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Reversing gut microbiome-driven adipose tissue inflammation alleviates metabolic syndrome.

ABSTRACT: Reversing gut microbiome-driven adipose tissue inflammation alleviates metabolic syndrome.

PROVIDER: PRJNA907777 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22501800.fastq.gz	Fastqsanger.gz
	SRR22501900.fastq.gz	Fastqsanger.gz
	SRR22501801.fastq.gz	Fastqsanger.gz
	SRR22501901.fastq.gz	Fastqsanger.gz
	SRR22501802.fastq.gz	Fastqsanger.gz

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Reversing gut microbiome-driven adipose tissue inflammation alleviates metabolic syndrome [RNA-seq: eWAT]

Project description:Reversing gut microbiome-driven adipose tissue inflammation alleviates metabolic syndrome [RNA-seq: eWAT]

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Reversing gut microbiome-driven adipose tissue inflammation alleviates metabolic syndrome [RNA-seq: ileum]

Project description:Reversing gut microbiome-driven adipose tissue inflammation alleviates metabolic syndrome [RNA-seq: ileum]

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Reversing gut microbiome-driven adipose tissue inflammation alleviates metabolic syndrome [RNA-seq: eWAT]

Project description:We performed unbiased transcriptional profiling of white adipose tissue (eWAT, epididymal white adipose tissue) from mice to determine mechanisms by which xanthohumol and tetrahydroxanthohumol supplementation could ameliorate hepatosteatosis induced by a HFD at the transcriptional level. We conducted RNA-seq analysis of total RNA of ewat obtained from mice after 16 weeks on the diet.

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Reversing gut microbiome-driven adipose tissue inflammation alleviates metabolic syndrome.

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-09-27 | GSE219235 | GEO

Reversing gut microbiome-driven adipose tissue inflammation alleviates metabolic syndrome [RNA-seq: ileum]

Project description:We performed unbiased transcriptional profiling of ileum from mice to determine mechanisms by which xanthohumol and tetrahydroxanthohumol supplementation could ameliorate hepatosteatosis induced by a HFD at the transcriptional level. We conducted RNA-seq analysis of total RNA of ileum obtained from mice after 16 weeks on the diet.

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Reducing gut microbiome-driven adipose tissue inflammation alleviates metabolic syndrome.

Project description:BackgroundThe gut microbiota contributes to macrophage-mediated inflammation in adipose tissue with consumption of an obesogenic diet, thus driving the development of metabolic syndrome. There is a need to identify and develop interventions that abrogate this condition. The hops-derived prenylated flavonoid xanthohumol (XN) and its semi-synthetic derivative tetrahydroxanthohumol (TXN) attenuate high-fat diet-induced obesity, hepatosteatosis, and metabolic syndrome in C57Bl/6J mice. This coincides with a decrease in pro-inflammatory gene expression in the gut and adipose tissue, together with alterations in the gut microbiota and bile acid composition.ResultsIn this study, we integrated and interrogated multi-omics data from different organs with fecal 16S rRNA sequences and systemic metabolic phenotypic data using a Transkingdom Network Analysis. By incorporating cell type information from single-cell RNA-seq data, we discovered TXN attenuates macrophage inflammatory processes in adipose tissue. TXN treatment also reduced levels of inflammation-inducing microbes, such as Oscillibacter valericigenes, that lead to adverse metabolic phenotypes. Furthermore, in vitro validation in macrophage cell lines and in vivo mouse supplementation showed addition of O. valericigenes supernatant induced the expression of metabolic macrophage signature genes that are downregulated by TXN in vivo.ConclusionsOur findings establish an important mechanism by which TXN mitigates adverse phenotypic outcomes of diet-induced obesity and metabolic syndrome. TXN primarily reduces the abundance of pro-inflammatory gut microbes that can otherwise promote macrophage-associated inflammation in white adipose tissue. Video Abstract.

