Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1010777 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25891100_1.fastq.gz | Fastqsanger.gz | |||
| SRR25891100_2.fastq.gz | Fastqsanger.gz | |||
| SRR25891101_1.fastq.gz | Fastqsanger.gz | |||
| SRR25891101_2.fastq.gz | Fastqsanger.gz | |||
| SRR25891102_1.fastq.gz | Fastqsanger.gz |
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Project description:Bazedoxifene and conjugated estrogens (CE+BZA) combination has been shown to prevent visceral adiposity and weight gain after menopause. However, its interaction with the microbiota has yet to be examined. In the present study, we use several –omics technologies to characterize the effects of various estrogens on the health of gut-liver axis. As reported in previous studies, CE+BZA combination is very effective at preventing ovariectomy-induced weight gain in mice fed a high-fat diet. Additionally, CE+BZA induces unique liver transcriptomic and blood metabolite profiles compared to estradiol, conjugated estrogens alone, and bazedoxifene alone. Several pathways and metabolites influenced are associated with lower rates of inflammation and overall benefits to gut and liver health. Finally, microbiome analysis shows that several bacterial species that potentially metabolize estrogens and affect their half-life in the body were significantly changed in CE+BZA treated mice. Our findings indicate a possible link between certain estrogens and gut microbiome and suggest a metabolic benefit of estrogens through manipulation of the gut-liver axis.
2018-02-13 | GSE92968 | GEO
Project description:Bazedoxifene and conjugated estrogens (CE+BZA) combination has been shown to prevent visceral adiposity and weight gain after menopause. However, its interaction with the microbiota has yet to be examined. In the present study, we use several –omics technologies to characterize the effects of various estrogens on the health of gut-liver axis. As reported in previous studies, CE+BZA combination is very effective at preventing ovariectomy-induced weight gain in mice fed a high-fat diet. Additionally, CE+BZA induces unique liver transcriptomic and blood metabolite profiles compared to estradiol, conjugated estrogens alone, and bazedoxifene alone. Several pathways and metabolites influenced are associated with lower rates of inflammation and overall benefits to gut and liver health. Finally, microbiome analysis shows that several bacterial species that potentially metabolize estrogens and affect their half-life in the body were significantly changed in CE+BZA treated mice. Our findings indicate a possible link between certain estrogens and gut microbiome and suggest a metabolic benefit of estrogens through manipulation of the gut-liver axis.
2019-12-28 | GSE93096 | GEO
Project description:Dietary fiber can suppress excess adipose tissue and weight gain in rodents and humans when fed high fat diets. The gut microbiome is thought to have a key role, although exactly how remains unclear. In a tightly controlled murine study, we explored how different types of dietary fiber and doses affect the gut microbiota and gut epithelial gene expression. We show that 10% pectin and 10% FOS suppress high fat diet (HFD)-induced weight gain, effects not seen at 2% doses. Furthermore, 2 and 10% mixtures of dietary fiber were also without effect. Distinct gut microbiota profiles were stimulated at the family and operational taxonomic unit (OTU) level by the different fiber treatments. Plasma levels of the gut hormone PYY were elevated by 10% pectin and FOS, but not 10% mixed fibers, and similarly RNA seq revealed some distinct effects of the 10% single fibers on gut epithelial gene expression. These data show how the ability of dietary fiber to suppress HFD-induced weight gain is dependent upon both fiber type and dose. It also shows that the microbial response to dietary fiber is distinct and that there is not a single microbial response associated with the inhibition of adiposity and weight gain. PYY seems key to the latter response, although the role of other factors such as Reg3g and CCK needs to be explored.
2025-02-05 | GSE288466 | GEO
Project description:Imeglimin is a recently developed anti-diabetic drug that could concurrently promote insulin secretion and insulin sensitivity, while its mechanisms of action are not fully understood. Here we show that imeglimin administration could protect mice from high fat diet-induced weight gain with enhanced energy expenditure and attenuated whitening of brown adipose tissue. Imeglimin administration led to significant alteration of gut microbiota, which included an increase of Akkermansia genus, with attenuation of obesity-associated gut pathologies. Ablation of microbiota by antibiotic treatment partially abrogated the insulin sensitizing effects of imeglimin, while not affecting its actions on body weight gain or brown adipose tissue. Collectively, our results characterize imeglimin as a potential agent promoting energy expenditure and gut integrity, providing new insights into its mechanisms of action.
2024-02-16 | GSE255432 | GEO
Project description:Morphine and its pharmacological derivatives are the most prescribed analgesics for moderate to severe pain management. However, chronic use of morphine reduces pathogen clearance and induces bacterial translocation across the gut barrier. The enteric microbiome has been shown to play a critical role in the preservation of the mucosal barrier function and metabolic homeostasis. Here, we show for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of the gram-positive pathogenic and reduction of bile-deconjugating bacterial strains. A significant reduction in both primary and secondary bile acid levels was seen in the gut, but not in the liver with morphine treatment. Morphine induced microbial dysbiosis and gut barrier disruption was rescued by transplanting placebo-treated microbiota into morphine-treated animals, indicating that microbiome modulation could be exploited as a therapeutic strategy for patients using morphine for pain management. In this study, we establish a link between the two phenomena, namely gut barrier compromise and dysregulated bile acid metabolism. We show for the first time that morphine fosters significant gut microbial dysbiosis and disrupts cholesterol/bile acid metabolism. Changes in the gut microbial composition is strongly correlated to disruption in host inflammatory homeostasis13,14 and in many diseases (e.g. cancer/HIV infection), persistent inflammation is known to aid and promote the progression of the primary morbidity. We show here that chronic morphine, gut microbial dysbiosis, disruption of cholesterol/bile acid metabolism and gut inflammation; have a linear correlation. This opens up the prospect of devising minimally invasive adjunct treatment strategies involving microbiome and bile acid modulation and thus bringing down morphine-mediated inflammation in the host.
