Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA318039 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Adipose Precursor HO-1 prevents healthy visceral adipose tissue expansion during obesity [I]
| PRJNA318040 | ENA
Project description:Adipose Precursor HO-1 determines healthy visceral adipose tissue expansion during obesity
| PRJNA318034 | ENA
Project description:Excessive accumulation of white adipose tissue (WAT) is a hallmark of obesity. The expansion of WAT in obesity involves proliferation and differentiation of adipose precursors (APs), however, the underlying molecular mechanisms remain unclear. Here, we identify Heme Oxygenase-1 (HO-1) as selectively being upregulated in the AP fraction of WAT, upon high-fat diet (HFD) feeding. Specific conditional deletion of HO-1 in APs of Hmox1fl/fl-Pdgfra Cre mice enhanced HFD-dependent visceral AP proliferation and differentiation, upstream of Cebpα and PPARγ. Opposite effects on human preadipocyte proliferation and differentiation in vitro were observed following HO-1 overexpression. Mechanistically, HO-1 acts upstream of AKT2 via ROS thresholding in mitochondria. Deletion of HO-1 in APs is sufficient to lower blood glucose, insulin and free fatty acid levels as well as liver steatosis during obesity, an effect not seen when HO-1 was conditionally deleted at later stages of adipogenesis using AdipoQ-Cre. Together, our data identify HO-1 as a diet-induced regulator limiting visceral adipose tissue hyperplasia during obesity.
2017-03-08 | GSE80147 | GEO
Project description:Excessive accumulation of white adipose tissue (WAT) is a hallmark of obesity. The expansion of WAT in obesity involves proliferation and differentiation of adipose precursors (APs), however, the underlying molecular mechanisms remain unclear. Here, we identify Heme Oxygenase-1 (HO-1) as selectively being upregulated in the AP fraction of WAT, upon high-fat diet (HFD) feeding. Specific conditional deletion of HO-1 in APs of Hmox1fl/fl-Pdgfra Cre mice enhanced HFD-dependent visceral AP proliferation and differentiation, upstream of Cebpα and PPARγ. Opposite effects on human preadipocyte proliferation and differentiation in vitro were observed following HO-1 overexpression. Mechanistically, HO-1 acts upstream of AKT2 via ROS thresholding in mitochondria. Deletion of HO-1 in APs is sufficient to lower blood glucose, insulin and free fatty acid levels as well as liver steatosis during obesity, an effect not seen when HO-1 was conditionally deleted at later stages of adipogenesis using AdipoQ-Cre. Together, our data identify HO-1 as a diet-induced regulator limiting visceral adipose tissue hyperplasia during obesity.
2017-03-08 | GSE80146 | GEO
Project description:Distinct characteristics of adipose tissue at different localization of human body has shown greater significance in development of metabolic disorders. Visceral adipose tissue in particular is known to be associated with obesity related metabolic complications that include type II diabetes. In this experiment, we attempt to profile transcriptome signatures of adipocyte, stromal vascular fraction (SVF) and adipose tissue from subcutaneous and visceral adipose tissue from obese individuals.
2019-11-04 | GSE135776 | GEO
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
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
Project description:In order to explore the effect of hypertension and overweight/obesity on human visceral adipose tissue transcriptome, we collected three visceral adipose tissue samples from normal weight individuals (non hypertension), overweight/obese individuals (non hypertension) and overweight/obese individuals with hypertension, and sequenced their transcriptome.
2023-07-03 | GSE217007 | GEO
Project description:Obesity-associated insulin resistance is characterized by a state of chronic, low-grade inflammation that is associated with the accumulation of M1 proinflammatory macrophages in adipose tissue. Although different evidence explains the mechanisms linking the expansion of adipose tissue and adipose tissue macrophage (ATM) polarization, in the current study we investigated the concept of lipid-induced toxicity as the pathogenic link that could explain the trigger of this response. We addressed this question using isolated ATMs and adipocytes from genetic and diet-induced murine models of obesity. Through transcriptomic and lipidomic analysis, we created a model integrating transcript and lipid species networks simultaneously occurring in adipocytes and ATMs and their reversibility by thiazolidinedione treatment. We show that polarization of ATMs is associated with lipid accumulation and the consequent formation of foam cell–like cells in adipose tissue. Our study reveals that early stages of adipose tissue expansion are characterized by M2-polarized ATMs and that progressive lipid accumulation within ATMs heralds the M1 polarization, a macrophage phenotype associated with severe obesity and insulin resistance. Furthermore, rosiglitazone treatment, which promotes redistribution of lipids toward adipocytes and extends the M2 ATM polarization state, prevents the lipid alterations associated with M1 ATM polarization. Our data indicate that the M1 ATM polarization in obesity might be a macrophage-specific manifestation of a more general lipotoxic pathogenic mechanism. This indicates that strategies to optimize fat deposition and repartitioning toward adipocytes might improve insulin sensitivity by preventing ATM lipotoxicity and M1 polarization. 15 samples; 2 genotypes and 2 time points
2012-03-22 | E-GEOD-36669 | biostudies-arrayexpress
Project description:Diabetes and obesity are widespread diseases with signifciant socioeconomic implications. We used three different types of human adipose tissue (epigastric, visceral, and subcutaneous) in order to determine differences in global gene expression between these adipose depots in severely obese patients. In this dataset, we include the expression data obtained from three types of adipose tissue; epigastric, subcutaneous, and visceral all obtained through open gastric bypass surgery. 18 total samples were analyzed. Tissues were paired together to run on one genechip, with three pairs of epigastric, three pairs of subcutaneous, and three pairs of visceral were ran on nine genechips. Comparisons of gene expression in the form of fold changes between pairs of adipose types (i.e., subcutaneous/epigastric, visceral/epigastric, and subcutaneous/visceral) were completed by Spotfire Analysis.
2013-08-22 | E-GEOD-42715 | biostudies-arrayexpress