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Fetal Sex Modulates Developmental Response to Maternal Malnutrition.

ABSTRACT: The incidence of obesity and metabolic diseases is dramatically high in rapidly developing countries. Causes have been related to intrinsic ethnic features with development of a thrifty genotype for adapting to food scarcity, prenatal programming by undernutrition, and postnatal exposure to obesogenic lifestyle. Observational studies in humans and experimental studies in animal models evidence that the adaptive responses of the offspring may be modulated by their sex. In the contemporary context of world globalization, the new question arising is the existence and extent of sex-related differences in developmental and metabolic traits in case of mixed-race. Hence, in the current study, using a swine model, we compared male and female fetuses that were crossbred from mothers with thrifty genotype and fathers without thrifty genotype. Female conceptuses evidence stronger protective strategies for their adequate growth and postnatal survival. In brief, both male and female fetuses developed a brain-sparing effect but female fetuses were still able to maintain the development of other viscerae than the brain (mainly liver, intestine and kidneys) at the expense of carcass development. Furthermore, these morphometric differences were reinforced by differences in nutrient availability (glucose and cholesterol) favoring female fetuses with severe developmental predicament. These findings set the basis for further studies aiming to increase the knowledge on the interaction between genetic and environmental factors in the determination of adult phenotype.

SUBMITTER: Gonzalez-Bulnes A

PROVIDER: S-EPMC4636307 | biostudies-other | 2015

REPOSITORIES: biostudies-other

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Maternal choline supplementation during murine pregnancy modulates placental markers of inflammation, apoptosis and vascularization in a fetal sex-dependent manner.

Project description:IntroductionNormal placental vascular development is influenced by inflammatory, angiogenic and apoptotic processes, which may be modulated by choline through its role in membrane biosynthesis, cellular signaling and gene expression regulation. The current study examined the effect of maternal choline supplementation (MCS) on placental inflammatory, angiogenic and apoptotic processes during murine pregnancy.MethodPregnant dams were randomized to receive 1, 2 or 4 times (X) the normal choline content of rodent diets, and tissues were harvested on embryonic day (E) 10.5, 12.5, 15.5 or 18.5 for gene expression, protein abundance and immunohistochemical analyses.ResultsThe choline-induced changes in the inflammatory and angiogenic markers were a function of fetal sex. Specifically, 4X (versus 1X) choline reduced the transcript (P ≤ 0.05) and protein (P ≤ 0.06) expression of TNF-a and IL-1β in the male placentas at E10.5 and E18.5, respectively. In the female placentas, 4X (versus 1X) choline modulated the transcript expression of Il1b in a biphasic pattern with reduced Il1b at E12.5 (P = 0.045) and E18.5 (P = 0.067) but increased Il1b at E15.5 (P = 0.031). MCS also induced an upregulation of Vegfa expression in the female placentas at E15.5 (P = 0.034; 4X versus 2X) and E18.5 (P = 0.026; 4X versus 1X). MCS decreased (P = 0.011; 4X versus 1X) placental apoptosis at E10.5. Additionally, the luminal area of the maternal spiral arteries was larger (P ≤ 0.05; 4X versus 1X) in response to extra choline throughout gestation.DiscussionMCS during murine pregnancy has fetal sex-specific effects on placental inflammation and angiogenesis, with possible consequences on placental vascular development.

| S-EPMC8140820 | biostudies-literature

Maternal protein-energy malnutrition during early pregnancy in sheep impacts the fetal ornithine cycle to reduce fetal kidney microvascular development.

Project description:This paper identifies a common nutritional pathway relating maternal through to fetal protein-energy malnutrition (PEM) and compromised fetal kidney development. Thirty-one twin-bearing sheep were fed either a control (n=15) or low-protein diet (n=16, 17 vs. 8.7 g crude protein/MJ metabolizable energy) from d 0 to 65 gestation (term, ∼ 145 d). Effects on the maternal and fetal nutritional environment were characterized by sampling blood and amniotic fluid. Kidney development was characterized by histology, immunohistochemistry, vascular corrosion casts, and molecular biology. PEM had little measureable effect on maternal and fetal macronutrient balance (glucose, total protein, total amino acids, and lactate were unaffected) or on fetal growth. PEM decreased maternal and fetal urea concentration, which blunted fetal ornithine availability and affected fetal hepatic polyamine production. For the first time in a large animal model, we associated these nutritional effects with reduced micro- but not macrovascular development in the fetal kidney. Maternal PEM specifically impacts the fetal ornithine cycle, affecting cellular polyamine metabolism and microvascular development of the fetal kidney, effects that likely underpin programming of kidney development and function by a maternal low protein diet.

| S-EPMC4216596 | biostudies-literature

Impact of Maternal Malnutrition on Gut Barrier Defense: Implications for Pregnancy Health and Fetal Development.

