Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1184377 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31303740_1.fastq.gz | Fastqsanger.gz | |||
| SRR31303740_2.fastq.gz | Fastqsanger.gz | |||
| SRR31303741_1.fastq.gz | Fastqsanger.gz | |||
| SRR31303741_2.fastq.gz | Fastqsanger.gz | |||
| SRR31303742_1.fastq.gz | Fastqsanger.gz |
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Project description:<p>The global rise in maternal obesity increases the risk of adverse maternal and neonatal outcomes. This study demonstrates that both long- (12 weeks) and short-term (gestational) exposure to a high-fat diet (HFD) induces uterine labor disorders, elevates stillbirth rates, and alters gut microbiota composition. Fecal microbiota transplantation (FMT) reveals that HFD inhibits uterine AMPK phosphorylation and reduces COX4 expression via gut microbiota modulation, further contributing to labor dysfunction. Faecalibaculum rodentium, a dominant gut bacterium, shows a negative correlation with stillbirth incidence. Transplantation of Faecalibaculum rodentium mitigates HFD-induced labor disorders, restores uterine ATP levels, and reduces stillbirth rates. This intervention increases serum butyric and acetic acid levels, which inhibit ERK phosphorylation via the GPR41 receptor and activate AMPK phosphorylation, promoting Nrf1 and PGC1 expression. These findings highlight the pivotal role of Faecalibaculum rodentium in counteracting HFD-induced uterine mitochondrial dysfunction and stillbirth.</p>
2025-08-22 | MTBLS12877 | MetaboLights
Project description:<p>Abstract</p><p>Background The gut microbiota mediates dietary impacts on host metabolism, but the roles of specific amino acids remain elusive. We investigated the mechanism by which dietary leucine restriction combats obesity.</p><p>Methods Combining Mendelian randomization in humans with intervention studies in high-fat diet mice, we assessed leucine restriction's effects. Mechanisms were probed via fecal microbiota transplantation, 16S rRNA sequencing, and serum non-targeted metabolomics.</p><p>Results Human genetics suggested a causal role for leucine in obesity. In mice, leucine restriction ameliorated metabolic disorders, and this effect was transferable by microbiota transplantation. We identified Faecalibaculum rodentium (F. rodentium) as a key enriched bacterium. Monocolonization with this strain replicated the anti-obesity benefits, which were linked to upregulated levels of the metabolite glycerophospho-N-oleoyl ethanolamine (GNOE), which correlated negatively with obesity phenotypes and was implicated in lipid and bile acid metabolism.</p><p>Conclusion Dietary leucine restriction confers metabolic benefits by enriching the gut microbe F. rodentium, which modulates host glycerophospholipid metabolite GONE to reduce obesity.</p><p>Key words: Obesity; Leucine restriction; Gut microbiota; Faecalibaculum rodentium; Glycerophospho-N-oleoyl ethanolamine</p>
2025-11-07 | MTBLS13281 | MetaboLights
Project description:Microbiota composition regulates colitis severity, yet mechanisms employed by the innate immune system to regulate this remain unclear. We show that severity of colitis in Clec12a deficient animals is dependent on microbiota composition. Microbiota from a Clec12a-/- animal has expanded Faecalibaculum rodentium and transplantation of the Clec12a-/- microbiota or treatment with F. rodentium is sufficient to worsen colitis in wild-type mice. However, Clec12a-/- animals are resistant to colitis developmemt when rederived into an 11-member community, while addition of F. rodentium worsens disease. Colitis in Clec12a-/- mice is dependent on monocytes and cytokine and sequencing analysis in Clec12a-/- macrophages and serum shows enhanced inflammation with a reduction in phagocytic genes. We demonstrate that F. rodentium specifically binds to Clec12a and Clec12a-/- deficient macrophages are specifically impaired in their ability to phagocytose F. rodentium. Thus, Clec12a is an innate-immune surveillance mechanism to control the expansion of potentially harmful commensals while limiting inflammation
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Project description:Faecalibaculum rodentium strain:Alo17 Genome sequencing and assembly
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Project description:Samples are small extracellular vesicles isolated from the serum of control mice (WTexo) and adipo-FtMT mice (TGexo) fed a high fat diet with doxycycline for 3 weeks. The adipo-FtMT mouse is a model of doxycycline-inducible, adipocyte-specific overexpression of mitochondrial ferritin (FtMT) to induce mitochondrial dysfunction and oxidative stress
2020-08-03 | MSV000085896 | MassIVE
Project description:Gut microbiota has profound effects on obesity and associated metabolic disorders. Targeting and shaping the gut microbiota via dietary intervention using probiotics, prebiotics and synbiotics can be effective in obesity management. Despite the well-known association between gut microbiota and obesity, the microbial alternations by synbiotics intervention, especially at the functional level, are still not characterized. In this study, we investigated the effects of synbiotics on high fat diet (HFD)-induced metabolic disorders, and systematically profiled the microbial profile at both the phylogenetic and functional levels. Synbiotics significantly reversed the HFD-induced change of microbial populations at the levels of richness, taxa and OTUs. Potentially important species Faecalibaculum rodentium and Alistipes putredinis that might mediate the beneficial effects of synbiotics were identified. At the functional level, short chain fatty acid and bile acid profiles revealed that interventions significantly restored cecal levels of acetate, propionate, and butyrate, and synbiotics reduced the elevated total bile acid level. Metaproteomics revealed the effect of synbiotics might be mediated through pathways involved in carbohydrate, amino acid, and energy metabolisms, replication and repair, etc. These results suggested that dietary intervention using our novel synbiotics alleviated HFD-induced weight gain and restored microbial ecosystem homeostasis phylogenetically and functionally.
