GNPS - Seed - Conturie Probiotic Supplement During Pregnancy
Ontology highlight
ABSTRACT:
INSTRUMENT(S): maXis
ORGANISM(S): Homo Sapiens (ncbitaxon:9606)
SUBMITTER: 
Louise Laurent
PROVIDER: MSV000084010 | GNPS | Mon Jun 24 10:23:00 BST 2019
REPOSITORIES: GNPS
Similar Datasets
Project description:The rate of probiotic usage by pregnant women in the US and Canada ranges from 1.3 to 3.6 %. Probiotic supplements are available without a prescription and have gained currency in treating a variety of ailment ranging from reducing risk of constipation, diarrhea, other gastrointestinal conditions, eczema, pre-term birth, and prevent adverse pregnancy outcomes, including gestational diabetes mellitus (GDM) and depression/anxiety. Three possible mechanisms by which maternal probiotic supplementation might influence the placenta are through 1) directly impacting possible bacteria residing in the placenta (placenta microbiome), 2) altering bacterial metabolites produced by gut microbiota within the mother that induce placental changes, and 3) maternal probiotics might affect the composition of the bacteria within the maternal gut that affects her immune cells and their responses to the heterologous placenta. For the second potential mechanism, bacterial metabolites that might influence placenta include short chain fatty acids (SCFAs), polyamines (PAs), and Vitamins B9 (Folic Acid) and 12 (Cobalamin), among others. This project aims to determine the effects maternal probiotic supplementation in mice might have on the fetal placenta. With the number of women taking over probiotic supplements increasing, further research is needed to determine how these bioactive agents may affect the placenta and health of the offspring.
2025-09-26 | GSE309308 | GEO
Project description:Children born to diabetic and obese or overweight mothers have a higher risk of heart disease at birth and later in life. Our previous work using chromatin immunoprecipitation sequencing revealed that late-gestation diabetes in combination with maternal high fat diet causes a distinct fuel-mediated epigenetic reprogramming of cardiac tissue during fetal cardiogenesis. We used gene expression profiling to investigate the overall transcriptional signature of newborn rat offspring exposed to the combination of maternal diabetes and maternal high fat diet.
2020-09-02 | GSE150649 | GEO
Project description:“Dysbiosis" of the maternal gut microbiome, in response to environmental challenges such as infection, altered diet and stress during pregnancy, has been increasingly associated with abnormalities in offspring brain function and behavior. However, whether the maternal gut microbiome regulates neurodevelopment in the absence of environmental challenge remains unclear. In addition, whether the maternal microbiome exerts such influences during critical periods of embryonic brain development is poorly understood. Here we investigate how depletion, and selective reconstitution, of the maternal gut microbiome influences fetal neurodevelopment in mice. Embryos from antibiotic-treated and germ-free dams exhibit widespread transcriptomic alterations in the fetal brain relative to conventionally-colonized controls, with reduced expression of several genes involved in axonogenesis. In addition, embryos from microbiome-depleted mothers exhibit deficient thalamocortical axons and impaired thalamic axon outgrowth in response to cell-extrinsic guidance cues and growth factors. Consistent with the importance of fetal thalamocortical axonogenesis for shaping neural circuits for sensory processing, restricted depletion of the maternal microbiome from pre-conception through mid-gestation yields offspring that exhibit tactile hyposensitivity in select sensorimotor behavioral tasks. Gnotobiotic colonization of antibiotic-treated dams with a limited consortium of spore-forming bacteria indigenous to the gut microbiome prevents abnormalities in fetal brain gene expression, fetal thalamocortical axonogenesis and adult tactile sensory behavior associated with maternal microbiome depletion. Metabolomic profiling reveals that the maternal microbiota regulates levels of numerous small molecules in the maternal serum as well as the brains of fetal offspring. Select microbiota-dependent metabolites – trimethylamine N-oxide, 5-aminovalerate, imidazole propionate, and hippurate – sufficiently promote axon outgrowth from fetal thalamic explants. Moreover, maternal supplementation with the metabolites during early gestation abrogates deficiencies in fetal thalamocortical axons and prevents abnormalities in tactile sensory behavior in offspring from microbiome-depleted dams. Altogether, these findings reveal that the maternal gut microbiome promotes fetal thalamocortical axonogenesis and select tactile sensory behaviors in mice, likely by signaling of microbially modulated metabolites to neurons in the developing brain.
