Dawley rats were randomly divided into either an IUGR group or a control group. Uteroplacental insufficiency surgery (IUGR) and sham surgery (control) were conducted. Offspring rats were spontaneously delivered on day 22 of pregnancy. On postnatal days 0 and 7, rats' pups were selected at random from the control and IUGR groups. Blood was withdrawn from the heart to determine leptin levels. The right lung was obtained for leptin and leptin receptor levels, immunohistochemistry, proliferating cell nuclear antigen (PCNA), western blot, and metabolomic analyses.
Results:
UPI-induced IUGR decreased leptin expression and impaired lung development, causing decreased surface area and volume in offspring. This results in lower body weight, decreased serum leptin levels, lung leptin and leptin receptor levels, alveolar space, PCNA, and increased alveolar wall volume fraction in IUGR offspring rats. The IUGR group found significant relationships between serum leptin, radial alveolar count, von Willebrand Factor, and metabolites.
Conclusion:
Leptin may contribute to UPI-induced lung development during the postnatal period, suggesting supplementation as a potential treatment.
Impact:
The neonatal rats with intrauterine growth restriction (IUGR) caused by uteroplacental insufficiency (UPI) showed decreased leptin expression and impaired lung development. UPI-induced IUGR significantly decreased surface area and volume in lung offspring. This is a novel study that investigates leptin expression and lung development in neonatal rats with IUGR caused by UPI. If our findings translate to IUGR infants, leptin may contribute to UPI-induced lung development during the postnatal period, suggesting supplementation as a potential treatment.
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