Search Results (185)

Prenatal and postnatal skeletal muscle development in ruminants is coordinated by interactions between genetic, nutritional, epigenetic, and endocrine factors. This review focuses on the influence of maternal nutrition during gestation on fetal myogenesis, satellite cell dynamics, and myogenic regulatory factors expression, including MYF5, MYOD1, and MYOG. Studies in sheep and cattle indicate that nutrient restriction or overnutrition alters muscle fiber number, the cross-sectional area, and the transcriptional regulation of myogenic genes in offspring. Postnatally, muscle hypertrophy is primarily mediated by satellite cells, which are activated via PAX7, MYOD, and MYF5, and regulated through mechanisms such as CARM1-induced chromatin remodeling and miR-31-mediated mRNA expression. Hormonal signaling via the GH–IGF1 axis and thyroid hormones further modulate satellite cell proliferation and protein accretion. Genetic variants, such as myostatin mutations in Texel sheep and Belgian Blue cattle, enhance muscle mass but may compromise reproductive efficiency. Nutritional interventions, including the plane of nutrition, supplementation strategies, and environmental stressors such as heat and stocking density, significantly influence muscle fiber composition and carcass traits. This review provides a comprehensive overview of skeletal muscle programming in ruminants, tracing the developmental trajectory from progenitor cell differentiation to postnatal growth and maturation. These insights underscore the need for integrated approaches combining maternal diet optimization, molecular breeding, and precision livestock management to enhance muscle growth, meat quality, and production sustainability in ruminant systems. Full article

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by restricted social communication and repetitive behaviors. Prenatal stress is critical in neurodevelopment and increases risk for ASD, particularly in those with greater genetic susceptibility to stress. Docosahexaenoic acid (DHA) is one of the most abundant ω-3 fatty acids in the membrane phospholipids of the mammalian brain, and dietary DHA plays an important role in brain development and maintenance of brain structure. In this study, we investigated whether peri-natal supplementation of DHA can alleviate autistic-like behaviors in a genetic risk/stress mouse model and how it alters lipid peroxidation activity and GABAergic system gene expression in the forebrain. Pregnant heterozygous serotonin transporter knockout (SERT-KO) and wild-type (WT) dams were placed in either non-stressed control conditions or chronic variable stress (CVS) conditions and fed either a control diet or a DHA-rich (1% by weight) diet. Offspring of each group were assessed for anxiety and autism-associated behavior at post-natal day 60 using an open field test, elevated plus maze test, repetitive behavior, and the 3-chamber social approach test. A liquid chromatography-mass spectrometry (LC-MS)-based method was used to follow changes in levels of lipid peroxidation products in the cerebral cortex. Male offspring of prenatally stressed SERT-het KO dams exhibited decreased social preference behaviors and increased repetitive grooming behaviors compared to WT control offspring. Moreover, DHA supplementation in male SERT-het mice decreased frequency of grooming behaviors albeit showing no associated effects on social behaviors. Regardless of stress conditions, supplementation of DHA to the WT mice did not result in alterations in grooming nor social interaction in the offspring. Furthermore, no apparent changes were observed in the lipid peroxidation products comparing the stressed and non-stressed brains. Gad2 was downregulated in the cortex of female offspring of prenatally stressed SERT-KO dams, and this change appeared to be rescued by DHA supplementation in offspring. Gad2 was upregulated in the striatum of male offspring of prenatally stressed SERT-KO dams, but DHA did not significantly alter the expression compared to the control diet condition. Full article

