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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

Proteomic analysis of inguinal white adipose tissue from obesity mice induced by high-fat diet

Project description:This project includes proteomic data of inguinal white adipose tissue from high-fat diet-induced obese mice versus wild-type mice. WTi reprents the inguinal white adipose tissue from wild-type mice.DIOi reprents the inguinal white adipose tissue from diet-induced obesity mice.

2026-05-22 | PXD067877 | Pride

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

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

| PRJEB83704 | ENA

Ubiquitin independent degradation pathway regulates browning of white adipose tissue

Project description:Obesity is a significant risk factor for diabetes, cardiovascular diseases, and certain cancers, and manifests as excessive fat accumulation. The browning of white adipose tissue (WAT) represents one of the most promising strategies for preventing and treating obesity and metabolic diseases. To date, an increasing number of studies have focused on key molecular mechanisms regulating fat thermogenesis, laying the foundation for effective intervention strategies.We analyzed the differentially expressed proteins in white adipose tissue of the inguinal region using mass spectrometry.

| PXD055441 |

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

A PPARγ-lncRNA axis modulatesthermoneutral remodeling of white adipose tissue

Project description:Interplay between parenchymal energy-storing white adipose cells and thermogenic beige adipocytes contributes to obesity and insulin resistance. Irrespective of cellular origin or specialized niche, adipocytes require the activity of the nuclear receptor peroxisome proliferator activated receptor gamma (PPARγ) for proper function. Exposure to cold or adrenergic signaling enriches thermogenic cells though multiple pathways that act synergistically with PPARγ, however, the molecular mechanisms by which PPARγ licenses white adipose tissue (WAT) to preferentially adopt a thermogenic or white adipose fate in response to dietary cues or thermoneutral conditions are not fully elucidated. Here, we show that a PPARγ-long noncoding RNA (lncRNA) axis integrates canonical and noncanonical thermogenesis to restrain white adipose tissue heat dissipation during thermoneutrality and diet-induced obesity (DIO). Pharmacologic inhibition or genetic deletion of the lncRNA Lexis, enhances UCP-1 dependent and independent thermogenesis. Adipose tissue specific deletion of Lexis counteracted diet-induced obesity, improved insulin sensitivity, and enhanced energy expenditure. Single-nuclei transcriptomics revealed that Lexis regulates a distinct population of thermogenic adipocytes. We systematically map Lexis motif preferences and show that it regulates the thermogenic program through the activity of the metabolic GWAS gene and WNT modulator TCF7L2. Collectively, our studies uncover a new mode of crosstalk between PPARγ and WNT signaling that preserves white adipose tissue plasticity.

2023-09-27 | GSE215870 | GEO

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