Project description:Small intestinal Paneth cells, enteric glial cells (EGC), and goblet cells maintain gut mucosal integrity, homeostasis, and influence host physiology locally and through the gut-brain axis. Little is known about their roles during pregnancy, or how maternal malnutrition impacts these cells and their development. Pregnant mice were fed a control diet (CON), undernourished by 30% vs. control (UN), or fed a high fat diet (HF). At day 18.5 (term = 19), gut integrity and function were assessed by immunohistochemistry and qPCR. UN mothers displayed reduced mRNA expression of Paneth cell antimicrobial peptides (AMP; Lyz2, Reg3g) and an accumulation of villi goblet cells, while HF had reduced Reg3g and mucin (Muc2) mRNA and increased lysozyme protein. UN fetuses had increased mRNA expression of gut transcription factor Sox9, associated with reduced expression of maturation markers (Cdx2, Muc2), and increased expression of tight junctions (TJ; Cldn-7). HF fetuses had increased mRNA expression of EGC markers (S100b, Bfabp, Plp1), AMP (Lyz1, Defa1, Reg3g), and TJ (Cldn-3, Cldn-7), and reduced expression of an AMP-activator (Tlr4). Maternal malnutrition altered expression of genes that maintain maternal gut homeostasis, and altered fetal gut permeability, function, and development. This may have long-term implications for host-microbe interactions, immunity, and offspring gut-brain axis function.

| S-EPMC6628366 | biostudies-literature

Fetal sex and risk of preeclampsia: Dose maternal race matter?

Project description:ObjectiveTo examine whether maternal race could affect the relationship between fetal sex and preeclampsia.Material and methodsThis study was a cohort analysis using prospectively collected data from pregnant women who participated in the Vitamin Antenatal Asthma Reduction Trial (VDAART). Preeclampsia was the secondary outcome of VDAART. We examined the association of fetal sex with preeclampsia and its potential interaction with maternal race in 813 pregnant women (8% with preeclampsia) in logistic regression models with adjustment for preterm birth (<37 weeks of gestation), maternal age, education, and body mass index at enrollment and clinical center. We further conducted a race stratified analysis and also examined whether any observed association was dependent on the gestational age at delivery and prematurity.ResultsIn an analysis of all races combined, preeclampsia was not more common among pregnant women with a male fetus compared to those with a female fetus (odds ratio [OR] = 1.3, 95% CI = 0.81, 2.24). There was an interaction between African American race and fetal sex in association with preeclampsia after adjustment for preterm delivery and other potential confounders (p = .014). In race stratified analyses, we observed higher odds of preeclampsia among African American pregnant women who carried male fetuses after adjustment for preterm delivery and other potential confounders (adjusted OR = 2.4, 95% CI = 1.12, 5.60).ConclusionWe observed fetal sexual dimorphic differences in the occurrence of preeclampsia in African American women, but not in Whites. Information on fetal sex may ultimately improve the prediction of pre-eclampsia in African American mothers, who might be at higher risk for this adverse condition in pregnancy.

| S-EPMC7954987 | biostudies-literature

Maternal nutrition modulates fetal development through inducing placental efficiency changes in gilts

Project description:Intra-uterine growth restriction (IUGR) and fetal overgrowth increase the risk of postnatal health. Maternal nutrition is the major intrauterine environmental factor that alters fetal weight. However, the mechanisms underlying maternal nutrition affect fetal development is not entirely clear. We developed a pig model and used isobaric tags for relative and absolute quantification (iTRAQ) to investigate alterations in the placental proteome were obtained from gilts in normal-energy-intake (Con) and high-energy-intake (HE) group, respectively.At 90 d of gestation, the heavy fetuses were found at the tubal ends and light fetuses at the cervical ends of the uterus in Con group and the heavy fetuses had higher glucose concentration than the light fetuses. However, a higher uniformity was noted in HE group. Placental promote between these two positions indicated that a total of 78 and 50 differentially expressed proteins were detected in Con and HE group, respectively. In Con group, these proteins related to lipid metabolism (HADHA, AACS, CAD), nutrient transport (GLUT, SLC27A1) and energy metabolism (NDUFV1, NDUFV2, ATP5C1). However, the differentially expressed proteins in HE group were mainly participation in transcriptional and translational regulation and intracellular vesicular transport.

