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

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

PROVIDER: PRJNA907780 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22501800.fastq.gz	Fastqsanger.gz
	SRR22501801.fastq.gz	Fastqsanger.gz
	SRR22501802.fastq.gz	Fastqsanger.gz
	SRR22501803.fastq.gz	Fastqsanger.gz
	SRR22501804.fastq.gz	Fastqsanger.gz

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

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

| PRJNA907777 | ENA

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]

| PRJNA907779 | ENA

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.

2023-09-27 | GSE219234 | GEO

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.

2023-09-27 | GSE219233 | GEO

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

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.

2023-11-12 | GSE247235 | GEO

Effects of β-glucan Rich Barley Flour on Glucose and Lipid Metabolism in the Ileum, Liver, and Adipose Tissues of High-Fat Diet Induced-Obesity Model Male Mice Analyzed by DNA Microarray

Project description:We evaluated whether intake of β-glucan-rich barley flour affects expression levels of genes related to glucose and lipid metabolism in the ileum, liver, and adipose tissues of mice fed a high-fat diet. C57BL/6J male mice were fed a high-fat diet supplemented with high β-glucan barley, for 92 days. We measured the expression levels of genes involved in glucose and lipid metabolism in the ileum, liver, and adipose tissues using DNA microarray and q-PCR. The concentration of short-chain fatty acids (SCFAs) in the cecum was analyzed by GC/MS. The metabolic syndrome indices were improved by barley flour intake. Microarray analysis showed that the expression of genes related to steroid synthesis was consistently decreased in the liver and adipose tissues. The expression of genes involved in glucose metabolism did not change in these organs. In liver, a negative correlation was showed between some SCFAs and the expression levels of mRNA related to lipid synthesis and degradation. Barley flour affects lipid metabolism at the gene expression levels in both liver and adipose tissues. We suggest that SCFAs are associated with changes in the expression levels of genes related to lipid metabolism in the liver and adipose tissues, which affect lipid accumulation

2020-11-20 | GSE157828 | GEO

Ileum and colon goblet cell proteome

Project description:This study is a comparative proteomics study of FACS sorted Muc2 expressing and non expressing cells in mouse ileum and colon.

2021-04-19 | PXD011527 | Pride

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.

| S-EPMC10512512 | biostudies-literature

Ileum content

Project description:Tan sheep ileum content 16s rRNA sequence

| PRJNA1156904 | ENA