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An early inflammatory gene profile in visceral adipose tissue in children

ABSTRACT: The aim of this study was to characterize expression profiles of visceral and subcutaneous adipose tissue in children. Adipose tissue samples were collected from children having elective surgery (n=71, [54 boys], 6.0 +- 4.3 years). Affymetrix microarrays (n=20) were performed to characterize the functional profile and identify genes of interest in adipose tissue. Visceral adipose tissue had an overrepresentation of Gene Ontology themes related to immune and inflammatory responses and subcutaneous adipose tissue had an overrepresentation of themes related to adipocyte growth and development. Likewise, qPCR performed in the whole cohort showed a 30-fold increase in haptoglobin (P < 0.005), 7-fold increase in IL-10 (P < 0.001), 8-fold decrease in VEGF (P < 0.01) and a 28-fold decrease in TBOX15 (P < 0.001) in visceral compared to subcutaneous adipose tissue.The inflammatory pattern in visceral adipose tissue may represent an early stage of the adverse effects of this depot, and combined with chronic obesity, may contribute to increased metabolic and cardiovascular risk.

ORGANISM(S): Homo sapiens

PROVIDER: GSE29718 | GEO | 2011/06/04

SECONDARY ACCESSION(S): PRJNA141093

REPOSITORIES: GEO

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An early inflammatory gene profile in visceral adipose tissue in children

Project description:The aim of this study was to characterize expression profiles of visceral and subcutaneous adipose tissue in children. Adipose tissue samples were collected from children having elective surgery (n=71, [54 boys], 6.0 +- 4.3 years). Affymetrix microarrays (n=20) were performed to characterize the functional profile and identify genes of interest in adipose tissue. Visceral adipose tissue had an overrepresentation of Gene Ontology themes related to immune and inflammatory responses and subcutaneous adipose tissue had an overrepresentation of themes related to adipocyte growth and development. Likewise, qPCR performed in the whole cohort showed a 30-fold increase in haptoglobin (P < 0.005), 7-fold increase in IL-10 (P < 0.001), 8-fold decrease in VEGF (P < 0.01) and a 28-fold decrease in TBOX15 (P < 0.001) in visceral compared to subcutaneous adipose tissue.The inflammatory pattern in visceral adipose tissue may represent an early stage of the adverse effects of this depot, and combined with chronic obesity, may contribute to increased metabolic and cardiovascular risk. 20 human samples from pre-pubertal boys and girls were assessed for differences in expression between subcutaneous (n=15) and visceral fat (n=5), with 1 microarray per subject

2011-06-04 | E-GEOD-29718 | biostudies-arrayexpress

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2013-08-22 | E-GEOD-42715 | biostudies-arrayexpress

SARS-CoV-2 infects adipose tissue in a fat depot- and viral lineage-dependent manner

Project description:Visceral adiposity is a risk factor for severe COVID-19, and a link between adipose tissue infection and disease progression has been proposed. Here we demonstrate that SARS-CoV-2 infects human adipose tissue and undergoes productive infection in human primary adipose-derived stromal-vascular cells differentiated into adipocytes. However, the permissiveness to infection and the cellular response depends on the anatomical origin of the cells and the viral lineage. Cells of visceral adipose tissue origin express more ACE2 and are more permissive to SARS-CoV-2 infection than their subcutaneous counterpart. SARS-CoV-2 infection leads to inhibition of lipolysis in cells of subcutaneous origin, while in visceral fat cells, it results in higher expression of pro-inflammatory cytokines. Viral load and cellular response are attenuated when visceral adipose tissue cells are infected with the SARS-CoV-2 gamma variant. A similar degree of cell death occurs 4-days after SARS-CoV-2 infection, regardless of the cell origin or viral lineage. Hence, SARS-CoV-2 infects human adipose tissue cells, replicating and altering cell function and viability in a fat depot- and viral lineage-dependent fashion.

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The Hidden Culprit of Visceral Fat: Dysfunctional Subcutaneous Adipose Tissue – Adipose tissue proteomics

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2019-02-27 | GSE127222 | GEO

Expression data from open bariatric surgery patients - various adipose samples

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Expression data from mice epididymal adipose tissue

Project description:Visceral white adipose tissue is closed correlated with obesity and metabolic dysfunction. Epididymal adipose tissue (eWAT) is considered as typical visceral white adipose tissue. Induction of browning of white adipose tissue improves metabolic dysfunction such as insulin resistance. In contrast to mice subcutaneous adipose tissue, visceral fat do not show significant browning under 4°C. However,under physiologically tolerable low temperature visceral adipose tissue can turn brown. We used microarrays to detail the global programme of gene expression in C57Bl/6 mice epididymal adipose tissue exposed to thermoneutral 30°C, 4°C and temperatures lower than 4°C.

2017-06-12 | GSE74062 | GEO

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Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White Preadipocytes (Microarray Expression)

Project description:Accumulation of subcutaneous white adipose tissue (WAT) is associated with increased insulin sensitivity, low levels of inflammation and a generally metabolically-healthy state, whereas accumulation of visceral adipose tissue is associated with insulin resistance, adipose tissue inflammation and metabolic syndrome. Membrane Metallo-Endopeptidase (MME/Neprislyin) is an extracellular, membrane-bound protease enriched in subcutaneous WAT that can target degradation of a variety of peptides, including insulin, IL6, and β-amyloids. Here, we show that MME in white preadipocytes is differently expressed in subcutaneous vs visceral WAT, and favors insulin signaling and a low inflammatory response. Thus, knockdown of MME in preadipocytes increases the inflammatory response to substance P and amyloidβ aggregates. This is associated with increased basal insulin signaling and decreased insulin-stimulated signaling. Moreover, MME differentially regulates the internalization and turnover of the α/β subunits of the insulin receptor. Thus, MME is a novel regulator of the insulin receptor in adipose tissue and may serve as a therapeutic target to increase insulin sensitivity and decrease inflammatory susceptibility.

2019-02-25 | GSE117352 | GEO

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