Fig. 7

Placental DHA metabolism regulates the amount of DHA available for the synthesis of signaling molecules and for fetal supply. The conversion of DHA into DHA-COA and lipids such as diacylglycerols (DG), triacylglycerols (TG), or phospholipids such as phosphatidylcholine (PC) or phosphatidylethanolamine-plasmalogen (PE-P) traps DHA in the placenta and prevents re-export. DHA released from lipids (blue arrows), may be remade into lipids, used to form signaling molecules such as eicosanoids or exported to the fetus. In our experiments, increased BMI (purple) and in-vitro glucose treatment (pink) was associated with the increased synthesis of most ¹³C-DHA-lipids, suggesting that upstream processes such as activation into DHA-CoA or the early stages of lipid synthesis may be affected. Glucose treatment also decreased PE-Ps suggesting a separate PE-P specific process may also be affected. Fasting glycemia (purple) is only associated with TGs, suggesting a link with TG specific processes. DHA lipid metabolism and change in response to glucose treatment, was also associated with birthweight centile (shown by brown arrows) suggesting that placental DHA metabolism could influence birthweight