Abstract
Leptin is secreted by the placenta and has a multi-facetted role in the regulation of functions related to pregnancy. Metabolic disorders and insufficient homeostatic compensatory mechanisms involving leptin during pregnancy play a decisive role in the development of pre-eclampsia (PE) and give rise to compromised intrauterine growth conditions and aberrant birth weight of offspring. This review was compiled to elucidate the metabolic background of PE and its relationship with adverse intrauterine growth conditions through the examination of leptin as well as to describe possible mechanisms linking leptin to fetal growth restriction. This review illustrates that leptin in PE is dysregulated in maternal, fetal, and placental compartments. There is no single set of unifying mechanisms within the spectrum of PE, and regulatory mechanisms involving leptin are specific to each situation. We conclude that dysregulated leptin is involved in fetal growth at many levels through complex interactions with parallel pregnancy systems and probably throughout the entirety of pregnancy.
Highlights
Normal fetal growth depends on complex interactions between maternal, placental, and fetal environments
We examine the latest information available about leptin action in PE to support the idea that dysregulated leptin is linked to aberrant intrauterine growth and subsequent low birth weight of offspring
Abnormalities within HIF1alpha’s oxygen sensing properties, rather than hypoxia, may promote conditions for the development of PE [94]. It remains unclear what impact this has on fetal growth, as pregnancies complicated by fetal growth restriction (FGR) have not typically been characterized by high placental leptin mRNA expression and leptin protein levels [56], which suggests that pregnancies complicated by FGR do not suffer from placental hypoxia as in PE
Summary
Normal fetal growth depends on complex interactions between maternal, placental, and fetal environments. An introductory overview of PE, fetal growth restriction (FGR), leptin and its receptors, and the role of leptin in normal pregnancy is provided. This is followed by a comprehensive examination of leptin action in PE and its association with FGR under the subsections of maternal, fetal, and placental leptin. Leptin from any origin (maternal, placental, fetal or neonatal
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