Placental dysfunction in maternal obesity is a key mechanism of fetal programming of metabolic syndrome

The placenta is a critical link between the maternal and fetal bodies and is therefore a central organ to be studied in the context of fetal programming of the metabolic syndrome. Obesity causes placental dysfunction through various mechanisms, including impaired expression of fatty acid transporter genes, esterification en zymes and lipid deposition. The resulting lipotoxic environment, by increasing proinflammatory markers in maternal plasma and placenta, activating placental inflammatory signaling, and upregulating proinflammatory genes, determines intraplacental functional abnormalities and programs long-term metabolic disorders in the fetus. Abnormalities in placental amino acid transport and mitochondrial dysfunction are observed. Evidence of increased placental reactive oxygen species (ROS) levels, protein nitrosylation, altered cytokine concentrations, and increased lipid peroxidation with subsequent endothelial dysfunction of the placental vascular network is recorded. Studies on hormone levels in placental tissues and fetal cord blood in obese women demonstrate various metabolic shifts. Of particular interest is the consideration of sexual dimorphism in the context of fetal programming, showing a cascade of differences in the genetic, metabolic, and inflammatory profile depending on the sex of the fetus. These changes represent mechanisms contributing to placental dysfunction and program ming of obesity and metabolic diseases in the fetus. However, many aspects of placental dysfunction in maternal obesity require further investigation.