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Foetoplacental epigenetic changes associated with maternal metabolic dysfunction.
Kerr, B, Leiva, A, Farías, M, Contreras-Duarte, S, Toledo, F, Stolzenbach, F, Silva, L, Sobrevia, L
Placenta. 2018;:146-152
Abstract
Metabolic-related diseases are attributed to a sedentary lifestyle and eating habits, and there is now an increased awareness regarding pregnancy as a preponderant window in the programming of adulthood health and disease. The developing foetus is susceptible to the maternal environment; hence, any unfavourable condition will result in foetal physiological adaptations that could have a permanent impact on its health. Some of these alterations are maintained via epigenetic modifications capable of modifying gene expression in metabolism-related genes. Children born to mothers with dyslipidaemia, pregestational or gestational obesity, and gestational diabetes mellitus, have a predisposition to develop metabolic alterations during adulthood. CpG methylation-associated alterations to the expression of several genes in the human placenta play a crucial role in the mother-to-foetus transfer of nutrients and macromolecules. Identification of epigenetic modifications in metabolism-related tissues of offspring from metabolic-altered pregnancies is essential to obtain insights into foetal programming controlling newborn, childhood, and adult metabolism. This review points out the importance of the foetal milieu in the programming and development of human disease and provides evidence of this being the underlying mechanism for the development of adulthood metabolic disorders in maternal dyslipidaemia, pregestational or gestational obesity, and gestational diabetes mellitus.
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Placental control of metabolic adaptations in the mother for an optimal pregnancy outcome. What goes wrong in gestational diabetes?
Hill, DJ
Placenta. 2018;:162-168
Abstract
As pregnancy progresses the placental syncytiotrophoblast increasingly assumes control of maternal glucose homeostasis through the release and counter-balancing effects of placental lactogen (PL) and placental variant growth hormone (GH-V). While local actions of these hormones on placental growth and function are likely to exist, each also exerts indirect actions to ensure fetal nutritional availability through modulation of the maternal insulin/insulin-like growth factor axis. Peripheral insulin resistance results from the increasing levels of GH-V in the maternal circulation and is counter-balanced by an increase in insulin availability through an expansion of maternal pancreatic β-cell mass. GH-V also increases maternal IGF-1 synthesis leading to enhanced placental growth and nutrient transporter activity. Maternal obesity and the presence of diabetes in pregnancy is associated with a disrupted balance in the placental expression of PL and GH-V. Several parallel mechanisms are likely to contribute to the increasing maternal β-cell mass as gestation progresses, including a reactivation of β-cell proliferation, an expansion of subsequent differentiation of resident β-cell progenitors, and α-to β-cell trans-differentiation. Each of these pathways could potentially be modulated during pregnancy to increase β-cell mass and prevent the onset of gestational diabetes.
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3.
Fetal DHA inadequacy and the impact on child neurodevelopment: a follow-up of a randomised trial of maternal DHA supplementation in pregnancy.
Mulder, KA, Elango, R, Innis, SM
The British journal of nutrition. 2018;(3):271-279
Abstract
DHA is an important component of neural lipids accumulating in neural tissue during development. Inadequate DHA in gestation may compromise infant development, but it is unknown whether there are lasting effects. We sought to determine whether the observed effects of fetal DHA inadequacy on infant development persist into early childhood. This follow-up study assessed children (5-6 years) whose mothers received 400 mg/d DHA or a placebo during pregnancy. Child neurodevelopment was assessed with several age-appropriate tests including the Kaufman Assessment Battery for Children. A risk-reduction model was used whereby the odds that a child from the maternal placebo group would fail to achieve a test score in the top quartile was calculated. The association of maternal DHA intake and status in gestation with child test scores, as well as with child DHA intake and status, was also determined. No differences were detected in children (n 98) from the maternal placebo and DHA groups achieving a high neurodevelopment test score (P>0·05). However, maternal DHA status was positively related to child performance on some tests including language and short-term memory. Furthermore, child DHA intake and status were related to the mother's intake and status in gestation. The neurodevelopment effects of fetal DHA inadequacy may have been lost or masked by other variables in the children. Although we provide evidence that maternal DHA status is related to child cognitive performance, the association of maternal and child DHA intake and status limits the interpretation of whether DHA before or after birth is important.
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Folic Acid Supplementation throughout pregnancy: psychological developmental benefits for children.