2016-06-01 | E-MTAB-3722 | biostudies-arrayexpress
Project description:Background & Aims: Non-alcoholic fatty liver disease (NALFLD)-associated changes in gut microbiota are important drivers of disease progression toward fibrosis. Therefore, reversing microbiota alterations could ameliorate NAFLD progression. Oat beta-glucan, a non-digestible polysaccharides, has shown promising therapeutic effects on hyperlipidemia associated with NAFLD, but its impact on gut microbiota and most importantly NAFLD fibrosis remains unknown. Methods: We performed detailed metabolic phenotyping including body composition, glucose tolerance, and lipid metabolism as well as comprehensive characterization of the gut-liver axis in a western-style diet (WSD)-induced model of NAFLD and assessed the effect of a beta-glucan intervention on early and advanced liver disease. Gut microbiota was modulated using broad-spectrum antibiotic (Abx) treatment. Results: Oat beta-glucan supplementation did not affect WSD-induced body weight gain, glucose intolerance, and the metabolic phenotype remained largely unaffected. Interestingly, oat beta-glucan dampened NAFLD inflammation, associated with significantly reduced monocyte-derived macrophages (MoMFs) infiltration, fibroinflammatory gene expression, and strongly reduced fibrosis development. Mechanistically, this protective effect was not mediated by changes in bile acid composition or signaling, but was dependent on gut microbiota and was lost upon Abx treatment. Specifically, oat beta-glucan partially reversed unfavorable changes in gut microbiota, resulting in an expansion of protective taxa, including Ruminococcus, and Lactobacillus followed by reduced translocation of TLR ligands. Conclusions: Our findings identify oat beta-glucan as a highly efficacious food supplement that dampens inflammation and fibrosis development in diet-induced NAFLD. These results, along with its favorable dietary profile, suggest that it may be a cost-effective and well-tolerated approach to preventing NAFLD progression and should be assessed in clinical studies.
2024-01-01 | GSE246738 | GEO
Project description:This pilot research trial studies the effects of chemotherapy on intestinal bacteria/organisms (microbiota) in patients newly diagnosed with breast cancer. Change in intestinal microbiota may be associated with weight gain in patients treated with chemotherapy. Weight gain has been also associated with cancer recurrence. Examining the types and quantity of bacterial composition in the stool of breast cancer patients treated with chemotherapy may help determine whether body weight and composition are associated with changes in the intestinal microbiota and allow doctors to plan better treatment to prevent weight gain and possibly disease recurrence.
| 2184354 | ecrin-mdr-crc
Project description:The gut microbiota influences both local and systemic inflammation. Inflammation contributes to development, progression and treatment of cancer, but it remains unclear whether commensal bacteria affect inflammation in the sterile tumor microenvironment. Here we show that disruption of the microbiota impairs the response of subcutaneous tumors to CpG-oligonucleotide immunotherapy and platinum chemotherapy. In antibiotic-treated or germ-free mice, tumor-infiltrating myeloid-derived cells responded poorly to therapy, resulting in lower cytokine production and tumor necrosis after CpG-oligonucleotide treatment, and deficient production of reactive oxygen species and cytotoxicity following chemotherapy. Thus, optimal responses to cancer therapy require an intact commensal microbiota that mediates its effects by modulating myeloid-derived cell functions in the tumor microenvironment. These findings underscore the importance of the microbiota in the outcome of disease treatment. Oxaliplatin treatment induces expression of pro-inflammatory genes, which are inhibited by antibiotic pretreatment. Our goal was to ascertain the effect of antibiotic on the tumor gene expression profile prior to treatment and early on after the treatment with chemotherapy (oxaliplatin). The time points were selected t
2013-12-03 | E-GEOD-51414 | biostudies-arrayexpress
Project description:We generate B-cell-specific Tlr9-deficient (Tlr9fl/fl/Cd19Cre+/-, KO) B6 mice and model obesity using a high-fat diet. Compared with control mice, B cell Tlr9-deficient mice exhibited increased weight gain, impaired glucose and insulin tolerance, reduced IL-10-producing B cells and increased inflammation in fat tissues. Tlr9 deficiency affected B cell differentiation, immunoglobulin levels, and T cell subsets. Furthermore, altered gut microbiota in B-cell-specific Tlr9-deficient mice led to a pro-inflammatory status in gut associated lymphoid tissues and glucose metabolism dysregulation. Using 16S rRNA sequencing we report altered gut microbial communities in the KO mice. Indeed, a reduction in Lachnospiraceae, may play a key role in the observed metabolic phenotypes in KO mice. Also, We identify an important network involving Tlr9, Irf4 and Il-10.
2024-04-11 | GSE263396 | GEO
Project description:Gut microbiota is involved in metabolic disorders. However, microbiome-based therapeutic interventions are not always effective, which might be due to interference of the host factors. Here, we first identified a strong positive correlation between OPN levels and BMI in humans. Next, we confirmed that OPN could aggravate high-fat diet induced metabolic disorders in mice. Importantly, we found that fecal microbiota transplantation from OPN-deficient mice significantly alleviated metabolic disorders in WT mice. OPN directly induces remodeling of the gut microbiota both in vitro and in vivo. These findings indicate that OPN could contribute to metabolic disorders by inducing an alteration of gut microbiota. OPN regulated the relative abundance of Lactobacillus by decreasing the adhesion of Lactobacillus to intestinal epithelial cells through Notch signaling pathway. These data identify OPN may serve as a potential pharmaceutical target for weight control and metabolic disorders treatment.
2022-10-26 | GSE216386 | GEO