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Obesity concerns 15% of the French population inlcuding women of reproductive age. Today, it has been well-established that maternal obesity is associated with complications such as repeated miscarriages, pre-eclampsia or gestational diabetes. In addition, the children born from obese or overweight mothers have a higher risk of developing obesity, cardiovascular diseases or metabolic syndromes as adults. The placenta, an interface between the mother and the fetus, ensures endocrine functions, exchanges and immune protection. With maternal obesity, the placenta is exposed to a lipotoxic and inflammatory environment.

An article that was published in JCEM by Marie-Noëlle Dieudonné and her partners of the Human Reproduction and Animal Model Teams (UMR 1198 BREED UVSQ-INRAE-ENVA) was focused on the study of the structure and function of the placenta in obese mothers without gestational diabetes.

Faced with chronic inflammation characterized by obesity, the placenta seems to adapt itself by decreasing the production of pro-inflammatory cytokines such as IL-6 and leptin associated with a reduced macrophagic and leucocyte infiltration. In addition, the exchange of nutrients is also modified in the placentas of obese women with a decrease 1) in the expression of GLUT1, a glucosetransporter, the SNAT1-2 amino acid transporters and 2) the density of fetal capillaries. Clinical data from this study showed no statistical difference between the weight of birth of newborns between obese women and nomal-weight women. These studies suggest that, faced with a deleterious environment such as that found with maternal obesity, the human placenta has a certain degree of plasticity and adapts to maintain normal fetal growth.