Protein expression of fatty acid transporter 2 is polarized to the trophoblast basal plasma membrane and increased in placentas from overweight/obese women

• Maternal and fetal circulating plasma NEFA levels do not correlate at term.
• FATP2 and FATP4 expressions were polarized to the basal plasma membrane (BPM) compared to microvillous membrane (MVM).
• FATP2 expression on the BPM was positively correlated with maternal BMI.
• Fatty acid transporters localized in syncytial plasma membranes are likely important for determining net lipid transfer.

BackgroundObese and overweight women are more likely to deliver a large infant or an infant with increased adiposity, however the underlying mechanisms are not well established. We tested the hypothesis that placental capacity to transport fatty acid is increased in overweight/obese women.MethodsPregnant women with body mass index (BMI) ranging from 18.4 to 54.3 kg/m2 and with uncomplicated term pregnancies were recruited for collection of blood samples and placental tissue. Maternal and fetal levels of non-esterified fatty acids (NEFAs) were measured in plasma. The expression and localization of CD36/fatty acid translocase (FAT), fatty acid transport protein (FATP)2, and FATP4 was determined in fixed placental tissue and in isolated syncytiotrophoblast plasma membranes from normal and high BMI mothers.ResultsMaternal and fetal plasma NEFA levels did not correlate (n = 42). FATP2 and FATP4 expressions were higher in the basal plasma membrane (BPM) compared to the microvillous membrane (P < 0.001; n = 7) per unit membrane protein. BPM expression of FATP2 correlated with maternal BMI (P < 0.01; n = 30); there was no association between CD36/FAT or FATP4 expression and maternal BMI.ConclusionThe polarization of FATPs to the BPM will facilitate fatty acid transfer across the placenta. In overweight/obese pregnancies, the increased FATP2 expression could contribute to increased fatty acid delivery to the fetus and while we have no direct data we speculate that this could lead accelerated fetal growth or increased fat deposition.