D M Farley1, J Choi, D J Dudley, C Li, S L Jenkins, L Myatt, P W Nathanielsz. 1. Center for Pregnancy and Newborn Research, Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, University of Texas Health Science Center at San Antonio, Texas 78229-3900, USA. farleyd3@uthscsa.edu
Abstract
UNLABELLED: HYPOTHESIS AND STUDY OBJECTIVES: We hypothesized that maternal obesity is associated with increased placental amino acid transport and hyperleptinemia. Our objectives were to study placental amino acid transport and the effect of leptin on placental amino acid transport in vitro in the setting of maternal obesity. MATERIALS AND METHODS: Seven lean, BMI at entry 22.4, and seven obese, BMI at entry 31.5 (p < 0.001), pregnant women were studied at 39 weeks. We measured baseline and leptin-stimulated placental system A sodium-dependent neutral amino acid transporter (SNAT) activity, placental immunoreactive protein expression of SNAT, leptin and leptin receptor, and maternal and fetal plasma leptin concentrations, with significance set at p <or= 0.05. The primary outcome measure was placental SNAT activity. RESULTS: The obese group had decreased placental SNAT activity (p = 0.005), maternal hyperleptinemia (p = 0.01) and decreased syncytiotrophoblast expression of leptin receptor (p = 0.01) and SNAT-4 (p < 0.001). Placental amino acid uptake was significantly stimulated by leptin in the lean group as compared to the obese group. Maternal weight gain and offspring birth weights were not different between groups. CONCLUSION: Maternal obesity was accompanied by decreased placental SNAT activity associated with maternal hyperleptinemia and placental leptin resistance in spite of appropriate maternal weight gain and normally grown neonates. These findings suggest altered placental function that may have clinical implications in obese pregnant women.
UNLABELLED: HYPOTHESIS AND STUDY OBJECTIVES: We hypothesized that maternal obesity is associated with increased placental amino acid transport and hyperleptinemia. Our objectives were to study placental amino acid transport and the effect of leptin on placental amino acid transport in vitro in the setting of maternal obesity. MATERIALS AND METHODS: Seven lean, BMI at entry 22.4, and seven obese, BMI at entry 31.5 (p < 0.001), pregnant women were studied at 39 weeks. We measured baseline and leptin-stimulated placental system A sodium-dependent neutral amino acid transporter (SNAT) activity, placental immunoreactive protein expression of SNAT, leptin and leptin receptor, and maternal and fetal plasma leptin concentrations, with significance set at p <or= 0.05. The primary outcome measure was placental SNAT activity. RESULTS: The obese group had decreased placental SNAT activity (p = 0.005), maternal hyperleptinemia (p = 0.01) and decreased syncytiotrophoblast expression of leptin receptor (p = 0.01) and SNAT-4 (p < 0.001). Placental amino acid uptake was significantly stimulated by leptin in the lean group as compared to the obese group. Maternal weight gain and offspring birth weights were not different between groups. CONCLUSION:Maternal obesity was accompanied by decreased placental SNAT activity associated with maternal hyperleptinemia and placental leptin resistance in spite of appropriate maternal weight gain and normally grown neonates. These findings suggest altered placental function that may have clinical implications in obese pregnant women.
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