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

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

PROVIDER: PRJNA589653 | 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 [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

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

Obesity drives depot-specific vascular remodeling in white adipose tissue

Project description:Obesity drives depot-specific vascular remodeling in white adipose tissue

| PRJEB62151 | ENA

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

YAP and TAZ protect against white adipocyte cell death during obesity

Project description:Investigation of the effect of YAP/TAZ on white adipocyte survival during obesity

2020-09-25 | GSE138911 | GEO

Adipocyte YTH N(6)-methyladenosine RNA-binding protein 1 protects against obesity by promoting white adipose tissue beiging in male mice

Project description:Obesity, one of the most serious public health issues, is caused by energy imbalance of energy intake and expenditure. N(6)-methyladenosine (m6A) RNA modification has been recently identified as a key regulator of obesity, while the detailed mechanism is elusive. Here, we found that YTH RNA binding protein 1 (YTHDF1), an m6A reader, acts as an essential regulator of white adipose tissue metabolism. The expression of YTHDF1 decreased in adipose tissue of mice fed a high-fat diet. Adipocyte-specific Ythdf1 deficiency exacerbated obesity-induced metabolic defects and inhibited beiging of inguinal white adipose tissue (iWAT) in mice. By contrast, mice with WAT-specific Ythdf1 overexpression were resistant to obesity and showed promotion of beiging. Mechanistically, YTHDF1 regulated the translation of diverse m6A-modified mRNAs. In particular, YTHDF1 facilitated the translation of bone morphogenetic protein 8b (Bmp8b) in an m6A-dependent manner to induce the beiging process. Together, these findings suggested that YTHDF1 may be an attractive therapeutic target for the management of obesity-associated diseases.

2023-02-02 | GSE197173 | GEO

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