Henry, LA, Cassidy, T, McLaughlin, M, Pentieva, K, McNulty, H, Walsh, CP, Lees-Murdock, D
Acta paediatrica (Oslo, Norway : 1992). 2018;(8):1370-1378
Abstract
AIM: To test the effect of folic acid supplements taken throughout pregnancy on children's psychosocial development. METHOD A randomised controlled trial of folic acid supplementation in pregnancy, with parental rating using the Resiliency Attitudes and Skills Profile (RASP), the Strengths and Difficulties Questionnaire (SDQ) and the Trait Emotional Intelligence Questionnaire Child Short Form (TEIQue-CSF). Children aged 6-7 whose mothers received folic acid throughout pregnancy (n = 22) were compared to those whose mothers only received it during the first trimester (n = 17). RESULTS Children whose mothers received the full-term supplement scored significantly higher on emotional intelligence and resilience. Hierarchical multiple regression analysis identified folate level at 36th gestational week as an important predictor of emotional intelligence (EI) and resilience. CONCLUSION Although conclusions must be drawn with caution, this research presents a number of potential implications, the main one being a proposed policy recommendation for women to take folic acid for the duration of pregnancy rather than stopping at the end of the first trimester. The second is the potential for future research to explore the possible psychological and social development benefits and in line with this to try and identify the explanatory mechanism involved.
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Atypical fetal development: Fetal alcohol syndrome, nutritional deprivation, teratogens, and risk for neurodevelopmental disorders and psychopathology.
Georgieff, MK, Tran, PV, Carlson, ES
Development and psychopathology. 2018;(3):1063-1086
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Abstract
Accumulating evidence indicates that the fetal environment plays an important role in brain development and sets the brain on a trajectory across the life span. An abnormal fetal environment results when factors that should be present during a critical period of development are absent or when factors that should not be in the developing brain are present. While these factors may acutely disrupt brain function, the real cost to society resides in the long-term effects, which include important mental health issues. We review the effects of three factors, fetal alcohol exposure, teratogen exposure, and nutrient deficiencies, on the developing brain and the consequent risk for developmental psychopathology. Each is reviewed with respect to the evidence found in epidemiological and clinical studies in humans as well as preclinical molecular and cellular studies that explicate mechanisms of action.
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Impact of Roux-en-Y gastric bypass and sleeve gastrectomy on fetal growth and relationship with maternal nutritional status.
Coupaye, M, Legardeur, H, Sami, O, Calabrese, D, Mandelbrot, L, Ledoux, S
Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery. 2018;(10):1488-1494
Abstract
BACKGROUND There is a lack of evidence on whether sleeve gastrectomy (SG), which induces fewer nutritional deficiencies than Roux-en-Y gastric bypass (RYGB), also affects fetal growth (FG). OBJECTIVES To compare neonatal outcomes after RYGB and SG and to assess the impact of maternal nutritional alterations on FG after both procedures. SETTING University Hospital, France. METHODS Women with singleton pregnancies who had at least 1 nutritional evaluation in our institution between 2004 and 2017 were included. FG was assessed with birth weight (BW) and BW-Z score (adjusted for sex and term), and maternal nutritional deficiencies were defined according to standard and pregnancy-specific norms. RESULTS During the study period 123 pregnancies were included, 77 after RYGB and 46 after SG. Weight loss was higher after RYGB than after SG (45.6 ± 12.4 versus 39.5 ± 13.7 kg, P = .02), but mean weight before pregnancy and weight gain during pregnancy were similar. Mean BW (3026 ± 677 versus 3162 ± 712 g), mean BW Z-score and incidence of small for gestational age (24% versus 19%) were not significantly different after RYGB and SG. Mean number of nutritional deficiencies during the second trimester was similar (2.2 ± 1.5 versus 2.1 ± 1.2 with specific norms), but the affected parameters differed between procedures. Urinary urea (R = .285, P = .04) was positively correlated to BW Z-score after both procedures. In contrast, serum iron parameters were negatively associated to BW Z-score. CONCLUSION FG restriction occurs after both SG and RYGB. FG after bariatric surgery is positively associated with protein supply and negatively correlated with maternal iron status.
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Perinatal Origins of Adult Disease.
Simeoni, U, Armengaud, JB, Siddeek, B, Tolsa, JF
Neonatology. 2018;(4):393-399
Abstract
Epidemiological and experimental studies have shown that the peri-conception period, pregnancy, and infancy are windows of particular sensibility to environmental clues which influence lifelong trajectories across health and disease. Nutrition, stress, and toxins induce epigenetic marks that control long-term gene expression patterns and can be transmitted transgenerationally. Chronic diseases of adulthood such as hypertension, diabetes, and obesity thus have early, developmental origins in the perinatal period. The early epigenome, in interaction with other actors such as the microbiome, add powerful layers of diversity to the biological predisposition generated by the genome. Such "programming" is a normal, adaptive component of development, including in normal pregnancies and births. However, perinatal disease, either maternal (such as pre-eclampsia, ges-tational diabetes, or inflammatory disease) or fetal, and neonatal diseases (such as intrauterine growth restriction and preterm birth) are major conditions of altered programming, translated into an increased risk for chronic disease in these patients when they reach adulthood. Early prevention, optimal perinatal nutrition, and specific follow-up measures are key factors in the early preservation of long-term health.
