Adipose Tissue Omics In Obesity
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PROVIDER: PRJNA1006496 | ENA |
REPOSITORIES: ENA
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Project description:Adipose Tissue Omics In Obesity
| PRJNA1006463 | ENA
Project description:Adipose Tissue Macrophage Accrual in Obesity
| PRJNA634570 | ENA
Project description:This SuperSeries is composed of the following subset Series: GSE25401: Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity [gene expression] GSE25470: Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity [miRNA data] GSE25910: Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity [differentiation data] Refer to individual Series
2012-08-12 | E-GEOD-25402 | biostudies-arrayexpress
Project description:Chronic, low-grade adipose tissue inflammation associated with adipocyte hypertrophy is an important link in the relationship between obesity and insulin resistance. Although ubiquitin ligases are essential regulators of inflammatory processes, the role of these enzymes in metabolically driven adipose tissue inflammation is relatively unexplored. In this study, we found that the ubiquitin ligase Siah2 is a central factor in obesity-related adipose tissue inflammation. When challenged with chronic excess energy intake, Siah2-null mice become obese with enlarged adipocytes, but do not develop obesity-induced insulin resistance. Proinflammatory gene expression is substantially reduced in the Siah2-null epididymal adipose tissue of the obese Siah2KO mice.
2015-09-29 | GSE61839 | GEO
Project description:Dysfunctional white adipose tissue contributes to the development of obesity-related morbidities, including insulin resistance, dyslipidemia, and other metabolic disorders. Adipose tissue macrophages (ATMs) accumulate in obesity and play both beneficial and harmful roles in the maintenance of adipose tissue homeostasis and function. Despite their importance, the molecules and mechanisms that regulate these diverse functions are not well understood. Lipid-associated macrophages (LAMs), the dominant subset of obesity-associated ATMs, accumulate in crown-like structures and are characterized by a metabolically activated and proinflammatory phenotype. We previously identified CD9 as a surface marker of LAMs. However, the contribution of CD9 to the activation and function of LAMs during obesity is unknown. Using a myeloid-specific CD9 knockout model, we show that CD9 supports ATM-adipocyte adhesion and crown-like structure formation. Furthermore, CD9 promotes the expression of pro-fibrotic and extracellular matrix remodeling genes. Loss of myeloid CD9 reduces adipose tissue fibrosis, increases visceral adipose tissue accumulation, and improves global metabolic outcomes during diet-induced obesity. These results identify CD9 as a causal regulator of pathogenic LAM functions, highlighting CD9 as a potential therapeutic target for treating obesity-associated metabolic disease.
2026-01-20 | GSE311351 | GEO
Project description:Human Adipose Tissue Microbiota in Obesity Study
| PRJEB53362 | ENA
Project description:Obesity drives significant changes in adipose tissue that precede development of tissue and systemic insulin resistance. Immune cell infiltration and inflammation are known contributors to these changes but there is limited understanding of their spatial context tissue-wide. We sought to identify spatial patterning in epididymal adipose tissue immune cells in a time course of diet-induced obesity in mice. Using spatial transcriptomics and single-cell RNA-sequencing, we identified dominant cell type signatures preserved in their anatomical context, quantified gene expression patterns at spots throughout adipose tissue, performed cell type network analysis, and investigated ligand-receptor colocalization. Our data support increased innate immune cells, including macrophages, monocytes, and innate lymphoid cells, with tissue-wide interspersion and dampened adaptive immune cell signatures with obesity. Network analysis identified increased heterogeneity in all major immune cell types, consistent with increased subtypes. To capture tissue dynamics at obesity onset, we draw on mathematical principles from linear algebra and spectral graph theory. We provide a framework for better understanding cell cooperation toward emergence of multicellular tissue function. Further, we adapt Turing's mathematical theory on morphogenesis to show lapse of emergence in adipose tissue.
2022-03-10 | GSE198012 | GEO
Project description:Different human adipose tissue depots may have functional differences. Subcutaneous human adipose tissue has been extensively studied, but less is known about other depots. Perithyroid (PT) adipose tissue contains not only white adipocytes but also brown adipocytes. The aim of this study was to compare the expression of brown adipocyte containing perithyroid adipose tissue with s.c. adipose tissue.role in the development of obesity. Expression profiling of adipose tissue may give insights into mechanisms contributing to obesity and obesity-related disorders. Expression analysis of paired biopsies from s.c and perithyriod (PT) adipose tissue from nine subjects undergoing surgery in the thyroid region.
2013-01-22 | E-GEOD-27657 | biostudies-arrayexpress
Project description:To assess changes in expression level of various chemokines and their receptors on diet-induced obesity, we analysed gene expression in adipose tissue of C56BL/6J mice fed a high-fat (HF) diet or normal chow diet for 8 weeks. HF diet-induced obese (DIO) mice showed adipose tissue inflammation and insulin resistance. Comprehensive gene expression analysis showed that MCP-1–CCR2 and CCL5–CCR5 signalling in epididymal white adipose tissue (eWAT) were enhanced during the development of obesity. Surprisingly, the gene expression of Cx3cl1 was decreased in the eWAT of DIO mice compared with lean mice. While Cx3cr1 expression showed no significant difference between DIO and lean mice. Decreased CX3CL1-CX3CR1 signalling in adipose tissue may also be involved in the development of obesity-induced adipose tissue inflammation and insulin resistance.
2021-04-01 | GSE167311 | GEO
Project description:Inflammasome activation in adipose tissue has been implicated in obesity-associated insulin resistance and type 2 diabetes. However, when and how inflammasome is activated in adipose tissue remains speculative. Here we test the hypothesis that extracellular ATP, a potent stimulus of inflammasome in macrophages via purinergic receptor P2X, ligand-gated ion channel, 7 (P2X7), may play a role in inflammasome activation in adipose tissue in obesity. Our data show that inflammasome is activated in adipose tissue upon 8-week feeding of 60% HFD, coinciding with the onset of hyperglycemia and hyperinsulinemia as well as the induction of P2X7 in adipose tissue. Unexpectedly, P2X7-deficient animals on HFD exhibit no changes in metabolic phenotypes, nor in inflammatory responses or inflammasome activation when compared to the wildtype controls. Similar observations have been obtained in hematopoietic cell-specific P2X7-deficient animals generated by bone marrow transplantation. Thus, we conclude that inflammasome activation in adipose tissue in obesity coincides with the onset of hyperglycemia and hyperinsulinemia, but unexpectedly, is not mediated by the ATP-P2X7 signaling axis. The nature of the inflammasome-activating danger signal(s) in adipose tissue in obesity remains to be characterized. Wild type and P2X7 knockout mice were fed a low fat diet (chow) or high fat diet for 12 weeks. After the diet intervention period, the animals were killed and epididymal white adipose tissue was removed. Total RNA was isolated and subjected to gene expression profiling.
2012-02-24 | E-GEOD-36033 | biostudies-arrayexpress