2022-02-22 | PXD009564 | Pride
Project description:Regulation of organismal homeostasis in response to nutrient availability is a vital physiological process that involves inter-organ communication. Understanding the mechanisms controlling systemic cross talk for maintenance of metabolic health is critical to counteract diet-induced obesity. Here, we show that cardiac-derived transforming growth factor beta 1 (TGF-b1) protects against weight gain and glucose intolerance in mice subjected to high-fat diet. Secretion of TGF-b1 by cardiomyocytes correlates with bioavailability of this factor in circulation. TGF-b1 prevents adipose tissue inflammation independent of body weight and glucose metabolism phenotypes, suggesting protection from adipocyte dysfunction-driven immune cell recruitment. TGF-b1 alters gene expression programs in white adipocytes, favoring their thermogenic fate and consequently increasing their mitochondrial oxygen consumption rates. Ultimately, subcutaneous and visceral white adipose tissue from heart-specific TGF-b1 transgenic mice fail to undergo cellular hypertrophy, leading to reduced overall adiposity during high-fat feeding. Thus, TGF-b1 is a critical mediator of heart-fat communication for regulation of systemic metabolism.
2021-11-03 | GSE179102 | GEO
Project description:Objective: To study if diabetic and insulin-resistant states lead to mitochondrial dysfunction in the liver, or alternatively, if there is adaption of mitochondrial function to these states in the long-term range. Results: High-fat diet (HFD) caused insulin resistance and severe hepatic lipid accumulation, but respiratory chain parameters were unchanged. Livers from insulin-resistant IR/IRS-1+/- mice had normal lipid contents and normal respiratory chain parameters, however showed mitochondrial uncoupling. Livers from severely hyperglycemic and hypoinsulimic, streptozotocin (STZ)-treated mice had massively depleted lipid levels, but respiratory chain abundance was unchanged. However, their mitochondria showed increased abundance and activity of the respiratory chain, which was better coupled compared to controls. Conclusions: Insulin resistance, either induced by obesity or by genetic manipulation, does not cause mitochondrial dysfunction in the liver of mice. However, severe insulin deficiency and high blood glucose levels in mice cause an enhanced performance of the respiratory chain, probably in order to maintain the high energy requirement of the unsuppressed gluconeogenesis. We performed gene expression microarray analysis on liver tissue derived from mice treated with STZ or standard diet (control).
2013-12-10 | E-GEOD-39752 | biostudies-arrayexpress
Project description:Long-term high fat feeding leads to hepatic steatosis, dyslipidemia, and a pro-inflammatory state. In a previous study, we observed this dysregulated metabolic phenotype when C57BL/6 mice were fed a high fat diet (HFD) for sixteen weeks. Additionally, a five-fold increase in liver gene expression of serum amyloid A-1 (SAA-1), an acute phase response protein that associates with high density lipoprotein (HDL), was observed. Inflammation induced changes composition may alter HDL functions, including anti-oxidant, anti-inflammatory and reverse cholesterol transport properties. Diet-induced onset and progression of HDL dysfunction is poorly understood. To examine the relationship between high fat diet and HDL dysfunction, we performed a short-term diet study. Four-week high fat feeding caused an increase in total plasma cholesterol compared with mice fed normal control diet (ND). No change in plasma triglycerides or development of hepatic steatosis was observed. These mice did however show evidence for increase in acute phase reactants, with a 3.25-fold increase in SAA-1 expression in liver. Heavy water labelling was used to determine the turnover rates of proteins associated with HDL. High fat diet resulted in increased fractional catabolic rate (HFD vs ND) of several acute phase response proteins involved ininnate immunity , including – Complement C3 (7.06 ± 0.99 vs 5.20 ± 0.56 %/h, p < 0.005), complement factor B (6.17 ± 0.59 vs 5.09 ± 0.87 %/h, p < 0.05), complement Factor H (4.16 ± 0.41 vs 3.56 ± 0.36 %/h, p < 0.05), and Complement factor I (3.50 ± 0.26 vs 2.75 ± 0.14 %/h, p < 0.005). Our findings suggest that early immune response-induced inflammatory remodeling of HDL precedes the diet-induced steatosis and dyslipidemia. Early HDL dysfunction reflected on impaired reverse cholesterol transport likely results in increase in plasma cholesterol in the absence of other lipid abnormalities.
2021-09-08 | PXD010272 | Pride