Smith–Lemli–Opitz syndrome (SLOS) is a rare, autosomal recessive genetic disorder caused by mutations in the DHCR7 gene, which encodes the enzyme responsible for the final step in cholesterol biosynthesis. Impaired enzyme function leads to cholesterol deficiency, affecting the development and function of the entire organism. The accumulation of cholesterol precursors enhances the formation of oxysterols, which are involved in the pathomechanism of neurological, ophthalmological, and vascular changes in patients. This review analyzes 53 studies published between 2020 and 2025 on the molecular mechanisms underlying the clinical features of SLOS, including cholesterol deficiency, oxysterol accumulation, and the latest diagnostic methods, including LC-MS/MS chromatography and biomarkers such as GFAP for monitoring disease progression. MRI is discussed as a supportive tool for neuroimaging, along with advances in prenatal diagnostics, such as the detection of cholesterol precursors in neonatal hair. Therapeutic options are also reviewed, with particular emphasis on cholesterol supplementation, cholic acid, and experimental treatments such as vitamin E supplementation, statin therapy, gene therapy, and liver transplantation. Current research indicates that expanding knowledge in this area not only improves patient prognosis but also provides hope for the development of effective therapies in the future. Full article

Background and Objectives: Maternal vitamin D (25-hydroxyvitamin D, 25(OH)D) deficiency during pregnancy is associated with adverse outcomes for both mother and fetus. While vitamin D supplementation is commonly recommended, dietary and lifestyle factors influencing maternal 25(OH)D levels at term remain underexplored, particularly in Southern Europe. Aim: This study aimed to investigate prenatal determinants of maternal 25(OH)D levels at the time of delivery, focusing on dietary intake, supplement use, and seasonal variation. Materials and Methods: We conducted a cross-sectional study on 248 pregnant women admitted for delivery at the General Hospital of Piraeus “Tzaneio” between September 2019 and January 2022. A structured questionnaire was used to assess prenatal intake of vitamin D-rich foods (such as fatty fish, eggs, dairy, and fortified products), supplement use (dose, frequency), sun exposure habits, and lifestyle factors. Maternal serum 25(OH)D concentrations were measured from blood samples collected at the time of admission for delivery. Statistical analysis included descriptive statistics and multivariate linear regression to identify independent dietary and supplemental predictors of maternal vitamin D status. Results: A high prevalence of maternal vitamin D deficiency (VDD) was observed, particularly during the autumn and winter months. Women who reported regular intake of vitamin D supplements (400–800 IU daily) had significantly higher 25(OH)D levels compared to those who did not. Dietary intake of vitamin D-rich foods was positively associated with maternal 25(OH)D status, although the effect size was smaller compared to supplementation. Seasonal variation, BMI, and limited sun exposure were also independent predictors. Conclusions: Both vitamin D supplementation and increased dietary intake were positively associated with maternal 25(OH)D concentrations at delivery. These findings underscore the importance of prenatal nutritional assessment and targeted supplementation strategies to prevent maternal VDD in Mediterranean populations. Full article

The intrauterine environment is increasingly recognised as a critical period for the emergence of mental health vulnerabilities. This review explores how adverse maternal exposures, such as psychological stress, infection, malnutrition, and environmental toxins, can disrupt foetal neurodevelopment via epigenetic mechanisms, contributing to the risk of psychiatric and neurodevelopmental disorders. Focusing primarily on human studies, we synthesise evidence on DNA methylation, histone modifications, and non-coding RNAs as key pathways through which the intrauterine environment influences gene regulation in the developing brain. We examine how timing of exposure, foetal sex, and gene–environment interactions modulate these effects, with particular attention to disorders such as schizophrenia, autism spectrum disorder, depression, and anxiety. The placenta emerges as a central mediator, both reflecting and shaping epigenetic changes in response to maternal signals. We also discuss the reversibility of epigenetic marks and highlight emerging interventions, including nutritional supplementation and maternal mental health support, that may buffer or reverse prenatal epigenetic programming. Methodological challenges are addressed, including tissue specificity and causal inference, and future directions are proposed toward integrating epigenetic biomarkers into early risk assessment and precision mental health and psychiatry. This review emphasises the importance of the prenatal period as a window of vulnerability and opportunity for shaping lifelong mental health. Full article

