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Glutamine Links Obesity to Inflammation in Human White Adipose Tissue

ABSTRACT: Glutamine Links Obesity to Inflammation in Human White Adipose Tissue

PROVIDER: PRJNA589657 | ENA |

REPOSITORIES: ENA

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Glutamine Links Obesity to Inflammation in Human White Adipose Tissue [array]

Project description:Glutamine Links Obesity to Inflammation in Human White Adipose Tissue [array]

| PRJNA589653 | ENA

Glutamine Links Obesity to Inflammation in Human White Adipose Tissue [ChIP-seq]

Project description:Glutamine Links Obesity to Inflammation in Human White Adipose Tissue [ChIP-seq]

| PRJNA589658 | ENA

Glutamine Links Obesity to Inflammation in Human White Adipose Tissue [array]

Project description:SP1-regulated transcriptome: Gene expression microarray following SP1 RNAi to define the SP1-regulated transcriptome in human in vitro differentiated adipocyte. Glutamine-regulated transcriptome: Gene expression microarray in human in vitro differentiated adipocyte incubated in high (10 mM) and low (0.5 mM) concentrations of glutamine.

2019-11-15 | GSE140424 | GEO

Glutamine Links Obesity to Inflammation in Human White Adipose Tissue [ChIP-seq]

Project description:Mapping of O-GlcNAcylated proteome along the genome by chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq) in in vitro differentiated human adipocytes incubated with low (0.5 mM) or high (10 mM) glutamine.

2019-11-15 | GSE140425 | GEO

Glutamine Links Obesity to Inflammation in Human White Adipose Tissue

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

2019-11-15 | GSE140426 | GEO

Adipose cDC1s contribute to obesity-associated white adipose tissue inflammation and metabolic dysfunction through STING-dependent IL-12 production

Project description:Obesity is associated with chronic low-grade white adipose tissue (WAT) inflammation that can contribute to the development of insulin resistance in mammals. Previous studies have identified interleukin (IL)-12 as a critical upstream regulator of WAT inflammation and metabolic dysfunction during obesity, however, the cell types and mechanisms that initiate WAT IL-12 production remain unclear. Analysis of mouse and human WAT single cell transcriptomic datasets, IL-12 reporter mice, and IL-12p70 protein levels by ELISA identified activated conventional type 1 dendritic cells (cDC1s) as the cellular source of WAT IL-12 during diet-induced obesity. cDC1s were required for the development of obesity-associated inflammation by increasing group 1 innate lymphocyte interferon (IFN)-γ production and inflammatory macrophage accumulation. Inducible depletion of cDC1s increased WAT insulin sensitivity and systemic glucose tolerance during diet-induced obesity. Endocytosis of apoptotic bodies containing self-DNA by WAT cDC1 drove STING-dependent IL-12 production. Together, these results suggest that WAT cDC1s act as critical regulators of adipose tissue inflammation and metabolic homeostasis during obesity.

2024-06-30 | GSE236110 | GEO

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Project description:The gut microbiota is a key environmental determinant of mammalian metabolism. Regulation of white adipose tissue (WAT) by the gut microbiota is a critical process that maintains metabolic fitness, while dysbiosis contributes to the development of obesity and insulin resistance (IR). However, how the gut microbiota controls WAT functions remain largely unknown. Herein, we show that tryptophan-derived metabolites produced by the microbiota control the expression of the miR-181 family in white adipocytes to regulate energy expenditure and insulin sensitivity. Moreover, we show that dysregulation of the microbiota-miR-181 axis is required for the development of obesity, IR, and WAT inflammation. Thus, our results indicate that regulation of miRNA levels in WAT by microbiota-derived cues is a central mechanism by which host metabolism is tuned in response to dietary and environmental changes. As MIR-181 is dysregulated in WAT from obese human individuals, the MIR-181 family may represent a potential therapeutic target to modulate WAT function in the context of obesity.

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2020-03-19 | GSE132706 | GEO

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