Effects of acute loss of mature adipocytes in adipose tissue on the liver
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA947589 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23942023_1.fastq.gz | Fastqsanger.gz | |||
| SRR23942023_2.fastq.gz | Fastqsanger.gz | |||
| SRR23942024_1.fastq.gz | Fastqsanger.gz | |||
| SRR23942024_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
Similar Datasets
Project description:To investigate the effects of acute loss of mature adipocytes in adipose tissue on the liver, we created tamoxifen-inducible adipocyte-specific insulin receptor knockout (iFIRKO) mice. We then performed comprehensive gene expression analysis on the liver of iFIRKO and control mice.
2023-04-18 | GSE227966 | GEO
Project description:Obesity is considered as a major public health concern with strong economic and social burdens. Exposure to pollutants such as heavy metals can contribute to the development of obesity and its associated metabolic disorders, including type 2 diabetes and cardiovascular diseases. Adipose tissue is an endocrine and paracrine organ that plays a key role in the development of these diseases and is one of the main target of heavy metal accumulation. In this study, we determined by inductively coupled plasma mass spectrometry cadmium concentrations in human subcutaneous and visceral adipose tissues, ranging between 2.5 nM and 2.5 µM. We found a positive correlation between cadmium levels and age, sex and smoking status and a negative correlation between cadmium and body mass index. Based on cadmium adipose tissue concentrations found in humans, we investigated the effects of cadmium exposure, at concentrations between 1 nM and 10 µM, on adipose-derived human mesenchymal stem cells differentiated into mature adipocytes in vitro. Transcriptomic analysis highlighted that such exposure altered the expression of genes involved in trace element homeostasis and heavy metal detoxification, such as Solute Carrier Family transporters and metallothioneins. This effect correlated with zinc level alteration in cells and cellular media. Interestingly, dysregulation of zinc homeostasis and transporters has been particularly associated with the development of obesity and type 2 diabetes. Moreover, we found that cadmium exposure induces the pro-inflammatory state of the adipocytes by enhancing the expression of genes such as IL-6, IL-1B and CCL2, cytokines also induced in obesity. Finally, cadmium modulates various adipocyte functions such as the insulin response signaling pathway and lipid homeostasis. Collectively, our data identified some of the cellular mechanisms by which cadmium alters adipocyte functions, thus highlighting new facets of its potential contribution to the progression of metabolic disorders.
2023-06-29 | MTBLS4128 | MetaboLights
Project description:Isolation of mature adipocytes from in vitro differentiated human adipose stem cells
| PRJNA947138 | ENA
Project description:Analysis of inguinal white adipose tissue (WAT) and liposarcoma (LPS) isolated from Notch1 overexpression mice (Ad/NICD). Results provide insight into molecular mechanisms underlying tumorigenic transformation of Ad/NICD mature adipocytes
2016-08-28 | GSE80433 | GEO
Project description:Thousands of human long intergenic noncoding RNAs (lincRNAs) have been detected in human adipose tissue. Here we characterized the function of one human adipse lincRNA, linc-ADAL (chr5:115292235-115296985) in mature adipcoytes through loss-of-function studies. Our results indicate that knockdown of linc-ADAL in differentiated adipocytes modulated expression of lipid metabolism genes.
2019-02-13 | GSE95173 | GEO
Project description:White adipose tissue (WAT) is a central factor in the development of type 2 diabetes. Despite the epidemiological importance of WAT there is a paucity of translational models to study long term changes in mature adipocytes. Here, we describe a novel method for the culture of mature white adipocytes under a permeable membrane. Compared to existing culture methods such as adipose tissue explants and adipocyte ceiling culture, Membrane mature Adipocyte Aggregate Cultures (MAAC) are superior at maintaining adipogenic gene expression through 2 weeks of culture, do not dedifferentiate, and are under reduced hypoxic stress relative to adipose tissue explants. Unbiased RNA-Sequencing analysis indicates that the gene expression profile of MAAC in culture for 1 or 2 weeks is more similar to starting patient material than cultured adipose tissue explants, floating adipocytes, or in vitro-differentiated precursors from the same donor, with the fewest number of differentially expressed genes and the smallest fold-change in gene expression. Importantly, adipocytes from lean and obese patients can be cultured as MAAC, as can subcutaneous and visceral adipocytes, while maintaining depot-specific gene expression signatures. MAAC remain fully functional after long term culture, with similar responses to insulin and lipolytic stimuli compared to recently isolated cells. In addition, MAAC maintain the ability to crosstalk with other cell types, producing synergistic increases in IL6 and IL8 when co-cultured with macrophages, and respond robustly and predictably to diverse pharmacological agonism. Together, these abilities make MAAC a powerful tool for studying phenotypic changes in mature adipocytes, crosstalk between adipocytes and other cell types, and provide an improved translational model for drug development for the modulation of adipose tissue function.
