Characterization of choline transporters in the human placenta over gestation

Baumgartner, Heidi K.; Trinder, Kinsey M.; Galimanis, Carly E.; Post, Annalisa; Phang, Tzu L.; Ross, Randal G.; Winn, Virginia D.

doi:10.1016/j.placenta.2015.10.001

Cited by 22 publications

(18 citation statements)

References 39 publications

(35 reference statements)

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“…Mothers received information on diets higher in choline, but dietary intake was not estimated because of the low relationship of self-reported intake to maternal choline levels in pregnant women, r = 0.2 (Wu et al ., 2012). The placental choline transporter CLT1 produces amniotic fluid levels approximately twice maternal plasma levels (Ilcol et al ., 2003; Baumgartner et al ., 2015). Uptake is proportional to maternal plasma concentration, which suggests that higher peak levels may be important determinants of amniotic fluid levels (Iwao et al ., 2016).…”

Section: Participants and Methodsmentioning

confidence: 99%

Interaction of maternal choline levels and prenatal Marijuana's effects on the offspring

et al. 2019

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BackgroundThis study investigated whether higher maternal choline levels mitigate effects of marijuana on fetal brain development. Choline transported into the amniotic fluid from the mother activates α7-nicotinic acetylcholine receptors on fetal cerebro-cortical inhibitory neurons, whose development is impeded by cannabis blockade of their cannabinoid-1(CB1) receptors.MethodsMarijuana use was assessed during pregnancy from women who later brought their newborns for study. Mothers were informed about choline and other nutrients, but not specifically for marijuana use. Maternal serum choline was measured at 16 weeks gestation.ResultsMarijuana use for the first 10 weeks gestation or more by 15% of mothers decreased newborns' inhibition of evoked potentials to repeated sounds (d’ = 0.55, p < 0.05). This effect was ameliorated if women had higher gestational choline (rs = −0.50, p = 0.011). At 3 months of age, children whose mothers continued marijuana use through their 10th gestational week or more had poorer self-regulation (d’ = −0.79, p < 0.05). This effect was also ameliorated if mothers had higher gestational choline (rs = 0.54, p = 0.013). Maternal choline levels correlated with the children's improved duration of attention, cuddliness, and bonding with parents.ConclusionsPrenatal marijuana use adversely affects fetal brain development and subsequent behavioral self-regulation, a precursor to later, more serious problems in childhood. Stopping marijuana use before 10 weeks gestational age prevented these effects. Many mothers refuse to cease use because of familiarity with marijuana and belief in its safety. Higher maternal choline mitigates some of marijuana's adverse effects on the fetus.

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Section: Participants and Methodsmentioning

confidence: 99%

Interaction of maternal choline levels and prenatal Marijuana's effects on the offspring

et al. 2019

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“…Mothers received information on diets higher in choline, but dietary intake was not estimated because of the low relationship of self-reported intake to maternal choline levels in pregnant women, r = 0.2 (Wu, Dyer, King, Richardson, & Innis, 2012). The placental choline transporter CLT1 produces amniotic fluid levels approximately twice maternal plasma levels (Baumgartner et al, 2015; Ilcol, Uncu, & Ulus, 2002). Uptake is proportional to maternal plasma concentration, which suggests that higher peak levels may be important determinants of amniotic fluid levels (Iwao et al, 2016).…”

Section: Participants and Methodsmentioning

confidence: 99%

Male fetus susceptibility to maternal inflammation: C-reactive protein and brain development

et al. 2019

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Background Maternal inflammation in early pregnancy has been identified epidemiologically as a prenatal pathogenic factor for the offspring's later mental illness. Early newborn manifestations of the effects of maternal inflammation on human fetal brain development are largely unknown. Methods Maternal infection, depression, obesity, and other factors associated with inflammation were assessed at 16 weeks gestation, along with maternal C-reactive protein (CRP), cytokines, and serum choline. Cerebral inhibition was assessed by inhibitory P50 sensory gating at 1 month of age, and infant behavior was assessed by maternal ratings at 3 months of age. Results Maternal CRP diminished the development of cerebral inhibition in newborn males but paradoxically increased inhibition in females. Similar sex-dependent effects were seen in mothers' assessment of their infant's self-regulatory behaviors at 3 months of age. Higher maternal choline levels partly mitigated the effect of CRP in male offspring. Conclusions The male fetal-placental unit appears to be more sensitive to maternal inflammation than females. Effects are particularly marked on cerebral inhibition. Deficits in cerebral inhibition 1 month after birth, similar to those observed in several mental illnesses, including schizophrenia, indicate fetal developmental pathways that may lead to later mental illness. Deficits in early infant behavior follow. Early intervention before birth, including prenatal vitamins, folate, and choline supplements, may help prevent fetal development of pathophysiological deficits that can have life-long consequences for mental health.

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“…VPA additionally reduced the mRNA levels of the main placental choline uptake transporter CTL1. 29 If a similar reduction occurs in pregnant women, it may lead to depletion of choline in the fetal compartment and placenta itself. Values are presented as percentage of control (mean values).…”

Section: Key Placental Carriers Are Targets Of Vpamentioning

confidence: 99%