Adolescent binge drinking has lasting behavioral consequences by disrupting the endocannabinoid system (ECS) and depleting brain omega-3. The natural accumulation of omega-3 fatty acids in cell membranes is crucial for maintaining the membrane structure, supporting interactions with the ECS, and restoring synaptic plasticity and cognition impaired by prenatal ethanol (EtOH) exposure. However, it remains unclear whether omega-3 supplementation can mitigate the long-term effects on the ECS, endocannabinoid-dependent synaptic plasticity, and cognition following adolescent binge drinking. Here, we demonstrated that omega-3 supplementation during EtOH withdrawal increases CB1 receptors in hippocampal presynaptic terminals of male mice, along with the recovery of receptor-stimulated [³⁵S]GTPγS binding to Gαi/o proteins. These changes are associated with long-term potentiation (LTP) at excitatory medial perforant path (MPP) synapses in the dentate gyrus (DG), which depends on anandamide (AEA), transient receptor potential vanilloid 1 (TRPV1), and N-methyl-D-aspartate (NMDA) receptors. Finally, omega-3 intake following binge drinking reduced the time and number of errors required to locate the escape box in the Barnes maze test. Collectively, these findings suggest that omega-3 supplementation restores Barnes maze performance to levels comparable to those of control mice after adolescent binge drinking. This recovery is likely mediated by modulation of the hippocampal ECS, enhancing endocannabinoid-dependent excitatory synaptic plasticity. Full article

Objectives: Dietary conditions are closely related to maternal health. This study aims to investigate the causal relationship between the first–second-trimester Dietary Inflammatory Index (DII) and developing anemia in the third trimester. Methods: This prospective cohort study comprised 545 pregnant women, with dietary data assessed via a semi-quantitative food frequency questionnaire (FFQ). Hemoglobin levels were obtained by hospital laboratory tests and used to diagnose anemia. Multivariable logistic regression models—adjusted for baseline serum iron, age, pre-pregnancy body mass index (BMI), occupation, education, history of adverse pregnancy outcomes, parity, serum iron, passive smoking exposure, and iron supplementation use during pregnancy—were employed to evaluate the relationships between the first-trimester DII, second-trimester DII, first–second-trimester average DII, and third-trimester anemia. Results: After multivariable adjustment, the first–second-trimester average DII in the pro-inflammatory diet group demonstrated a 3.73-fold elevated risk of third-trimester anemia compared to the anti-inflammatory diet group (Odds Ratio [OR] = 3.73, 95% Confidence Interval [CI]: 1.50–9.25). Conclusions: Pro-inflammatory dietary patterns during pregnancy exhibit a significant correlation with developing third-trimester anemia. This study demonstrates that reducing dietary pro-inflammatory components through prenatal nutrition programs may lower third-trimester anemia risk. Notably, this study carries potential risks of bias, including self-reporting bias in dietary data and incompletely controlled confounding factors (such as unmeasured biomarkers). Full article

Background: Docosahexaenoic acid (DHA) is the most important fatty acid (FA) for the development and function of brain and retina. Mother’s milk is the predominant source of DHA for the baby’s postnatal life, and the omega 3 FA content of a mother’s diet is highly correlated with the cognitive and visual functions of the infant. However, clinical trials aimed at increasing the DHA content of mother’s milk and thereby improving infant cognitive function have been inconclusive. Methods: In this study, we tested the hypothesis that the molecular form of dietary DHA is important in enriching DHA in mother’s milk as well as in pup tissues. Lactating dams were fed defined diets containing DHA either in the form of triacylglycerol (TAG) or lysophosphatidylcholine (LPC), and the FA composition of mother’s milk and pup tissues was determined on postnatal day 16. Results: The results showed that LPC-DHA was 5-fold more efficient than TAG-DHA in enriching milk DHA. Moreover, DHA content was increased by 31% in the brain, 56% in the retina, and 14% in the liver of the pups by LPC-DHA in the maternal diet, whereas no increases were observed with TAG-DHA. The DHA content of the pup adipose tissue, however, was increased equally by the DHA supplements. Conclusions: These results show that dietary LPC-DHA is a promising new strategy to increase milk DHA content and to potentially improve brain and retinal health in infants. This strategy may be more important in the care of premature infants who miss the critical prenatal period of DHA accretion in the last trimester of pregnancy. Full article