2019-04-02 | GSE115020 | GEO
Project description:We took a systematic approach to determine the transcriptional programs that are specifically regulated by C/EBP? in mature white adipocytes of mice on chow diet or high fat diet. The hypothesis tested in the present study was that C/EBP?, as a lipogenic transcription factor, has unique direct targets compared to PPAR?. Our inducible adipocyte specific knockout system allows us to test the direct targets of C/EBP? and PPAR? in adipocytes by short-term C/EBP? or PPAR? elimination in mature adipocytes in vivo. Results indicate that although it has been shown that C/EBP? and PPAR? cross-regulate each other, they have distinct direct responsive targets. Moreover, there are very few C/EBP? specific targets in mice on a chow diet, most of the C/EBP? targets in mature adipocytes are genes modulated by HFD feeding. Total RNA obtained from subcutaneous adipose tissue of Adn-C/EBP?-/- mice on doxycycline chow diet for 3 days, doxycycline high fat diet for 3 days or 1 month and Adn-PPAR?-/- mice on doxycycline chow diet for 3 days, compared to control littermates.
2014-11-04 | E-GEOD-62937 | biostudies-arrayexpress
Project description:Background: Adipose tissue homeostasis is a complex process influenced by many mechanisms that become dysregulated with obesity. We have previously shown that Maternal Separation and Early Weaning (MSEW), a mouse model of early life stress, exacerbates high-fat diet (HF)-induced fat deposition in female mice, but not male mice. In addition, we have shown that this exacerbated adiposity is due to an increase in visceral adipose tissue, and fat depot known to be linked with cardio-metabolic dysfunction. Purpose: The aim of this study was to determine differential gene expression patterns in gonadal white adipose tissue (gWAT), a visceral fat, in female mice exposed to MSEW compared to controls. Adipose tissue is composed of many different stromal cell types including preadipocytes, mature adipocytes, and immune cells. Preadipocytes are the precursor stem cells that differentiate into mature adipocytes that can uptake and store lipids and have a more predominte endocrine function. Methods: Control and MSEW mice were weaned onto either a low-fat diet (LF) or a high-fat diet (HF) for 20 weeks. Fresh gonadal white adipose tissue was harvested after euthanasia and subjected to collagenase digestion. Tissue was centrifuged and filtered to separate the mature fraction from the stromal vascular fraction. Magnetic Activated Cell Sorting (MACs) was used to further isolate adipocytes from other cell types. Pre-and mature adipocytes were collected and saved in Purezol at -80oC for later RNA extraction using the Promega ReliaPrep RNA miniprep systems. Total RNA was sent to Novogene for scRNAseq analysis.
2021-12-31 | GSE168751 | GEO
Project description:Obesity and associated metabolic outcomes define the metabolic syndrome. Interestingly, an under-appreciated fact is that body fat distribution, rather than total body fat amount, is a key determinant of metabolic disease. Indeed, in contrast to upper-body obesity, lower-body fat accumulation inversely correlates with metabolic risks. Understanding processes regulating upper- vs. lower-body fat expansion is paramount to predict (and prevent) these risks. We combine functional, proteomics, transcriptomics and epigenomics analyses to identify chromatin-associated mechanisms of adipose depot-specific fat expansion. Here, we analyze by RNA-seq the transcriptome of adipocytes differentiated in vitro from human gluteal (lower-body) and abdominal subcutaneous (upper-body) depots-derived adipose stem cells. We aim to identify adipose depot-specific and temporal differences in the up- or down-regulation of gene expression, and relate these differences to changes in chromatin states.
2024-04-01 | GSE227819 | GEO
Project description:Olfactomedin-2 (OLFM2) participates in brain development and appears to be involved in energy handling. In adipose tissue, we here show expression of OLFM2 to be adipocyte-specific and opposed to obesity. OLFM2 levels are increased during adipogenesis, and impaired when differentiated fat cells are challenged with conditions emulating inflammation in the context of obesity. On the molecular level, examination of OLFM2 deficiency in human adipocytes indicated down-regulation of genes related to cell cycle. At the cellular level, the loss of OLFM2 compromised adipogenesis, while its over-production enhanced the adipogenic transformation of 3T3-L1 cells. Complementary loss and gain of function assays coupled to untargeted proteomics revealed the modulation of key protein pathways, including regulation of citrate cycle, fatty acid degradation, axon guidance and focal adhesion in mature adipocytes and precursor cells. Transferring these findings into animal models using a whole-body knockout and transcriptionally depleted adipose Olfm2 highlighted, respectively, a cluster of molecular changes connected with defective cell cycle (in both), fat mass accretion and impaired metabolism (in the latter). Our data underscores a key role for OLFM2 in fat cells, and suggests that the association between adipose OLFM2 and obesity is not only correlative but also causative.
2023-11-16 | MSV000093409 | MassIVE