Review: Placental transport and metabolism of energy substrates in maternal obesity and diabetes

Gallo, Linda A.; Barrett, Helen L.; Nitert, Marloes Dekker

doi:10.1016/j.placenta.2016.12.006

Cited by 59 publications

(48 citation statements)

References 97 publications

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“…Fetal growth is affected by maternal nutrient availability, placenta nutrient transport efficiency, and fetal demand. A recent review has shown that the adaptation of placenta may partially determine fetal outcomes . In male placentas from HF dams, mTORC1 signaling was activated and nutrient transporter expression was increased in this study.…”

Section: Discussionsupporting

confidence: 53%

Prenatal high‐fat diet alters placental morphology, nutrient transporter expression, and mtorc1 signaling in rat

Song

Sun

Boersma

et al. 2017

Obesity

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Objective: This study aimed to determine how the rat placenta and fetus respond to maternal high-fat (HF) diet during gestation and to identify the possible mechanisms. Methods: Pregnant Sprague-Dawley rats were fed with standard chow (13.5% fat) or HF (60% fat) diet during gestation. Placentas were collected on gestation day 21. Results: HF dams had greater fat mass, higher plasma leptin, lower plasma adiponectin, and impaired glucose tolerance during pregnancy. The placental labyrinth thickness was reduced in both male and female fetuses of HF dams. In HF male placentas, glucose transporter 3 gene expression, system A amino acid transporter (SNAT) 2 gene expression, and SNAT2 protein expression were increased through the activation of the mTORC1 4EBP1 branch. In HF female placentas, gene expression of insulin-like growth factor 2 (IGF2) and IGF2 receptor was elevated compared to placentas of females fed standard chow. Although male and female placentas responded differently to prenatal HF diet exposure, both male and female fetal weight was not altered by maternal HF diet. Conclusions: Placenta responds and adapts to maternal metabolic changes by altering placental layer thickness, mTORC1 signaling, expression of nutrient transporters, and growth factors in a sex-specific manner.Obesity (2017) 25, 909-919.

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Section: Discussionsupporting

confidence: 53%

Prenatal high‐fat diet alters placental morphology, nutrient transporter expression, and mtorc1 signaling in rat

Song

Sun

Boersma

et al. 2017

Obesity

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“…Physiological hypertriglyceridemia of pregnancy is exacerbated by GDM and pre‐existing type‐2 diabetes . Maternal triglycerides do not cross the placental barrier but are hydrolysed by placental lipoprotein lipase to non‐esterified fatty acids (NEFA) . Hence, maternal NEFA may be an even better predictor of neonatal adiposity than Tg.…”

Section: Introductionmentioning

confidence: 99%

“…5 Maternal triglycerides do not cross the placental barrier but are hydrolysed by placental lipoprotein lipase to non-esterified fatty acids (NEFA). 6,7 Hence, maternal NEFA may be an even better predictor of neonatal adiposity than Tg. Increased insulin resistance in pregnancy is a physiological adaptation that provides the necessary nutrients for fetal growth, i.e.…”

Section: Introductionmentioning

confidence: 99%

Maternal lipids are associated with newborn adiposity, independent of GDM status, obesity and insulin resistance: a prospective observational cohort study

Samsuddin

Arumugam

Amin

et al. 2019

BJOG

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Objective To determine the association between maternal lipaemia and neonatal anthropometrics in Malaysian mother-offspring pairs. Design Prospective observational cohort study.Setting Single tertiary multidisciplinary antenatal clinic in Malaysia.Population A total of 507 mothers: 145 with gestational diabetes mellitus (GDM); 94 who were obese with normal glucose tolerance (NGT) (pre-gravid body mass index, BMI ≥ 27.5 kg/m 2 ), and 268 who were not obese with NGT.Methods Maternal demographic, anthropometric, and clinical data were collected during an interview/examination using a structured questionnaire. Blood was drawn for insulin, C-peptide, triglyceride (Tg), and non-esterified fatty acid (NEFA) during the 75-g 2-hour oral glucose tolerance test (OGTT) screening, and again at 36 weeks of gestation. At birth, neonatal anthropometrics were assessed and data such as gestational weight gain (GWG) were extracted from the records.Main outcome measures Macrosomia, large-for-gestational-age (LGA) status, cohort-specific birthweight (BW), neonatal fat mass (NFM), and sum of skinfold thickness (SSFT) > 90th centile.Results Fasting Tg > 95th centile (3.6 mmol/L) at screening for OGTT was independently associated with LGA (adjusted odds ratio, aOR 10.82, 95% CI 1.26-93.37) after adjustment for maternal glucose, pre-gravid BMI, and insulin sensitivity. Fasting glucose was independently associated with a birthweight ratio (BWR) of >90th centile (aOR 2.06, 95% CI 1.17-3.64), but not with LGA status, in this well-treated GDM cohort with predelivery HbA1c of 5.27%. In all, 45% of mothers had a pre-gravid BMI of <23 kg/m 2 and 61% had a pre-gravid BMI of ≤ 25 kg/m 2 , yet a GWG of >10 kg was associated with a 4.25-fold risk (95% CI 1.71-10.53) of BWR > 90th centile.Conclusion Maternal lipaemia and GWG at a low threshold (>10 kg) adversely impact neonatal adiposity in Asian offspring, independent of glucose, insulin resistance and pre-gravid BMI. These may therefore be important modifiable metabolic targets in pregnancy.

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“…Placental amino acid transport is tightly regulated with more than 20 known amino acid transporters. These include seven neutral amino acid transporters, including system A and system L. These systems are distinct in their substrate specificity and sodium dependency [87]. The role of amino acid transport activity in modulating fetal growth in obesity has been demonstrated in studies investigating various regulatory pathways.…”

Section: Amino Acidsmentioning

confidence: 99%

The impact of maternal obesity in pregnancy on placental glucocorticoid and macronutrient transport and metabolism

Johns

Denison

Reynolds

2020

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Maternal obesity is the most common metabolic disturbance in pregnancy affecting more than 1 in 5 women in some countries. Babies born to obese women are heavier with more adiposity at birth, and are vulnerable to obesity and metabolic disease across the lifespan suggesting offspring health is 'programmed' by fetal exposure to an obese intra-uterine environment. The placenta plays a major role in dictating the impact of maternal health on prenatal development. Maternal obesity impacts the function of integral placental receptors and transporters for glucocorticoids and nutrients, key drivers of fetal growth, though mechanisms remain poorly understood. This review aims to summarise current knowledge in this area, and considers the impact of obesity on the epigenetic machinery of the placenta at this vital juncture in offspring development. Further research is required to advance understanding of these areas in the hope that the trans-generational cycle of obesity can be alleviated.

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Review: Placental transport and metabolism of energy substrates in maternal obesity and diabetes

Cited by 59 publications

References 97 publications

Prenatal high‐fat diet alters placental morphology, nutrient transporter expression, and mtorc1 signaling in rat

Prenatal high‐fat diet alters placental morphology, nutrient transporter expression, and mtorc1 signaling in rat

Maternal lipids are associated with newborn adiposity, independent of GDM status, obesity and insulin resistance: a prospective observational cohort study

The impact of maternal obesity in pregnancy on placental glucocorticoid and macronutrient transport and metabolism

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