2018-10-26 | PXD004951 | Pride

Maternal nutrition modulates fetal development by inducing placental efficiency changes in gilts.

Project description:BackgroundIntra-uterine growth restriction (IUGR) and fetal overgrowth increase risks to postnatal health. Maternal nutrition is the major intrauterine environmental factor that alters fetal weight. However, the mechanisms underlying the effects of maternal nutrition on fetal development are not entirely clear. We developed a pig model, and using isobaric tags for relative and absolute quantification (iTRAQ), we investigated alterations in the placental proteome of gilts on a normal-energy-intake (Con) and high-energy-intake (HE) diet.ResultsIn the Con group, heavy and light fetuses were found at the tubal and cervical ends of the uterus respectively at 90 d of gestation. Moreover, the heavy fetuses had a higher glucose concentration than the light fetuses. However, a higher uniformity was noted in the HE group. Placental promoters between these two positions indicated that 78 and 50 differentially expressed proteins were detected in the Con and HE groups respectively. In the Con group, these proteins were involved in lipid metabolism (HADHA, AACS, CAD), nutrient transport (GLUT, SLC27A1), and energy metabolism (NDUFV1, NDUFV2, ATP5C1). However, in the HE group they mainly participated in transcriptional and translational regulation, and intracellular vesicular transport.ConclusionsOur findings revealed that maternal nutrition may alter birth weight mainly through the modulation of placental lipid and energy metabolism, which also provides a possible mechanism to explain the higher uniformity of fetal weight in gilts fed a HE diet.

| S-EPMC5331709 | biostudies-literature

Fetal sex and maternal pregnancy outcomes: a systematic review and meta-analysis.

Project description:BACKGROUND:Since the placenta also has a sex, fetal sex-specific differences in the occurrence of placenta-mediated complications could exist. OBJECTIVE:To determine the association of fetal sex with multiple maternal pregnancy complications. SEARCH STRATEGY:Six electronic databases Ovid MEDLINE, EMBASE, Cochrane Central, Web-of-Science, PubMed, and Google Scholar were systematically searched to identify eligible studies. Reference lists of the included studies and contact with experts were also used for identification of studies. SELECTION CRITERIA:Observational studies that assessed fetal sex and the presence of maternal pregnancy complications within singleton pregnancies. DATA COLLECTION AND ANALYSES:Data were extracted by 2 independent reviewers using a predesigned data collection form. MAIN RESULTS:From 6522 original references, 74 studies were selected, including over 12,5 million women. Male fetal sex was associated with term pre-eclampsia (pooled OR 1.07 [95%CI 1.06 to 1.09]) and gestational diabetes (pooled OR 1.04 [1.02 to 1.07]). All other pregnancy complications (i.e., gestational hypertension, total pre-eclampsia, eclampsia, placental abruption, and post-partum hemorrhage) tended to be associated with male fetal sex, except for preterm pre-eclampsia, which was more associated with female fetal sex. Overall quality of the included studies was good. Between-study heterogeneity was high due to differences in study population and outcome definition. CONCLUSION:This meta-analysis suggests that the occurrence of pregnancy complications differ according to fetal sex with a higher cardiovascular and metabolic load for the mother in the presence of a male fetus. FUNDING:None.

| S-EPMC7216628 | biostudies-literature

The eutheria-specific miR-290 cluster modulates placental growth and maternal-fetal transport.

