ISSN 1662-4009 (online)

ESPE Yearbook of Paediatric Endocrinology (2021) 18 2.20 | DOI: 10.1530/ey.18.2.20

J Clin Endocrinol Metab. 2021 Mar 25;106(4):e1880–e1896. doi: 10.1210/clinem/dgaa660. PMID: 32936881.

By studying placentas from normal weight mothers and obese (non-diabetic) mothers, the authors found that maternal obesity was associated with lower expression of nutrient transporters (such as for glucose and amino acids), surprisingly fewer immune cells, and compromised endocrine function.

Maternal health and fetal development are closely linked via the placenta. Normal pregnancy is characterized by a proinflammatory state and this is exacerbated in pregnancies associated with maternal obesity. Maternal obesity may alter placental morphology and placental function by affecting the transport of nutrients such as glucose and amino acids. Previous studies have highlighted the impact of maternal obesity on the development and exchange functions of the placenta but the results are often conflicting and debatable. So, the aim of the present study was to evaluate the impact of maternal obesity on the inflammatory status, the morphology and levels of nutrient transporter expression and activity of the placenta.

The current findings were in contrast to the original hypothesis that there would be increased inflammatory markers (immune cells) in the placenta. The birth weight of the newborn was not affected. This suggests that the placenta has the capacity or plasticity to adapt to an obesogenic environment during pregnancy so that the fetus is protected. It is possible that the immune and inflammatory changes are dampened and nutrient exchange are differentially regulated in maternal obesity in the placenta as a protective mechanism for the fetus. This adaptive capacity or plasticity of the placenta is probably compromised in pregnancies where there is gestational diabetes.

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