Mouse gut metagenome
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR161989_1.fastq.gz | Fastqsanger.gz | |||
| DRR161989_2.fastq.gz | Fastqsanger.gz | |||
| DRR161990_1.fastq.gz | Fastqsanger.gz | |||
| DRR161990_2.fastq.gz | Fastqsanger.gz | |||
| DRR161991_1.fastq.gz | Fastqsanger.gz |
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Project description:Postnatal gut microbiota does not directly impact the obesity of offspring of GF mother
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Project description:Maternal obesity is increasingly common and negatively impact offspring health. Children born to mothers with obesity are at higher risk of developing diseases associated with abnormalities within the hematopoietic system such as atypical immune profiles, hematopoiesis, and metabolic diseases such as type 2 diabetes. Interestingly, disease risks are often dependent on the offspring’s sex, suggesting sex-specific reprogramming effect of maternal obesity on offspring hematopoietic stem and progenitor cell (HSPC) function. However, the impact of maternal obesity exposure on offspring HSPC function is largely unknown, and the capability of HSPC to regulate offspring metabolic health has not been studied. Here we examined differential transcriptomes of hematopoietic stem and progenitor cells from male and female pups (postnatal day 21) from dams given western diet or control diet. RNA-seq revealed inflammatory gene pathways in female MatOb offspring that potentially protect HSPC function.
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Project description:Gut microbiota play an important role in regulating individual health. It is also increasingly apparent that changes in maternal gut microbiota result can render her offspring more susceptible to diseases later in life. Such bacterial induced changes likely originate in the womb. As the placenta is the primary communication organ between mother and conceptus, it is vulnerable to in utero environmental changes, including those associated with maternal gut microbiota. The placenta also relays nutritional and other factors, including serotonin, to the developing fetal brain that help guide development of this organ. Thus, placental disruptions can influence the placenta-brain axis and subsequently neurobehavioral programming with potential long-term consequences. One mechanism by which changes in maternal gut microbiota might effect the placenta are through alterations in bacterial short chained fatty acids (SCFA). The hypothesis, thus, tested in the current studies is that absence of a maternal gut microbiota, as occurs in germ-free (GF) mice, would impact bacterial SCFA in her fecal samples and in the fetal placenta and brain. Secondarily, we tested whether transcriptomic changes would be evident in the placenta and fetal brain from conceptuses derived from GF relative to multi-pathogen free (MPF) pregnant females.
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Project description:Postnatal gut microbiota in offspring of propionate-supplemented mothers
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Project description:Maternal gut microbiota in pregnancy influences obesity in offspring
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Project description:Postnatal gut microbiota in offspring of high-fiber diet-fed mothers
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Project description:Early-life factors, including nutrition, shape long-term health outcomes. Despite the essential role of lactation in maternal nutritional support, the influence of epigenetic factors on lactation and postnatal growth remains poorly understood. Zinc-finger protein 57 (ZFP57), is an epigenetic regulator of genomic imprinting, a process that directs gene expression based on parental origin, playing a vital role in mammalian prenatal growth. Here, we identify a novel function of ZFP57 in the mammary gland, where it serves as a key modulator of postnatal resource control, independently of imprinted genes. ZFP57 regulates multiple aspects of mammary gland functions, including ductal branching and cellular homeostasis. Its absence leads to significant differential gene expression, related to alveologenesis, lactogenesis and milk synthesis, associated with delayed lactation and altered milk composition. This results in life-long impacts on offspring including the development of metabolic syndrome. Cross-fostering reveals intricate dynamics between mother and offspring during lactation. Pups raised by a dam of a different genotype than their birth-mother exhibit exacerbated metabolic features in adulthood. This study shows a novel mechanism responsible for the programming of offspring long-term health by maternal context.
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Project description:To characterize the effect of microbiota on global gene expression in the distal small intestine during postnatal gut development we employed mouse models with experimental colonization by intestinal microbiota. Using microarray analysis to assess global gene expression in ileal mucosa at the critical stage of intestinal development /maturation associated with weaning, and asking how expression is affected by microbial colonization In the study presented here, preweaned and postweaned GF, SPF mouse small intestinal total RNAs were used. Also, 3-week-old gnotobiotic mouse as well as GF mouse small intestinal RNAs were used.
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Project description:Alterations in the gastrointestinal microbiota have been implicated in obesity in mice and humans, but the conserved microbial functions that influence host energy metabolism and adiposity have not been determined. Here we show that bacterial bile salt hydrolase (BSH) controls a microbe-host dialogue which functionally regulates host lipid metabolism and weight gain. Expression of cloned BSH enzymes in the GI tract of gnotobiotic or conventional mice significantly altered plasma bile acid signatures and regulated transcription of key genes involved in lipid metabolism (PPARgamma angptl4), cholesterol metabolism (abcg5/8), gastrointestinal homeostasis (regIIIgamma) and circadian rhythm (dbp, per1/2) in the liver or small intestine. High-level expression of BSH in conventionally raised mice resulted in significant reduction of host weight-gain, plasma cholesterol and liver triglycerides. We demonstrate that bacterial BSH activity significantly impacts systemic metabolic processes and adiposity in the host, and represents a key mechanistic target for the control of obesity and hypercholesterolaemia. Germ free Swiss Webster mice were monocolonised with EC containing the bacterial gene, Bile salt hydroalse. The treatment groups and relevant controls were; 1. Germ Free(GF) n=4 , 2. GF and EC n=4, 3. GF and EC +BSH1 n=4, 4. GF and EC+ BSH2 n=4, 5. GF re-conventionalised (CONV-D) n= 5. The Ileum and Liver were removed and the RNA extracted (RNAeasy plus universal kit (Qiagen), quantified and Microarrays were carried out using mouse Exon ST1.0 arrays (Affymetrix) by Almac Group, Craigavon, Northern Ireland. Analysis and pathway mapping was carried out by ALMAC and using Subio Platform software (Subio Inc) and Genesis Software.
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Project description:Maternal health and diet can have important consequences for offspring nutrition and metabolic health. Signals are communicated from the mother to the infant during lactation through milk via macronutrients, hormones and bioactive molecules. In this study we designed experiments to probe the mother-milk-infant triad in the condition of normal maternal health and upon exposure to high fat diet (HFD) with or without concurrent metformin exposure. We examined maternal characteristics, milk composition and offspring metabolic parameters on postnatal day 16, prior to offspring beginning to wean. We found that lactational HFD increased maternal adipose tissue, mammary gland adipocytes, and altered milk lipid composition causing a higher amount of n-6 long chain fatty acids and lower n-3. Offspring of HFD dams were heavier with more body fat during suckling. Metformin exposure decreased maternal glucose and several amino acids. Offspring of met dams were smaller during suckling. Gene expression in the lactating mammary glands was impacted to a greater extent by metformin but both metformin and HFD altered genes related to muscle contraction, indicating that these genes may be more susceptible to lactational stressors. Our study demonstrates the impact of common maternal exposures during lactation on milk composition, mammary gland function and offspring growth with metformin having little capacity to recuse from the effects of a maternal HFD during lactation.
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