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

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

PROVIDER: PRJNA589658 | ENA |

REPOSITORIES: ENA

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Glutamine Links Obesity to Inflammation in Human White Adipose Tissue

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

| PRJNA589657 | ENA

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 [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

The microbiota regulates white adipose tissue inflammation and progression of obesity through a highly conserved family of microRNAs.

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.

2019-04-03 | GSE126135 | GEO

Increased phosphocreatine/creatine ratio in white adipocytes promotes inflammation

Project description:The mechanisms promoting disturbed white adipocyte function in obesity remain largely unclear. Herein, we integrate white adipose tissue (WAT) metabolomic and transcriptomic data from clinical cohorts and find that the WAT phosphocreatine/creatine ratio is increased and creatine kinase-B expression and activity is decreased in the obese state. . In human in vitro and murine in vivo models, we demonstrate that decreased phosphocreatine metabolism in white adipocytes alters AMPK activity via effects on ATP/ADP levels, independently of WAT beigeing. This disturbance promotes a pro-inflammatory profile characterized, in part, by increased CCL2 production. These data suggest that the phosphocreatine/creatine system links cellular energy shuttling with pro-inflammatory responses in human and murine white adipocytes. Our findings provide unexpected perspectives on the mechanisms driving WAT inflammation in obesity and may present avenues to target adipocyte dysfunction.

2022-01-27 | GSE192361 | GEO

Obesity drives depot-specific vascular remodeling in white adipose tissue

Project description:Obesity-driven pathological expansion of white adipose tissue (WAT) is a key driver of endothelial dysfunction. Contrary to this paradigm, early vascular alterations associated with over nutrition also exacerbate AT dysfunction. To dissect this complex cause and consequence relationship, here we perform a single-cell transcriptomics screen to generate a detailed landscape of endothelial heterogeneity and vascular alterations in murine model of obesity. Given the differences in ontogeny and function of distinct WAT depots, we demarcate key differences in subcutaneous and visceral WAT vasculature. In addition to descriptive taxonomy, we perform in-depth validation and characterization of our in silico data. We identify a sWAT specific fenestrated endothelial cell subtype, which is drastically reduced in obese conditions. This reduction was associated with a decrease in VEGFA expressing perivascular cells. The novel endothelial subtypes provide a basis for future research and new directions for therapeutic interventions.

2023-05-26 | E-MTAB-12855 | biostudies-arrayexpress

Systemic approaches reveal anti-adipogenic signals at the onset of obesity–related inflammation in white adipose tissue [RNA-seq]

Project description:HFD feeding induces a rapid adipocyte progenitors (APs) proliferation in visceral adipose tissue (vWAT), followed by a block of differentiation. In contrast, subcutaneous adipose tissue (scWAT), in obesity, undergoes trans-differentiation of beige adipocytes to white and, consequently, a hyperplastic growth at later stages. We performed RNA-seq to investigate the global transcriptomic changes induced by HFD feeding

2020-03-19 | GSE132706 | GEO

Systemic approaches reveal anti-adipogenic signals at the onset of obesity–related inflammation in white adipose tissue [ChIP-seq]

Project description:HFD feeding induces a rapid adipocyte progenitors (APs) proliferation in visceral adipose tissue (vWAT), followed by a block of differentiation. In contrast, subcutaneous adipose tissue (scWAT), in obesity, undergoes trans-differentiation of beige adipocytes to white and, consequently, a hyperplastic growth at later stages. We performed ChIP-seq to profile RNA pol II recruitment and the global epigenetic changes of H3K4me1 and H3K27Ac induced by HFD feeding.

2020-03-19 | GSE132726 | GEO

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