Abstract
Background/Objectives:Maternal obesity increases the risk of poor pregnancy outcome including stillbirth, pre-eclampsia, fetal growth restriction and fetal overgrowth. These pregnancy complications are associated with dysfunctional syncytiotrophoblast, the transporting epithelium of the human placenta. Taurine, a β-amino acid with antioxidant and cytoprotective properties, has a role in syncytiotrophoblast development and function and is required for fetal growth and organ development. Taurine is conditionally essential in pregnancy and fetal tissues depend on uptake of taurine from maternal blood. We tested the hypothesis that taurine uptake into placental syncytiotrophoblast by the taurine transporter protein (TauT) is lower in obese women (body mass index (BMI)⩾30 kg m−2) than in women of ideal weight (BMI 18.5–24.9 kg m−2) and explored potential regulatory factors.Subjects/Methods:Placentas were collected from term (37–42-week gestation), uncomplicated, singleton pregnancies from women with BMI 19–49 kg m−2. TauT activity was measured as the Na+-dependent uptake of 3H-taurine into placental villous fragments. TauT expression in membrane-enriched placental samples was investigated by western blot. In vitro studies using placental villous explants examined whether leptin or IL-6, adipokines/cytokines that are elevated in maternal obesity, regulates TauT activity.Results:Placental TauT activity was significantly lower in obese women (BMI⩾30) than women of ideal weight (P<0.03) and inversely related to maternal BMI (19–49 kg m−2; P<0.05; n=61). There was no difference in TauT expression between placentas of ideal weight and obese class III (BMI⩾40) subjects. Long-term exposure (48 h) of placental villous explants to leptin or IL-6 did not affect TauT activity.Conclusions:Placental TauT activity at term is negatively related to maternal BMI. We propose that the reduction in placental TauT activity in maternal obesity could lower syncytiotrophoblast taurine concentration, compromise placental development and function, and reduce the driving force for taurine efflux to the fetus, thereby increasing the risk of poor pregnancy outcome.
Highlights
Around 1 in 5 women in the UK are obese at the start of pregnancy (body mass index (BMI): kg m−2) 430)[1] and 1 in 1000 expectant mothers has a BMI of ⩾ 50 at delivery.[2]
This study demonstrates that the placental taurine transporter protein (TauT) activity is negatively related to maternal BMI, with the greatest reduction in activity in women with a BMI ⩾ 40 compared with their ideal weight counterparts
Taurine facilitates the maintenance of syncytiotrophoblast and the reduction in TauT activity could contribute to placental dysfunction in maternal obesity and increase susceptibility to pregnancy complications
Summary
Around 1 in 5 women in the UK are obese at the start of pregnancy (body mass index (BMI): kg m−2) 430)[1] and 1 in 1000 expectant mothers has a BMI of ⩾ 50 (morbidly obese) at delivery.[2]. Successful pregnancy depends on appropriate development and function of the placenta to ensure adequate delivery of oxygen and nutrients from mother to fetus.[10] Pre-eclampsia and disorders of fetal growth (FGR, macrosomia) are associated with placental dysfunction,[11] and maternal obesity is likely to increase the risk of these pregnancy complications through effects on the placenta. Maternal circulating levels of leptin and IL-6 are increased, whereas adiponectin levels are reduced,[18,19,20] disrupting the normal adaptation in maternal endocrine milieu associated with pregnancy.[21] Maternal obesity is associated with heightened levels of placental oxidative[22] and nitrative[23] stress, conditions that dysregulate syncytiotrophoblast renewal in vitro.[24,25] plasma amino-acid concentrations in pregnant obese women may be different to women of ideal weight,[26] altering the availability of nutrients for maternal– fetal transfer across the placenta. We investigated whether long-term exposure to leptin and IL-6, which are elevated in maternal obesity, modulates placental TauT activity in vitro
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