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Altered maternal and placental lipid metabolism and fetal fat development in obesity: Current knowledge and advances in non-invasive assessment.
Delhaes, F, Giza, SA, Koreman, T, Eastabrook, G, McKenzie, CA, Bedell, S, Regnault, TRH, de Vrijer, B
Placenta. 2018;:118-124
Abstract
Abnormal maternal lipid profiles, a hallmark of increased maternal adiposity, are associated with pregnancy complications such as preeclampsia and gestational diabetes, and offspring long-term metabolic health is impacted as the consequence of altered fetal growth, physiology and often iatrogenic prematurity. The metabolic changes associated with maternal obesity and/or the consumption of a high-fat diet effecting maternal lipid profiles and metabolism have also been documented to specifically affect placental function and may underlie changes in fetal development and life course disease risk. The placenta plays a critical role in mediating nutritional signals between the fetus and the mother. As obesity rates in women of reproductive age continue to increase, it is becoming evident that inclusion of new technologies that allow for a better understanding of early changes in placental lipid transport and metabolism, non-invasively in maternal circulation, maternal tissues, placenta, fetal circulation and fetal tissues are needed to aid timely clinical diagnosis and treatment for obesity-associated diseases. This review describes pregnancy lipid homeostasis, with specific reference to changes arising from altered maternal body composition on placental and fetal lipid transport and metabolism. Current technologies for lipid assessments, such as metabolomics and lipidomics may be impacted by labour or mode of delivery and are only reflective of a single time point. This review further addresses how established and novel technologies for assessing lipids and their metabolism non-invasively and during the course of pregnancy may guide future research into the effect of maternal metabolic health on pregnancy outcome, placenta and fetus.
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Maternal and Foetal Health Implications of Vitamin D Status during Pregnancy.
Larqué, E, Morales, E, Leis, R, Blanco-Carnero, JE
Annals of nutrition & metabolism. 2018;(3):179-192
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Abstract
BACKGROUND To what extent does the circulating 25-hydroxyvitamin D (25[OH]D) concentration help to meet the physiological needs of humans is an ongoing subject of debate. Remaining unexposed to the sun to reduce melanoma cancer risk, current lifestyle with less out door activities, and increasing obesity rates, which in turn increases the storage of vitamin D in the adipose tissue, are presumably factors that contribute to the substantial upsurge in the prevalence of vitamin D deficiency in humans. Since evidence is lacking regarding the appropriate cut-off points to define vitamin D status during pregnancy, references used to establish the intake recommendations and vitamin D content of prenatal vitamin supplements are quite conservative. SUMMARY The foetus depends fully on maternal 25(OH)D supply. 25(OH)D readily crosses the placenta and it is activated into 1,25(OH)2D by foetal kidneys. Moreover, 1,25(OH)2D can also be synthesized within the placenta to regulate placental metabolism. The importance of vitamin D during pregnancy for maintaining maternal calcium homeostasis and therefore for foetal bone development is well recognized; major discussions are in progress regarding the potential maternal detrimental effects on pregnancy outcomes, foetal development, and the long-term health of children. Interventional studies have also evaluated the effect of vitamin D for reduction on preterm birth and asthma programming. Key Messages: Clinically, by understanding the effects of vitamin D on perinatal outcomes, we could individualize antenatal counselling regarding vitamin D supplementation to ensure vitamin D repletion without increasing the risk of foetal hypercalcemia.
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Maternal Non-glycemic Contributors to Fetal Growth in Obesity and Gestational Diabetes: Spotlight on Lipids.
Barbour, LA, Hernandez, TL
Current diabetes reports. 2018;(6):37
Abstract
PURPOSE OF REVIEW Excess fetal growth is increasingly recognized as a risk factor for childhood obesity, and mounting evidence supports that maternal glucose is not the only driver. This review focuses on the role of clinically applicable maternal non-glycemic contributors to excess fetal growth, particularly lipids, in addition to amino acids (AA), insulin resistance, inflammation, maternal nutrition, and gestational weight gain (GWG) in obesity and gestational diabetes mellitus (GDM). RECENT FINDINGS Lipids, specifically triglycerides and free fatty acids, appear to be strong contributors to excess fetal fat accretion and adiposity at birth, particularly in obese pregnancies, which account for the largest number of large-for-gestational-age infants. Maternal pre-pregnancy body mass index (BMI), GWG, insulin resistance, inflammation, and glucose, lipid, and AA concentrations have both independent and interacting effects on fetal growth, operating both early and late in pregnancy. All are sensitive to maternal nutrition. Early vs. later gestational exposure to excess maternal fuels in fasting and postprandial conditions may differentially impact fetoplacental outcomes. Compelling evidence suggests that targeting interventions early in pregnancy beyond glucose may be critical to improve fetal growth patterns.