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Project description:Background: Congenital heart disease (CHD) is a leading cause of death in newborns, yet many of its molecular mechanisms remain unknown. Both maternal obesity and diabetes increase the risk of CHD in offspring, with recent studies suggesting these conditions may have distinct teratogenic mechanisms. The global prevalence of obesity is rising, and while maternal obesity is a known risk factor for fetal CHD, the specific mechanisms are largely unexplored. Methods: We used a murine model of diet-induced maternal obesity, without diabetes, to produce dams that were overweight but had normal blood glucose levels. Embryos were generated and their developing hearts analyzed. Transcriptome analysis was performed using single-nuclei (snRNAseq) and bulk RNA sequencing (RNA-seq). Global and phospho-enriched proteome analysis was performed using tandem-mass tag mass spectroscopy (TMT-MS). Immunobloting and histologic evaluation were also performed. Results: Analysis revealed disrupted oxidative phosphorylation and reactive oxygen species formation, with reduced antioxidant capacity, evidenced by downregulation of genes Sod1 and Gp4x, and disrupted Hif1a signaling. Evidence of oxidative stress, cell death signaling, and alteration in Rho GTPase and actin cytoskeleton signaling was also observed. Genes involved in cardiac morphogenesis, including Hand2, were downregulated, and fewer mature cardiomyocytes were present. Histologic analysis confirmed increased cardiac defects in embryos exposed to maternal obesity. Conclusion: These findings demonstrate maternal obesity alone can result in cardiac defects through mechanisms similar to those associated with maternal hyperglycemia. This study provides valuable insights into the role of maternal obesity, a growing and modifiable risk factor, in the development of the most common birth defect, CHD.
2025-06-30 | PXD062087 | Pride
Project description:Maternal exposures during pregnancy influence the risk of many chronic adult-onset diseases in the offspring. We investigated whether feeding pregnant rats a high fat (HF) or ethinyl-estradiol (EE2)-supplemented diet affects carcinogen-induced mammary cancer risk in daughters, granddaughters and great-granddaughters. Here we show that mammary tumorigenesis is higher in daughters and granddaughters of HF rat dams and in daughters, granddaughters and great-granddaughters of EE2 rat dams. Outcross experiments indicate that increased mammary cancer risk is transmitted to HF granddaughters equally through the female or male germlines, but it is only transmitted to EE2 granddaughters through the female germline. The effects of maternal EE2 exposure on offspring's mammary cancer risk are associated with alternations in the DNA methylation machinery and methylation patterns in mammary tissue of all three EE2 generations. We conclude that dietary and estrogenic exposures in pregnancy increase breast cancer risk in multiple generations of offspring, possibly through non-genetic means We examined the whole genome methylation status of both control and EE2-supplemented diet rats in three consecutive generations
2012-09-20 | E-GEOD-40251 | biostudies-arrayexpress
Project description:Nephron number in the mouse kidney is lowered when maternal protein intake is reduced to 6-8% down from 20% (normal diet). We used single cell sequencing to study the transcriptional response to maternal low protein diet in the mouse embryonic kidney at days E14.5 and P0 (birth).
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Project description:The early-life period is increasingly being recognized as a window of opportunity to shape immunity where microbiota and related probiotics have an important impact. Innate γδ T cells are the first T cells generated in utero populating epithelial tissues such as the lung contributing to tissue protection through, for example, IL17 production. Here, we studied the influence of maternal microbiota and probiotic supplementation during pregnancy on innate γδ T cells in the lung and thymus of newborn mice. Detailed time-kinetic experiments showed that at birth the murine lung T cell population was specifically dominated by IL17-committed γδ T cells expressing an invariant Vγ6Vδ1 TCR. Single-cell-RNA-sequencing showed that the biased IL17-commitment of perinatal lung γδT cells is highly conserved between mice and humans. While maternal microbiota depletion with antibiotics tended to decrease the frequency of the lung Vγ6 T cells of the offspring at birth, the maternal administration of Lacticaseibacillus rhamnosus(L.rhm.), but not of Bifidobacterium animalis subsp.lactis(B.lac.), increased significantly their frequency resulting in the augmentation of the IL17-commitment of the mouse lung T cell compartment. Altogether, our data indicate that the maternal microbiota contributes to the shaping of IL17-committed γδT cells in the lungs of newborns and that maternal administration of specific probiotic strains can enhance this process.
2025-09-16 | GSE278178 | GEO
Project description:Gestational protein restriction is a model for low birth size. We hypothesized that taurine supplementation would protect against changes in newborn liver and muscle caused by a maternal low protein diet. Pregnant mouse dams were subjected to different diet schemes from day 1 of pregnancy until birth. Pups were killed following birth and liver and hindleg skeletal muscle taken out and frozen at -80C until analysis. Diet schemes: Normal Protein (20% casein; NP), Normal Protein + taurine (1% taurine supplementation in water ad libitum; NP+tau), Low Protein (8% casein; LP) and LP+tau The liver and muscle samples were normalized separately.
2009-11-07 | E-GEOD-12730 | biostudies-arrayexpress