Fig. 5

Summary of the influence of fetal sex in ester, ether and plasmalogen PC and PE containing DHA and ARA in the maternal–fetal unit in response to maternal obesity. The phenotype of obese mothers includes reduced ester, ether and plasmalogen PC and PE containing DHA but not those phospholipids containing ARA regardless of fetal sex. In obese mother carrying a male baby: in placenta, all the ester linked PC containing DHA and ARA are decreased by obesity and only one ether PC with DHA species while all ester linked PE were unchanged suggesting downregulated PEMT enzyme activity to convert PE into PC. In addition, decreased LPC-DHA is likely due to decreased iPLA2 protein expression. In fetal circulation, several ester PC DHA and ARA species and ester, ether and plasmalogen PE with DHA and ARA were reduced suggesting a defect of LCPUFA transfer capacity. In obese mother carrying a female baby: in placenta, all PE species with DHA and ARA were decreased but not PC species and LPCAT4 expression was lower. These results suggest an upregulated PEMT activity to maintain PC production. No change was observed in female umbilical cord. By decreasing all ether and plasmalogen PE, species considered as reservoir for DHA and ARA in the placenta, female fetuses of obese mothers show a high fetal–placental adaptability and placental reserve capacity that can maintain the PC-LCPUFA synthesis and the transfer of these crucial species to the fetus to preserve growth and brain development