Maternal obesity: new placental paradigms unfolded

Brombach, Carolin; Tong, Wen Ting; Giussani, Dino A.

doi:10.1016/j.molmed.2022.05.013

Cited by 22 publications

(20 citation statements)

References 148 publications

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“…In pregnancy, the maternal metabolism changes dramatically to support fetal growth and meet maternal additional energy requirements. However, maternal obesity in pregnancy increases maternal complications and enhances the risk of developing obesity, cardiovascular disease, diabetes, and cognitive dysfunction in offspring in adult life [ 25 , 26 ]. Obesity-induced metaflammation results in aberrant changes at the cellular and humoral levels that contribute to pregnancy complications.…”

Section: Impacts Of Obesity On Maternal Endocrine Factors and Fetal B...mentioning

confidence: 99%

Maternal Obesity and Gut Microbiota Are Associated with Fetal Brain Development

et al. 2022

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Obesity in pregnancy induces metabolic syndrome, low-grade inflammation, altered endocrine factors, placental function, and the maternal gut microbiome. All these factors impact fetal growth and development, including brain development. The lipid metabolic transporters of the maternal-fetal-placental unit are dysregulated in obesity. Consequently, the transport of essential long-chain PUFAs for fetal brain development is disturbed. The mother’s gut microbiota is vital in maintaining postnatal energy homeostasis and maternal-fetal immune competence. Obesity during pregnancy changes the gut microbiota, affecting fetal brain development. Obesity in pregnancy can induce placental and intrauterine inflammation and thus influence the neurodevelopmental outcomes of the offspring. Several epidemiological studies observed an association between maternal obesity and adverse neurodevelopment. This review discusses the effects of maternal obesity and gut microbiota on fetal neurodevelopment outcomes. In addition, the possible mechanisms of the impacts of obesity and gut microbiota on fetal brain development are discussed.

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Section: Impacts Of Obesity On Maternal Endocrine Factors and Fetal B...mentioning

confidence: 99%

Maternal Obesity and Gut Microbiota Are Associated with Fetal Brain Development

et al. 2022

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“…Development of maternal insulin resistance and a proinflammatory state in the setting of hyperglycemia and hyperlipidemia may also contribute to an abnormal metabolic transition in early postnatal life ( 75 ). Further, exposure to elevated metabolic substrates may cause direct glucotoxic and lipotoxic effects on placental proteins, which in turn have been shown to contribute to oxidative stress, endoplasmic reticulum (ER) stress and proinflammatory pathways affecting overall placental function ( 76 ). In response to increased placental transport of glucose to the fetus, fetal hyperinsulinemia develops which is hypothesized to contribute to obesity conditioning in the offspring ( 77 ).…”

Section: Mechanisms Of Metabolic Conditioning Of Obesity and Cardiova...mentioning

confidence: 99%

“…Maternal circulating levels of metabolic substrates and hormones, as discussed above, significantly impact placental function, likely mediated by mTOR signaling on the placenta by activating amino acid and glucose transport as well as mitochondrial biogenesis and protein synthesis, ultimately contributing to excess fetal nutrient delivery with increased risk for fetal overgrowth in obese women ( 75 , 76 ).…”

Section: Mechanisms Of Metabolic Conditioning Of Obesity and Cardiova...mentioning

confidence: 99%

The metabolic conditioning of obesity: A review of the pathogenesis of obesity and the epigenetic pathways that “program” obesity from conception

2022

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Understanding the developmental origins of health and disease is integral to overcome the global tide of obesity and its metabolic consequences, including atherosclerotic cardiovascular disease, type 2 diabetes, hyperlipidemia, and nonalcoholic fatty liver disease. The rising prevalence of obesity has been attributed, in part, to environmental factors including the globalization of the western diet and unhealthy lifestyle choices. In this review we argue that how and when such exposures come into play from conception significantly impact overall risk of obesity and later health outcomes. While the laws of thermodynamics dictate that obesity is caused by an imbalance between caloric intake and energy expenditure, the drivers of each of these may be laid down before the manifestation of the phenotype. We present evidence over the last half-century that suggests that the temporospatial evolution of obesity from intrauterine life and beyond is, in part, due to the conditioning of physiological processes at critical developmental periods that results in maladaptive responses to obesogenic exposures later in life. We begin the review by introducing studies that describe an association between perinatal factors and later risk of obesity. After a brief discussion of the pathogenesis of obesity, including the systemic regulation of appetite, adiposity, and basal metabolic rate, we delve into the mechanics of how intrauterine, postnatal and early childhood metabolic environments may contribute to adult obesity risk through the process of metabolic conditioning. Finally, we detail the specific epigenetic pathways identified both in preclinical and clinical studies that synergistically “program” obesity.

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“…Maternal obesity is likely to have a deleterious impact on chronic inflammation and pre-programmed chronic inflammatory pathways and metabolism of the placental compared to gestational DM. Adverse effects of obesity on maternal and fetal health are mediated by complex interactions between metabolic, inflammatory, and oxidative stress signaling in the placenta [ 58 ]. However, there are overlapping mechanisms of the impact of maternal obesity and diabetes on the placenta.…”

Section: Limitationmentioning

confidence: 99%

Associations between Maternal Risk Factors and Intrinsic Placental and Fetal Brain Functional Properties in Congenital Heart Disease

Rajagopalan

Schmithorst

El-Ali

et al. 2022

IJMS

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The relationship between maternal risk factors (MRFs) (particularly pre-gravid obesity, diabetes, and hypertension) and congenital heart disease (CHD) to placental and fetal brain outcomes is poorly understood. Here, we tested the hypothesis that MRF and CHD would be associated with reduced intrinsic placental and fetal brain function using a novel non-invasive technique. Pregnant participants with and without MRF and fetal CHD were prospectively recruited and underwent feto-placental MRI. Using intrinsic properties of blood oxygen level dependent imaging (BOLD) we quantified spatiotemporal variance of placenta and fetal brain. MRFs and CHD were correlated with functional characteristics of the placenta and fetal brain. Co-morbid MRF (hypertension, diabetes, and obesity) reduced spatiotemporal functional variance of placenta and fetal brain (p < 0.05). CHD predicted reduced fetal brain temporal variance compared to non-CHD (p < 0.05). The presence of both MRF and CHD was associated with reduced intrinsic pBOLD temporal variance (p = 0.047). There were no significant interactions of MRFs and CHD status on either temporal or spatial variance of intrinsic brain BOLD. MRF and CHD reduced functional characteristic of placenta and brain in fetuses. MRF modification and management during pregnancy may have the potential to not only provide additional risk stratification but may also improve neurodevelopmental outcomes.

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Maternal obesity: new placental paradigms unfolded

Cited by 22 publications

References 148 publications

Maternal Obesity and Gut Microbiota Are Associated with Fetal Brain Development

Maternal Obesity and Gut Microbiota Are Associated with Fetal Brain Development

The metabolic conditioning of obesity: A review of the pathogenesis of obesity and the epigenetic pathways that “program” obesity from conception

Associations between Maternal Risk Factors and Intrinsic Placental and Fetal Brain Functional Properties in Congenital Heart Disease

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