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Adipose tissue retains an epigenetic memory of obesity after weight loss [snRNAseq]

ABSTRACT: Adipose tissue retains an epigenetic memory of obesity after weight loss [snRNAseq]

PROVIDER: PRJNA991596 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25152654_1.fastq.gz	Fastqsanger.gz
	SRR25152654_2.fastq.gz	Fastqsanger.gz
	SRR25152655_1.fastq.gz	Fastqsanger.gz
	SRR25152655_2.fastq.gz	Fastqsanger.gz
	SRR25152656_1.fastq.gz	Fastqsanger.gz

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Adipose tissue retains an epigenetic memory of obesity after weight loss [snRNAseq]

Project description:Reducing body weight to improve metabolic health and related comorbidities is a primary goal in treating obesity. However, maintaining weight loss is a considerable challenge, especially as the body appears to retain an obesogenic memory that defends against body weight changes. Overcoming this barrier for long-term treatment success is difficult because the molecular mechanisms underpinning this phenomenon remain largely unknown. Here, by using single-nuclei RNA-sequencing, we show that both human and mouse adipose tissue retain cellular transcriptional changes after appreciable weight loss. Furthermore, we find persistent obesity-induced alterations in the mouse adipocyte epigenome, negatively affecting their function and response to metabolic stimuli. Mice carrying this obesogenic memory show accelerated rebound weight gain, and the epigenetic memory can explain future transcriptional deregulation in adipocytes in response to further high-fat diet feeding. In summary, our findings indicate the existence of an obesogenic memory, largely based on stable epigenetic changes, in mouse adipocytes, and likely other cell types. These changes appear to prime cells for pathological responses in an obesogenic environment, contributing to the problematic "yo-yo" effect often seen with dieting. Targeting these changes in the future could improve long-term weight management and health outcomes.

2024-11-14 | GSE236579 | GEO

Adipose tissue retains an epigenetic memory of obesity after weight loss

Project description:Adipose tissue retains an epigenetic memory of obesity after weight loss

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Adipose tissue retains an epigenetic memory of obesity after weight loss [TRAP]

Project description:Adipose tissue retains an epigenetic memory of obesity after weight loss [TRAP]

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Adipose tissue retains an epigenetic memory of obesity after weight loss [CUT&TAG]

Project description:Adipose tissue retains an epigenetic memory of obesity after weight loss [CUT&TAG]

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Adipose tissue retains an epigenetic memory of obesity after weight loss [ATAC-seq]

Project description:Adipose tissue retains an epigenetic memory of obesity after weight loss [ATAC-seq]

| PRJNA991593 | ENA

Adipose tissue retains an epigenetic memory of obesity after weight loss [TRAP]

2024-11-14 | GSE236578 | GEO

Adipose tissue retains an epigenetic memory of obesity after weight loss [CUT&TAG]

2024-11-14 | GSE236577 | GEO

Adipose tissue retains an epigenetic memory of obesity after weight loss [ATAC-seq]

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Obesity Weight Loss Study

Project description:Obesity Weight Loss Study

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Multiomics reveals persistence of obesity-associated immune cell phenotypes in adipose tissue during weight loss and subsequent weight regain

Project description:Most individuals do not maintain weight loss, and weight regain increases cardio-metabolic risk beyond that of obesity. Adipose inflammation directly contributes to insulin resistance; however, immune-related changes that occur with weight loss and weight regain are not well understood. Single cell RNA-sequencing was completed with CITE-sequencing and biological replicates to profile changes in murine immune subpopulations following obesity, weight loss, and weight cycling. Weight loss normalized glucose tolerance, however, type 2 immune cells did not repopulate adipose following weight loss. Many inflammatory populations persisted with weight loss and increased further following weight regain. Obesity drove T cell exhaustion and broad increases in antigen presentation, lipid handing, and inflammation that persisted with weight loss and weight cycling. This work provides critical groundwork for understanding the immunological causes of weight cycling-accelerated metabolic disease.

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