Analytical review uncovers how placental dysfunction alters fetal adipose tissue programming, highlighting the placenta–adipose axis as a driver of long-term metabolic diseases.
The placenta plays a central role in the developmental programming of fetal metabolic health by regulating nutrient transfer, endocrine signalling, and responses to changes in the maternal environment. Increasing evidence indicates that placental dysfunction associated with maternal obesity, gestational diabetes mellitus, hypoxia, and inflammation may influence not only fetal growth but also the development and long-term function of adipose tissue. The aim of this study was to analyse the current concept of the placenta–adipose tissue axis and summarize recent evidence regarding the role of placental dysfunction in the developmental programming of adipose tissue and susceptibility to metabolic diseases. An analytical review of recent scientific publications in placental biology, developmental programming, adipose tissue morphology, endocrinology, and metabolic research was conducted. The available evidence suggests that alterations in placental nutrient transport, lipid metabolism, endocrine signalling, and inflammatory pathways may affect adipogenesis, adipose progenitor cell development, and adipose tissue plasticity. These changes may contribute to persistent disturbances in energy homeostasis and increase susceptibility to obesity, insulin resistance, and other metabolic disorders later in life. The placenta–adipose tissue axis represents a promising conceptual framework for understanding the developmental origins of metabolic diseases and may provide new opportunities for the identification of early biomarkers and preventive strategies.
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T.V. Pankiv (2026) studied this question.
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