Dept. of Pediatrics, Division of Neonatology, Baylor College of Medicine & Texas Children's Hospital, Houston, TX, USA.
Dept. of Obstetrics & Gynecology, Maternal-Fetal Medicine, Baylor College of Medicine & Texas Children's Hospital, Houston, TX, USA.
Pediatr Res. 2024 May;95(6):1410-1411. doi: 10.1038/s41390-024-03038-1. Epub 2024 Jan 23.
Uteroplacental insufficiency (UPI) is a major cause of fetal growth restriction (FGR). Leptin, an adipokine, has been shown to play a vital role in fetal organogenesis. There is evidence reporting leptin deficiency in preterm and growth-restricted fetuses. In this issue of Pediatric Research, Yuliana et al. report leptin expression and lung development in UPI-induced FGR rats. UPI-induced FGR rats expressed decreased lung leptin and had impaired lung development, as shown by decreased surface area and lung volume. They also found a significant association between lung radial alveolar count, serum leptin, von Willebrand factor, and specific metabolites on metabolomic analyses. Previous studies on leptin supplementation in vivo have been associated with improvement in lung maturation; supporting the evidence, that leptin improves lung growth and development in FGR and may have future therapeutic potential in the improvement of respiratory outcomes in these infants. Future studies to support evidence of this association in humans are warranted.
胎盘功能不全（UPI）是胎儿生长受限（FGR）的主要原因。瘦素作为一种脂肪细胞因子，在胎儿器官发生中起着至关重要的作用。有证据表明，早产儿和生长受限胎儿存在瘦素缺乏。在本期《儿科研究》中，Yuliana 等人报告了 UPI 诱导的 FGR 大鼠中瘦素的表达和肺发育情况。UPI 诱导的 FGR 大鼠肺组织中瘦素表达降低，肺发育受损，表现为肺表面积和肺容量减少。他们还发现，肺径向肺泡计数、血清瘦素、血管性血友病因子和代谢组学分析中的特定代谢物之间存在显著关联。先前关于体内补充瘦素的研究与改善肺成熟有关；这一证据支持了这样一种观点，即瘦素可改善 FGR 中的肺生长和发育，并可能在改善这些婴儿的呼吸结局方面具有未来的治疗潜力。有必要进行进一步的研究以支持这种关联在人类中的证据。