Background: Vitamin D deficiency (VDD) during pregnancy has been associated with various obstetric complications, including preeclampsia, gestational diabetes, and premature rupture of membranes. However, its potential link to placental abruption remains underexplored. The aim of this study was to investigate whether low maternal vitamin D levels are associated with an increased risk of placental abruption in pregnancies considered otherwise low-risk. Methods: We conducted a cross-sectional study involving 248 pregnant women who were admitted for delivery at a public hospital in Athens, Greece. Serum levels of 25-hydroxyvitamin D [25(OH)D] were measured upon admission. Levels below 30 ng/mL were classified as insufficient. Although this threshold corresponds to insufficiency according to the Endocrine Society, for the purposes of this study, levels < 30 ng/mL were treated as indicative of vitamin D deficiency in order to capture broader physiological implications. Cases of placental abruption were identified based on obstetric history and clinical documentation at the time of delivery. A Chi-square test was used to assess the association between vitamin D status and placental abruption, and a multivariate logistic regression model was applied to control for potential confounders, including hypertensive disorders of pregnancy, smoking, and preterm birth. The potential role of vitamin D supplementation during pregnancy was also explored as part of the analysis. Results: Our analysis revealed that women with VDD had a significantly higher incidence of placental abruption (p < 0.05). In the multivariate model, VDD remained an independent risk factor (adjusted OR: 3.2, 95% CI: 1.1–9.6). Additional risk factors that showed significant associations with placental abruption included pregnancy-induced hypertension and maternal smoking. Conclusions: These findings support the hypothesis that insufficient maternal vitamin D levels may contribute to adverse pregnancy outcomes, including placental abruption. Further prospective studies are warranted to clarify the causal mechanisms and to evaluate whether early detection and correction of vitamin D deficiency could serve as a preventive strategy in prenatal care. Full article

Prolonged exposure to fine particulate matter (PM_2.5) has been implicated in accelerated aging, including organ fibrosis. This study aimed to investigate whether prenatal and postnatal PM_2.5 exposure promotes renal fibrogenesis in adulthood and whether long-term vitamin D supplementation alleviates associated renal injury. Pregnant Sprague-Dawley rats were randomly assigned to three groups: control (normal saline, NS), PM_2.5 exposure, and PM_2.5 exposure with vitamin D supplementation during gestation and lactation (n = 3/group). Male offspring were subsequently exposed to the same conditions from postnatal weeks 3 to 8 (n = 7/group). On postnatal day 56, PM_2.5-exposed rats showed lower body weight and more severe glomerular and tubulointerstitial damage compared to controls. Serum calcium levels were elevated in the PM_2.5 group. The expression of intrarenal renin, transforming growth factor-β1, α-smooth muscle actin, and vimentin was upregulated, accompanied by increased collagen deposition. Long-term vitamin D supplementation reversed most of these changes, except for intrarenal vimentin expression and serum calcium levels. These findings indicate that prenatal and postnatal PM_2.5 exposure can activate intrarenal renin signaling and fibrogenic pathways, contributing to renal fibrosis later in life. Long-term vitamin D supplementation may provide partial protective effects against PM_2.5-induced renal fibrogenesis. Full article

