Hirschmugl, Birgit, Crozier, Sarah, Matthews, Nina, Kitzinger, Eva, Klymiuk, Ingeborg, Inskip, Hazel, Harvey, Nicholas, Cooper, Cyrus, Sibley, Colin P., Glazier, Jocelyn D., Wadsack, Christian, Godfrey, Keith, Desoye, Gernot and Lewis, Rohan (2018) Relation of placental alkaline phosphatase expression in human term placental to maternal and offspring fat mass. International Journal of Obesity, 42 (6), 1202-1210. (doi:10.1038/s41366-018-0136-8).
Abstract
Introduction: alkaline phosphatase is implicated in intestinal lipid transport and to the development of obesity. Placental alkaline phosphatase is localised to the microvillous plasma membrane of the placental syncytiotrophoblast at the maternal-fetal interface, but its role is unclear. We investigated the relations of placental alkaline phosphatase activity and mRNA expression with maternal body composition and offspring fat mass in humans. Methods: term human placentas from the UK Birthright cohort (n=52) and the Southampton Women’s Survey (SWS)(n=95) were studied. In the Birthright cohort, alkaline phosphatase activity was measured in placental microvillous plasma membrane vesicles. In the SWS, alkaline phosphatase mRNA was measured using Nanostring. Alkaline phosphatase gene expression was compared to other lipid related genes. Results: in Birthright samples placental microvillous plasma membrane alkaline phosphatase activity was positively associated with maternal triceps skinfold thickness and BMI (β=0.04 (95%CI 0.01, 0.06) and β=0.02 (0.00, 0.03) µmol/mg protein/min per SD, P=0.002 and P=0.05, respectively) adjusting for potential confounders. In SWS samples placental alkaline phosphatase mRNA expression in term placenta was positively associated with maternal triceps skinfold (β=0.24 (0.04, 0.44) SD/SD, P=0.02), had no association with neonatal %fat mass (β=0.01 (-0.20, 0.21) SD/SD, P=0.93) and was negatively correlated with %fat mass at ages 4 (β=-0.28 (-0.52, -0.04) SD/SD, P=0.02), 6-7 (β=-0.25 (-0.49, -0.02) SD/SD, P=0.03) years. When compared with placental expression of other genes, alkaline phosphatase expression was positively related to genes including the lysophosphatidylcholine transporter MFSD2A (major facilitator superfamily domain containing 2A, P<0.001) and negatively related to genes including the fatty acid transport proteins 2 and 3 (P=0.001, P<0.001). Conclusions: our findings suggest relationships between placental alkaline phosphatase and both maternal and childhood adiposity. The inverse relationship between placental alkaline phosphatase gene expression and childhood %fat mass suggests placental alkaline phosphatase may help to protect the fetus from the adverse effects of maternal obesity.
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