Abstract
BackgroundFetal docosahexaenoic acid (DHA) supply relies on preferential transplacental transfer, which is regulated by placental DHA lipid metabolism. Maternal hyperglycemia and obesity associate with higher birthweight and fetal DHA insufficiency but the role of placental DHA metabolism is unclear.MethodsExplants from 17 term placenta were incubated with 13C-labeled DHA for 48 h, at 5 or 10 mmol/L glucose treatment, and the production of 17 individual newly synthesized 13C-DHA labeled lipids quantified by liquid chromatography mass spectrometry.ResultsMaternal BMI positively associated with 13C-DHA-labeled diacylglycerols, triacylglycerols, lysophospholipids, phosphatidylcholine and phosphatidylethanolamine plasmalogens, while maternal fasting glycemia positively associated with five 13C-DHA triacylglycerols. In turn, 13C-DHA-labeled phospholipids and triacylglycerols positively associated with birthweight centile. In-vitro glucose treatment increased most 13C-DHA-lipids, but decreased 13C-DHA phosphatidylethanolamine plasmalogens. However, with increasing maternal BMI, the magnitude of the glucose treatment induced increase in 13C-DHA phosphatidylcholine and 13C-DHA lysophospholipids was curtailed, with further decline in 13C-DHA phosphatidylethanolamine plasmalogens. Conversely, with increasing birthweight centile glucose treatment induced increases in 13C-DHA triacylglycerols were exaggerated, while glucose treatment induced decreases in 13C-DHA phosphatidylethanolamine plasmalogens were diminished.ConclusionsMaternal BMI and glycemia increased the production of different placental DHA lipids implying impact on different metabolic pathways. Glucose-induced elevation in placental DHA metabolism is moderated with higher maternal BMI. In turn, findings of associations between many DHA lipids with birthweight suggest that BMI and glycemia promote fetal growth partly through changes in placental DHA metabolism.
Highlights
Fetal docosahexaenoic acid (DHA) supply relies on preferential transplacental transfer, which is regu‐ lated by placental DHA lipid metabolism
While the bulk of endogenous 12C-DHA lipids was found in Phosphatidylethanola‐ mine plasmalogen (PE-P) (51.6% of total 12C-DHA lipids ± SD 8.4) followed by Phos‐ phatidylcholine (PC) (36.4% ± 9.9), TGs (6.7% ± 2), for freshly produced 13C-DHA lipids, most were found in TGs (38.7% of total 13C-DHA lipids ± 10.5) and PCs (30.7% ± 7.4) followed by PE-Ps (19.7% ± 3.7) (Fig. 1A)
Glucose‐treatment‐induced changes in placental DHA metabolism and birthweight we examined the association between glucose response and birthweight, since how the placenta responds to glucose during pregnancy might impact fetal growth
Summary
Fetal docosahexaenoic acid (DHA) supply relies on preferential transplacental transfer, which is regu‐ lated by placental DHA lipid metabolism. Transplacental DHA supply is regulated by placental lipid metabolism, but there is limited understanding of the specific pathways involved (Haggarty 2010; Lewis et al 2018). Understanding these mechanisms could pave the way to optimizing in-utero DHA supply for fetal development and designing strategies to rectify possible fetal DHA insufficiency in pathological conditions such as gestational diabetes (GDM) and maternal obesity (Haggarty 2010; Harris and Baack 2015). DHA and related derivatives act as signaling molecules (Larqué et al 2014; Herrera and Ortega-Senovilla 2018a; Delhaes et al 2018; Gallo et al 2017) that regulate fetal growth, inflammatory processes and labor onset (Duttaroy 2016; Rogers et al 2013; Farhat et al 2020), and protect against oxidative stress (Yavin et al 2002; Lessig and Fuchs 2009; Wang and Wang 2010)
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