Background/Objectives: Neonatal outcomes, including low birth weight, preterm birth, and neonatal mortality, pose significant global health challenges, particularly in low- and middle-income countries. Prenatal care has emerged as a critical intervention in mitigating these risks through medical, nutritional, and psychosocial support. This study aimed to systematically assess the effectiveness of prenatal care interventions in preventing neonatal outcomes across diverse settings. Methods: A systematic review and meta-analysis were conducted according to PRISMA guidelines, with the protocol registered in PROSPERO (CRD42024601066). Fourteen peer-reviewed studies were included following a comprehensive search across five major databases. Eligible studies reported quantitative neonatal outcomes associated with prenatal care interventions, including nutritional supplementation, mental health services, telehealth, and routine antenatal care. Random-effects models were used for meta-analysis, and the risk of bias was assessed using RoB 2 and the Newcastle–Ottawa Scale. Results: Nutritional interventions, especially folic acid and iron supplementation, significantly reduced neonatal mortality by up to 40% (RR = 0.60, 95% CI: 0.54–0.68). High-quality prenatal care was associated with a 41% reduction in neonatal mortality. Psychosocial support reduced the risk of low birth weight and preterm birth, while telehealth interventions lowered NICU admissions in low-risk populations (RR = 0.88, 95% CI: 0.75–1.03). Heterogeneity was substantial (I² = 70%), and publication bias was suggested. Conclusions: Comprehensive prenatal care, integrating medical, nutritional, and mental health interventions, significantly improves neonatal outcomes. The global implementation of accessible, high-quality prenatal services is essential, particularly in underserved populations, to reduce neonatal morbidity and mortality. Full article

Background: Neurobehavioral developmental disorders significantly affect children’s future well-being and contribute to the global disease burden. While prenatal micronutrient supplementation is crucial for fetal neural development, their individual and combined effects on subsequent neurobehavioral outcomes in childhood remain poorly understood. This study aimed to examine the individual and combined effects of prenatal micronutrient supplementation on neurobehavioral developmental disorders in preschool children, and to explore their effects across specific developmental domains. Methods: 15,636 mother-child dyads were recruited from the 2022 children’s survey in Shenzhen, China. Mothers provided information on prenatal supplementation of calcium, folic acid, iron, and multivitamins. Five domains of children’s neurobehavioral functioning were assessed using the Ages and Stages Questionnaire-Third Edition (communication, gross motor, fine motor, problem-solving, and personal-social status). Logistic regression models were used to estimate the effect of micronutrient supplementations on NDDs across crude, adjusted, and full-inclusion models. Combined effects were assessed by multiplicative and additive interactions calculated from crossover analysis. Results: 11.7% of preschool children were identified as at risk for neurobehavioral developmental disorders, with the highest prevalence in the gross motor domain. Prenatal multivitamin supplementation showed a protective effect against neurobehavioral developmental disorders (OR = 0.73, 95% CI = 0.66–0.81). Interaction analysis revealed that the combination of iron and multivitamins further enhanced this protection, with both multiplicative (IOR = 1.26, 95% CI = 1.02–1.57) and additive interactions (RERI = 0.18, 95% CI = 0.02–0.35). The problem-solving domain consistently showed the greatest benefit from the supplementation of these micronutrients individually and in combination. Conclusions: Prenatal multivitamin supplementation reduces the risk of neurobehavioral developmental disorders, especially when combined with iron supplementation. These findings highlight the potential benefits of prenatal co-supplementation strategies to improve neurobehavioral outcomes in offspring. Further studies are recommended to confirm these findings and explore underlying mechanisms. Full article

Fetal programming suggests that maternal nutrition during gestation influences offspring growth, development, and productivity. This study evaluated the effects of prenatal protein-energy supplementation on the lifetime performance of Nellore cattle. Twenty-eight nulliparous heifers were inseminated and assigned to one of two groups: Non-Programmed; receiving only mineral supplementation; or Fetal Programmed (FP); receiving additional protein-energy supplementation throughout gestation. Cows in the FP group maintained significantly better body condition score during gestation (p < 0.01), and their calves exhibited greater body weight (BW) during the first 56 days (p < 0.05) and a tendency to grow to a greater BW up to 250 days (p < 0.10) in addition to improved morphological traits, such as increased rump width and length at 45 days of age (p ≤ 0.02). However, these advantages were not sustained in later growth stages, as no significant differences were observed in final body weight, ultrasound carcass traits, or overall feedlot performance. These findings suggest that while prenatal nutrition can influence early developmental traits, its long-term impact on offspring performance may be limited under consistent postnatal management. Nonetheless, the limited sample size, combined with the absence of molecular data and individual feed intake and efficiency measurements, constrains a more comprehensive interpretation of the programming effects on offspring performance. Further research is needed to explore the molecular mechanisms of fetal programming, particularly its epigenetic effects and interactions with postnatal nutrition, to optimize strategies for improving the efficiency and sustainability of beef cattle. Full article

