Mouse gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB17165 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR524557_1.fastq.gz | Fastqsanger.gz | |||
| DRR524557_2.fastq.gz | Fastqsanger.gz | |||
| DRR524558_1.fastq.gz | Fastqsanger.gz | |||
| DRR524558_2.fastq.gz | Fastqsanger.gz | |||
| DRR524559_1.fastq.gz | Fastqsanger.gz |
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Project description:Introduction: Chronic sleep fragmentation (SF) is prevalent in contemporary human society, highlighting detrimental effects on glucose metabolism and adipose tissue morphology, which is closely linked to gut microbiota composition. However, it remains unclear whether sleep recovery (SR) after prolonged SF can ameliorate glucose metabolism, influence the transcriptome of inguinal white adipose tissue (iWAT), and whether these effects align with alterations in the gut microbiota. Methods: Mice were subjected to 8 weeks of SF and subsequently allowed 2 weeks of SR. We assessed glucose tolerance through intraperitoneal glucose tolerance tests (ipGTT), analyzed gut microbiota via 16s rDNA amplicon sequencing, and examined transcriptomic alterations in iWAT using RNA sequencing. Results: Despite the two-week SR following chronic SF, significant glucose intolerance persisted, accompanied by subtle shifts in the gut microbiota and alterations in gene expression within iWAT. The top hub genes Ncapg, Cenpe, and Tik were identified from the protein-protein interaction network. Conclusion: Even followed by a brief period of SR, prolonged SF still led to ongoing glucose intolerance and alterations in the adipose tissue transcriptome in mice. These changes were intertwined with modifications in the gut microbiome. The shifts in gut microbiota may play a pivotal role in understanding the sustained negative effects of SF.
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Project description:Dietary lipids and gut microbiota may both influence adipose tissue physiology. By feeding conventional and germ-free mice high fat diets with different lipid compositon we aimed to investigate how dietary lipids and the gut microbiota interact to influence inflammation and metabolism in the liver
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Project description:Dietary lipids and gut microbiota may both influence adipose tissue physiology. By feeding conventional and germ-free mice high fat diets with different lipid compositon we aimed to investigate how dietary lipids and the gut microbiota interact to influence inflammation and metabolism in epididymal adipiose tissue (EWAT)
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Project description:Dietary lipids can affect metabolic health through gut microbiota-mediated mechanisms, but the influence of lipid-microbiota interaction on liver steatosis is unknown. We investigated the effect of dietary lipid composition on human microbiota in an observational study and combined diet experiments with microbiota transplants to study lipid-microbiota interactions and liver status in mice. In humans, low intake of saturated fatty acids (SFA) was associated with increased microbial diversity independent of fiber intake. In mice, cecum levels of SFA correlated negatively with microbial diversity and were associated with a shift in butyrate and propionate producers. Mice fed poorly absorbed SFA had improved metabolism and liver status. These features were transmitted by microbial transfer. Diets enriched in n-6- and/or n-3-polyunsaturated fatty acids were protective against steatosis but had minor influence on the microbiota. In summary, we find that unabsorbed SFA correlate with microbiota features that may be targeted to decrease liver steatosis.
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Project description:The immune system is shaped by the balance of n-3 and n-6 polyunsaturated fatty acids (PUFAs), but how these dietary lipids influence dendritic cells (DCs)— key inducers of adaptive immunity—remains largely unexplored. Importantly, whether an excess of n-6 PUFAs, a hallmark of modern diets, could undermine DC function and immune surveillance remains largely unexplored. Here, we uncover a striking link between dietary lipids and DC dysfunction. We found that an n-6 PUFA-rich diet promotes ferroptosis in DCs via suppression of the Nrf2 antioxidant pathway, impairing their antigen presenting capacity. Accordingly, interventions with dietary n-3 PUFAs or ferroptosis inhibitors reversed these effects, restoring DC function and enhancing responses to DC-based chemo-immunotherapy in a preclinical model of metastatic ovarian cancer. These findings suggest that dietary lipids are not just passive components of metabolism but active regulators of DC function and fate. These findings are critical for the creating novel nutritional interventions that improve vaccination and immunotherapy outcomes.
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Project description:Dietary lipids and gut microbiota may both influence adipose tissue physiology. By feeding conventional and germ-free mice high fat diets with different lipid compositon we aimed to investigate how dietary lipids and the gut microbiota interact to influence inflammation and metabolism in the liver Wild-type C57Bl/6 male mice 11 weeks of age were fed isocaloric diets (45% kcal fat) with either menhaden fish oil (Research Diets, D05122102) or lard (Research Diets, D10011202) for 11 weeks. Liver samples were harvested at the end of the experiment and analyzed by microarray.
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Project description:Dietary lipids and gut microbiota may both influence adipose tissue physiology. By feeding conventional and germ-free mice high fat diets with different lipid compositon we aimed to investigate how dietary lipids and the gut microbiota interact to influence inflammation and metabolism in epididymal adipiose tissue (EWAT) Wild-type C57Bl/6 male mice 11 weeks of age were fed isocaloric diets (45% kcal fat) with either menhaden fish oil (Research Diets, D05122102) or lard (Research Diets, D10011202) for 11 weeks. Epididymal WAT samples were harvested at the end of the experiment and analyzed by microarray.
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Project description:We have previously shown that paramylon (PM) supplementation to a high fat diet reduces the postprandial glucose rise, serum total and LDL-cholesterol, and abdominal fat accumulation in mice; however, the mechanism has not been determined. We evaluated the potential mechanism in male C57BL/6J mice fed a high-fat diet supplemented with 5% PM powder, extracted from Eu-glena gracilis, for 12 weeks. Abdominal fat weight, and serum lipids were measured; ileal and hepatic mRNA expression were assessed using DNA microarray and real-time PCR. The poten-tial mechanism of PM on modulating lipid metabolism was explored by gene ontology (GO) classification and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. Dietary supplementation with PM resulted in decreased abdominal fat accumulation and serum LDL-cholesterol concentrations via suppression of the digestion and absorption pathway in the ileum and activation of the hepatic PPAR signaling pathway. Improvement in glucose tolerance may be the result of lipid metabolism modification because the glucose metabolism pathway was not detected by GO classification and KEGG pathway analysis. PM intake also directly enhanced immunoglobulin production.
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