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Deletion of the mitochondrial calcium uniporter in adipose tissue promotes energy expenditure and alleviates diet-induced obesity

Project description:Objectives: Studies have shown a correlation between obesity and mitochondrial calcium homeostasis, yet it is unclear whether and how Mcu regulates adipocyte lipid deposition. This study aims to provide new potential target for the treatment of obesity and related metabolic diseases, and to explore the function of Mcu in adipose tissue. Methods: We firstly investigated the role of mitoxantrone, an Mcu inhibitor, in the regulation of glucose and lipid metabolism in mouse adipocytes (3T3-L1 cells). Secondly, C57BL/6J mice were used as a research model to investigate the effects of Mcu inhibitors on fat accumulation and glucose metabolism in mice on a high-fat diet (HFD), and by using CRISPR/Cas9 technology, adipose tissue-specific Mcu knockdown mice (Mcu fl/+ AKO) and Mcu knockout of mice (Mcu fl/fl AKO) were obtained, to further investigate the direct effects of Mcu on fat deposition, glucose tolerance and insulin sensitivity in mice on a high-fat diet. Results: we found the Mcu inhibitor reduced adipocytes lipid accumulation and adipose tissues mass in mice fed an HFD. Both Mcu fl/+ AKO mice and Mcu fl/fl AKO mice were resistant to HFD-induced obesity, compared to control mice. Mice with Mcu fl/fl AKO showed improved glucose tolerance and insulin sensitivity as well as reduced hepatic lipid accumulation. Mechanistically, inhibition of Mcu promoted mitochondrial biogenesis and adipocyte browning, increase energy expenditure and alleviates diet-induced obesity. Conclusion: Our study demonstrates a link between adipocyte lipid accumulation and mCa2+ levels, suggesting that adipose-specific Mcu deficiency alleviates HFD-induced obesity and ameliorates metabolic disorders such as insulin resistance and hepatic steatosis. These effects may be achieved by increasing mitochondrial biosynthesis, promoting white fat browning and enhancing energy metabolism.

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Hydrogen Attenuates Allergic Inflammation by Reversing Energy Metabolic Pathway Switch.

Project description:Mechanisms mediating the protective effects of molecular hydrogen (H2) are not well understood. This study explored the possibility that H2 exerts its anti-inflammatory effect by modulating energy metabolic pathway switch. Activities of glycolytic and mitochondrial oxidative phosphorylation systems were assessed in asthmatic patients and in mouse model of allergic airway inflammation. The effects of hydrogen treatment on airway inflammation and on changes in activities of these two pathways were evaluated. Monocytes from asthmatic patients and lungs from ovalbumin-sensitized and challenged mice had increased lactate production and glycolytic enzyme activities (enhanced glycolysis), accompanied by decreased ATP production and mitochondrial respiratory chain complex I and III activities (suppressed mitochondrial oxidative phosphorylation), indicating an energy metabolic pathway switch. Treatment of ovalbumin-sensitized and challenged mice with hydrogen reversed the energy metabolic pathway switch, and mitigated airway inflammation. Hydrogen abrogated ovalbumin sensitization and challenge-induced upregulation of glycolytic enzymes and hypoxia-inducible factor-1?, and downregulation of mitochondrial respiratory chain complexes and peroxisome proliferator activated receptor-? coactivator-1?. Hydrogen abrogated ovalbumin sensitization and challenge-induced sirtuins 1, 3, 5 and 6 downregulation. Our data demonstrates that allergic airway inflammation is associated with an energy metabolic pathway switch from oxidative phosphorylation to aerobic glycolysis. Hydrogen inhibits airway inflammation by reversing this switch. Hydrogen regulates energy metabolic reprogramming by acting at multiple levels in the energy metabolism regulation pathways.

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Tubuloside B alleviates inflammation of murine macrophages

Project description:Tubuloside B alleviates inflammation of murine macrophages

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