Background: Prenatal alcohol exposure (PAE) can reduce fetal growth and cause neurodevelopmental disability. Prenatal choline supplements attenuate PAE-induced behavioral and growth deficits; however, the underlying mechanisms are unknown. Alcohol alters nutrient metabolism and potentially increases nutrient needs. Here, we investigate how alcohol affects choline metabolism in the maternal–fetal dyad and the role of supplemental choline. Methods: Pregnant C57BL/6J mice were assigned to one of four groups: alcohol-exposed (3 g/kg alcohol/day) or control +/− 100 mg/kg choline daily from embryonic day (E)8.5–17.5. We performed an exploratory hypothesis-generating analysis of targeted metabolomics on choline-related metabolites in the maternal liver, plasma, placenta, and fetal brain at E17.5 and Spearman correlation analyses to determine their association with gestational and fetal growth outcomes. Results: Although choline levels were largely unaffected by alcohol or choline, alcohol increased many lipid products in the CDP–choline pathway; this was not normalized by choline. Alcohol increased placental CDP–ethanolamine and reduced the maternal hepatic SAM/SAH ratio as well as dimethylglycine and the serine/glycine ratio across the dyad, suggesting a functional insufficiency in methyl donor pools. These outcomes were rescued by supplemental choline. Correlation analyses among choline metabolites and fetal growth outcomes suggest that maternal plasma methionine, serine, and the serine/glycine ratio may be predictive of maternal–fetal choline status. Conclusions: The increased hepatic lipid synthesis that characterizes chronic alcohol exposure may draw choline into phospholipid biosynthesis at the expense of its use as a methyl donor. We propose that PAE increases choline needs, and that its supplementation is necessary to fulfill these competing demands for lipid and methyl use. Full article

Vitamin D is an essential nutrient, involved in various biological processes including calcium homeostasis, bone health, immune function, and brain development. Vitamin D from the mother crosses the placenta during pregnancy, directly impacting the neurodevelopment of the fetus. Vitamin D insufficiency is a substantial global health problem, influencing almost 47.9% of individuals, with especially high predominance rates among pregnant women. Background/Objectives: Preclinical studies suggest that maternal vitamin D deficiency results in significant alterations in the development of the offspring’s brain. Nonetheless, randomized clinical trials in humans have produced conflicting results on the beneficial effect of high-dose vitamin D supplementation during pregnancy on neurodevelopmental outcomes. This review aims to evaluate the association of maternal prenatal vitamin D levels and vitamin D supplementation during pregnancy with offspring neurodevelopment. Methods: This study thoroughly reviewed the literature and searched throughout PubMed, ScienceDirect, Cochrane Library, and Google Scholar, adhering to PRISMA guidelines. Studies assessing maternal vitamin D levels, supplementation, and offspring neurodevelopmental outcomes were included based on predefined eligibility criteria. Results: Among 9686 screened studies, only 20 met the inclusion criteria, representing 18,283 mother–child pairs. A small, non-significant trend suggested a positive association between higher maternal vitamin D levels and offspring cognitive, language, motor, and social-emotional development. The strongest associations were observed in cognitive performance and language acquisition, though inconsistencies emerged across studies. Cord blood vitamin D levels showed no consistent effects on neurodevelopment. Maternal vitamin D supplementation during pregnancy demonstrated no reliable benefits for offspring neurodevelopment, with results varying by study design and participant characteristics. Conclusions: Large-scale, multicenter randomized trials, with standardized neurodevelopmental assessments at multiple ages are needed to define the effects of vitamin D deficiency and supplementation during pregnancy on offspring neurodevelopmental outcomes. Future research should investigate the confounding factors contributing to inconsistencies, including supplementation protocols, genetic variations, and assessment methodologies. Clarifying these aspects will enhance the understanding of maternal vitamin D’s role in fetal neurodevelopment and aid in refining prenatal supplementation guidelines. Full article