The Role of Placental Nutrient Sensing in Maternal-Fetal Resource Allocation1

Díaz, Paula; Powell, Theresa L.; Jansson, Thomas

doi:10.1095/biolreprod.114.121798

Cited by 124 publications

(90 citation statements)

References 129 publications

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“…Furthermore, antenatal complications also associate with LBW [28,31]. It has been reported that the placenta may act as a nutrient sensor that adjust maternal nutrient supply to fetal growth [27,30]. In our study, the combined effect of pre-eclampsia and anaemia were the respective placental and antenatal complications seen associating strongly with term LBW.…”

Section: Discussionsupporting

confidence: 53%

“…Studies in Pakistan and China showed that maternal low primary education, anaemia, hypertension and socio-economic factors were strong factors that influenced term LBW [8,9]. Intrauterine malnutrition as a result of poor maternal nutrition can lead to restricted growth in utero and it can serve as a proxy to LBW [29,30]. A single mother in Ghana, especially in the low income range, will have difficulty obtaining adequate income to afford enough, well-balanced food to eat.…”

Section: Discussionmentioning

confidence: 99%

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Maternal Demographic and Placental Risk Factors in Term Low Birth Weight in Ghana

Aleksenko

Tettey

Richard³

et al. 2017

J Preg Child Health

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Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Maternal Demographic and Placental Risk Factors in Term Low Birth Weight in Ghana

Aleksenko

Tettey

Richard³

et al. 2017

J Preg Child Health

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“…Changes in placental nutrient transport alter nutrient flux to the fetus and, ultimately, fetal growth, independent of maternal nutrient levels (30,31). Indeed, large infants of obese nondiabetic women are more likely to have elevated cord serum glucose (26,32), which may be related to an increased placental glucose transport capacity rather than elevated maternal blood glucose levels (26).…”

Section: Discussionmentioning

confidence: 99%

Adiponectin supplementation in pregnant mice prevents the adverse effects of maternal obesity on placental function and fetal growth

Aye

Rosario

Powell

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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137

136

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Mothers with obesity or gestational diabetes mellitus have low circulating levels of adiponectin (ADN) and frequently deliver large babies with increased fat mass, who are susceptible to perinatal complications and to development of metabolic syndrome later in life. It is currently unknown if the inverse correlation between maternal ADN and fetal growth reflects a cause-and-effect relationship. We tested the hypothesis that ADN supplementation in obese pregnant dams improves maternal insulin sensitivity, restores normal placental insulin/mechanistic target of rapamycin complex 1 (mTORC1) signaling and nutrient transport, and prevents fetal overgrowth. Compared with dams on a control diet, female C57BL/ 6J mice fed an obesogenic diet before mating and throughout gestation had increased fasting serum leptin, insulin, and C-peptide, and reduced high-molecular-weight ADN at embryonic day (E) 18.5. Placental insulin and mTORC1 signaling was activated, peroxisome proliferator-activated receptor-α (PPARα) phosphorylation was reduced, placental transport of glucose and amino acids in vivo was increased, and fetal weights were 29% higher in obese dams. Maternal ADN infusion in obese dams from E14.5 to E18.5 normalized maternal insulin sensitivity, placental insulin/mTORC1 and PPARα signaling, nutrient transport, and fetal growth without affecting maternal fat mass. Using a mouse model with striking similarities to obese pregnant women, we demonstrate that ADN functions as an endocrine link between maternal adipose tissue and fetal growth by regulating placental function. Importantly, maternal ADN supplementation reversed the adverse effects of maternal obesity on placental function and fetal growth. Improving maternal ADN levels may serve as an effective intervention strategy to prevent fetal overgrowth caused by maternal obesity.adipokines | maternal-fetal exchange | amino acids | glucose | insulin resistance

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“…39 In support of this model, maternal obesity is associated with increased placental expression of system A amino acid transporters 1 and 2 (SNAT1 and SNAT2) in conjunction with greater activity of the mTOR (mechanistic target of rapamycin) and insulin growth factor 1 (IGF-1) signaling pathways, which presumably contribute to fetal overgrowth. 40 By contrast, a recent report found that maternal obesity decreased placental taurine transporter activity in villous explants, without changes in protein expression.…”

Section: Placental Changes Associated With Maternal Obesitymentioning

confidence: 95%

Obesity and pregnancy: mechanisms of short term and long term adverse consequences for mother and child

Catalano

Shankar

2017

BMJ

882

749

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Obesity is the most common medical condition in women of reproductive age. Obesity during pregnancy has short term and long term adverse consequences for both mother and child. Obesity causes problems with infertility, and in early gestation it causes spontaneous pregnancy loss and congenital anomalies. Metabolically, obese women have increased insulin resistance in early pregnancy, which becomes manifest clinically in late gestation as glucose intolerance and fetal overgrowth. At term, the risk of cesarean delivery and wound complications is increased. Postpartum, obese women have an increased risk of venous thromboembolism, depression, and difficulty with breast feeding. Because 50-60% of overweight or obese women gain more than recommended by Institute of Medicine gestational weight guidelines, postpartum weight retention increases future cardiometabolic risks and prepregnancy obesity in subsequent pregnancies. Neonates of obese women have increased body fat at birth, which increases the risk of childhood obesity. Although there is no unifying mechanism responsible for the adverse perinatal outcomes associated with maternal obesity, on the basis of the available data, increased prepregnancy maternal insulin resistance and accompanying hyperinsulinemia, inflammation, and oxidative stress seem to contribute to early placental and fetal dysfunction. We will review the pathophysiology underlying these data and try to shed light on the specific underlying mechanisms.

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The Role of Placental Nutrient Sensing in Maternal-Fetal Resource Allocation1

Cited by 124 publications

References 129 publications

Maternal Demographic and Placental Risk Factors in Term Low Birth Weight in Ghana

Maternal Demographic and Placental Risk Factors in Term Low Birth Weight in Ghana

Adiponectin supplementation in pregnant mice prevents the adverse effects of maternal obesity on placental function and fetal growth

Obesity and pregnancy: mechanisms of short term and long term adverse consequences for mother and child

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