Project description:The vertebrate-specific ESCC microRNA family arises from two genetic loci in mammals: miR-290/miR-371 and miR-302. The miR-302 locus is found broadly among vertebrates, whereas the miR-290/miR-371 locus is unique to eutheria, suggesting a role in placental development. Here, we evaluate that role. A knock-in reporter for the mouse miR-290 cluster is expressed throughout the embryo until gastrulation, when it becomes specifically expressed in extraembryonic tissues and the germline. In the placenta, expression is limited to the trophoblast lineage, where it remains highly expressed until birth. Deletion of the miR-290 cluster gene (Mirc5) results in reduced trophoblast progenitor cell proliferation and a reduced DNA content in endoreduplicating trophoblast giant cells. The resulting placenta is reduced in size. In addition, the vascular labyrinth is disorganized, with thickening of the maternal-fetal blood barrier and an associated reduction in diffusion. Multiple mRNA targets of the miR-290 cluster microRNAs are upregulated. These data uncover a crucial function for the miR-290 cluster in the regulation of a network of genes required for placental development, suggesting a central role for these microRNAs in the evolution of placental mammals.

| S-EPMC5675445 | biostudies-literature

Fetal sex and maternal postpartum depressive symptoms: findings from two prospective pregnancy cohorts.

Project description:BackgroundFetal sex is known to modify the course and complications of pregnancy, with recent evidence of sex-differential fetal influences on the maternal immune and endocrine systems. In turn, heightened inflammation and surges in reproductive hormone levels associated with pregnancy and parturition have been linked with the development of perinatal depression. Here, we examined whether there is an association between fetal sex and maternal depression assessed during the prenatal and postnatal periods.MethodsThe study included two multi-ethnic, prospective pregnancy cohorts that enrolled women from prenatal clinics in the Northeastern United States between 2001 and 2018. Maternal depressive symptoms were measured during the prenatal and postnatal periods using the Edinburgh Postpartum Depression Scale (EPDS), and newborn sex was reported by the mother following delivery. We used logistic regression to examine associations between fetal sex and maternal depressive symptoms (EPDS > 10) during the prenatal period only, postnatal period only, or both periods versus no depressive symptoms during either period. We considered both unadjusted models and models adjusted for a core set of sociodemographic and lifestyle variables.ResultsIn adjusted models using PRISM data (N = 528), women pregnant with a male versus female fetus had significantly greater odds of depressive symptoms during the postnatal period compared to women without depressive symptoms during either period (odds ratio [OR] = 5.24, 95% confidence interval [CI] = 1.93, 14.21). The direction of results was consistent in the ACCESS cohort, although the findings did not reach statistical significance (OR = 2.05, 95% CI = 0.86, 4.93). Significant associations were not observed in either cohort among women with prenatal symptoms only or women with prenatal and postnatal symptoms.ConclusionsMale fetal sex was associated with the onset of depressive symptoms during the postnatal period.

| S-EPMC7789145 | biostudies-literature

Independent influences of maternal obesity and fetal sex on maternal cardiovascular adaptation to pregnancy: a prospective cohort study.

Project description:Background/objectivesSuccessful pregnancy requires the de novo creation of low-resistance utero-placental and feto-placental circulations and incomplete remodeling of this vasculature can lead to maternal or fetal compromise. Maternal BMI and fetal sex are known to influence vascular compliance and placental development, but it is unknown if these are independent or synergistic effects. Here we aim to investigate the impact of maternal obesity, fetal sex, and any interaction thereof on maternal cardiovascular adaptation to pregnancy, by assessing the physiological drop of uterine artery doppler pulsatility (UtA-PI) and umbilical artery doppler pulsatility index (UA-PI) over gestation.Subjects/methodsNulliparous women with a singleton pregnancy participating in a prospective cohort study (n = 4212) underwent serial UtA-PI and UA-PI measurements at 20-, 28- and 36-weeks gestation. Linear mixed regression models were employed to investigate the influence of maternal BMI, fetal sex and interactions thereof on the magnitude of change in UtA-PI and UA-PI.ResultsThroughout gestation, UtA-PI was higher for male fetuses and UA-PI was higher for female fetuses. The physiological drop of UtA-PI was significantly smaller in overweight (change -24.3% [95%CI -22.3, -26.2]) and obese women (change -21.3% [-18.3, -24.3]), compared to normal-weight women (change -25.7% [-24.3, -27.0]) but did not differ by fetal sex. The physiological drop in UA-PI was greater for female than male fetuses (-32.5% [-31.5, -33.5] vs. -30.7% [-29.8, -31.7]) but did not differ by maternal BMI. No interactions between maternal BMI and fetal sex were found.ConclusionsMaternal cardiovascular adaptation to pregnancy is independently associated with maternal BMI and fetal sex. Our results imply sexual dimorphism in both maternal cardiovascular adaptation and feto-placental resistance.

| S-EPMC7577853 | biostudies-literature

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