Placental regulation of fetal nutrient supply

Larqué, Elvira; Ruiz-Palacios, María; Koletzko, Berthold

doi:10.1097/mco.0b013e32835e3674

Cited by 107 publications

(72 citation statements)

References 39 publications

(40 reference statements)

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“…Because ADN supplementation also reduced maternal insulin levels, it is likely that the effects of ADN on placental insulin signaling were a result of both the direct effects of ADN in attenuating placental insulin signaling as well as the indirect effects through reduced circulating insulin levels. Insulin signaling regulates critical functions of the placenta, including nutrient transport, and therefore is believed to be essential in determining fetal growth (24,39). Thus, we propose that the normalization of placental insulin signaling by maternal ADN infusion constitutes the critical event that ultimately prevents fetal overgrowth caused by maternal obesity.…”

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.

128

124

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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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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.

128

124

View full text Add to dashboard Cite

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“…Chen et al (21) observed that decreased miR-143 expression promoted adipogenic growth and differentiation of adipose tissue-derived stromal cells by targeting MAPK kinase 5. Compared with control placenta, placenta from macrosomic pregnancies has greater capacity to support growth and differentiation, as it must provide more space and transport more nutrients to a larger fetus (40). Therefore, it can be explained why miR-143 expression was reduced in macrosomic placenta.…”

mentioning

confidence: 99%

Decreased miR-143 and increased miR-21 placental expression levels are associated with macrosomia

Zhang

Cai

et al. 2016

Molecular Medicine Reports

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Abstract. Macrosomia, a birth weight ≥4,000 g, is associated with maternal and infant health problems. The dysregulation of microRNAs (miRNAs) in the placenta is associated with adverse birth outcomes, yet whether aberrantly expressed placental miRNAs are associated with macrosomia remains unknown. The aim of the current study was to characterize the expression of three placental miRNAs (miR-6, -21 and -143) and evaluate their association with macrosomia. The miRNA expression in placental tissues from 67 macrosomic pregnancies and 64 normal pregnancies were analyzed using reverse transcription-quantitative polymerase chain reaction. The expression of miR-21 was observed to be elevated in macrosomic placenta compared with control samples, while miR-143 expression was significantly lower than in control placenta (P<0.05). No significant differences were identified in the miR-16 expression levels between the groups (P= 0.955). Following division of miRNA expression levels by quartile, logistic regression models demonstrated that the odds of macrosomia increased with miR-21 expression quartile: Q2, odds ratio (OR)=6.67 [95% confidence interval (CI), 1.39-32.05]; Q3, OR=4.10 (95% CI, 0.88-19.11); Q4, OR=16.19 (95% CI, 2.46-106.68). Conversely, higher levels of miR-143 expression were protective against macrosomia: Q2, OR= 0.22 (95% CI, 0.049-0.98); Q3, OR= 0.11 (95% CI, 0.024-0.55), and Q4, OR= 0.16 (95% CI, 0.032-0.79). Thus, statistical analysis demonstrated that high levels of miR-21 expression and low levels of miR-143 expression predict the risk for macrosomia, indicating an interaction between the two miRNAs. Bioinformatic analysis suggested that they are likely to function in the mitogen-activated protein kinases signaling pathway to influence the risk of macrosomia. The results of the present study provide evidence that placental miR-21 and -143 are important in the formation of macrosomia.

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“…There is a total of 1000 gram protein increase throughout the pregnancy and half of this belongs to the fetus and the fetoplacental tissues (32). Maternal serum albumin decreases and globulin increases in pregnancy.…”

Section: Maternal Protein Metabolismmentioning

confidence: 99%

“…High density lipoprotein stimulates human placental lactogen through its receptors on the placenta (32). Lipids, lipoproteins and apolipoproteins decrease at various rates in the postpartum period also by the contribution of lactation (32). Alterations in lipid metabolism cause accumulation of maternal fat stores in the early pregnancy in order to enhance lipolysis in the late pregnancy by human chorionic somotomammotrophin.…”

Section: Maternal Lipid Metabolismmentioning

confidence: 99%

“…Maternal serum albumin decreases and globulin increases in pregnancy. Placental lactogen and human chorionic gonodotrophin suppress deamination in the liver to prevent loss of amino acids to preserve amino acids for fetus (32). If mother gets insufficient carbohydrates and lipids, proteins are used as the energy source which is an undesirable condition.…”

Section: Maternal Protein Metabolismmentioning

confidence: 99%

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