Genome-wide discovery and integrative genomic characterization of insulin resistance loci using serum triglycerides to HDL-cholesterol ratio [bulk RNA-seq]
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE274839 | GEO | 2024/09/01
REPOSITORIES: GEO
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Project description:Hypoxia in adipose tissue is suggested to be involved in the development of a chronic mild inflammation, which in obesity can further lead to insulin-resistance. The effect of hypoxia on gene expression in adipocytes seems to play a central role in this inflammatory response observed in obesity. However, the global impact of hypoxia on transcriptional changes in human adipocytes is unclear. Therefore, we compared gene expression profiles of human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes under normoxic or hypoxic conditions to detect hypoxia-responsive genes in adipocytes by using whole human genome microarrays.
2011-04-14 | GSE28603 | GEO
Project description:Hypoxia in adipose tissue is suggested to be involved in the development of a chronic mild inflammation, which in obesity can further lead to insulin-resistance. The effect of hypoxia on gene expression in adipocytes seems to play a central role in this inflammatory response observed in obesity. However, the global impact of hypoxia on transcriptional changes in human adipocytes is unclear. Therefore, we compared gene expression profiles of human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes under normoxic or hypoxic conditions to detect hypoxia-responsive genes in adipocytes by using whole human genome microarrays. Human SGBS adipocytes were cultured in a hypoxic environment (1% O2) for 3, 6 and 16 hours and the control group was cultured under normoxic conditions (21% O2). Total RNA was prepared from control and treated SGBS cells, in triplicate experiments, and probes were hybridized on ‘Human Genome U133 2.0’ arrays (Affymetrix).
2011-04-14 | E-GEOD-28603 | biostudies-arrayexpress
Project description:The pathogenesis of obesity-related metabolic diseases has been linked to the inflammation of white adipose tissue (WAT), but the molecular interconnections are still not fully understood. MiR-146a controls inflammatory processes by suppressing pro-inflammatory signaling pathways. The aim of this study was to characterize the role of miR-146a in obesity and insulin sensitivityresistance . MiR-146a-/- mice were subjected to a high fat diet followed by metabolic tests and WAT transcriptomics. Gain- and loss-of-function studies were performed using human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes. Compared to controls, miR-146a-/- mice gained significantly more body weight on a high fat diet with increased fat mass and adipocyte hypertrophy. This was accompanied by exacerbated liver steatosis, insulin resistance, and glucose intolerance. Likewise, adipocytes transfected with an inhibitor of miR-146a displayed a decrease in insulin-stimulated glucose uptake, while transfecting miR-146a mimics caused the opposite effect. Natriuretic peptide receptor 3 (NPR3) was identified as a direct target gene of miR-146a in adipocytes and CRISPR/Cas9-mediated knockout of NPR3 increased insulin-stimulated glucose uptake and enhanced de-novo lipogenesis. In summary, miR-146a regulates systemic and adipocyte insulin sensitivity via downregulation of NPR3.
2020-10-12 | GSE151268 | GEO
Project description:SGBS cells were used as a model system to investigate the cellular mode of action of a variety of plasticizers in human adipocytes. In brief, cells were cultured at 5% CO2 and 37°C in 95% humidity. Cells of generation 40 and passage 3 after thawing were grown to confluence with DMEM/F12 containing 33 µM biotin, 17 µM pantothenate, 100 U/l penicillin, and 0.1 mg/l streptomycin (basal medium) supplemented with 10% FCS (Gibco, Carlsbad, CA, USA). According to the standard differentiation protocol, differentiation was initiated (day 0) after changing to serum-free basal medium supplemented with 0.1 μM cortisol, 0.01 mg/ml apo-transferrin, 0.2 nM triiodothyronine, and 20 nM human insulin (differentiation medium) with the addition of 2 µM rosiglitazone, 25 nM dexamethasone, and 200 µM 3-isobutyl-1-methylxanthine for the first four days. SGBS cells were first differentiated according to the standard protocol for 12 days. Obtained adult adipocytes were then exposed to the plasticizers for 8 days with medium changes every second day. The control contained equivalent amounts of solvent (0.01% MeOH). Additinally, a control on day 12 before exposure was sampled. All SGBS cell culture experiments were conducted in quadruplets.
2022-06-20 | PXD030843 | Pride
Project description:SGBS cells were used as a model system to investigate the cellular mode of action of a variety of plasticizers in human adipocytes. In brief, cells were cultured at 5% CO2 and 37°C in 95% humidity. Cells of generation 40 and passage 3 after thawing were grown to confluence with DMEM/F12 containing 33 µM biotin, 17 µM pantothenate, 100 U/l penicillin, and 0.1 mg/l streptomycin (basal medium) supplemented with 10% FCS (Gibco, Carlsbad, CA, USA). According to the standard differentiation protocol, differentiation was initiated (day 0) after changing to serum-free basal medium supplemented with 0.1 μM cortisol, 0.01 mg/ml apo-transferrin, 0.2 nM triiodothyronine, and 20 nM human insulin (differentiation medium) with the addition of 2 µM rosiglitazone, 25 nM dexamethasone, and 200 µM 3-isobutyl-1-methylxanthine for the first four days. The positive control was differentiated using the standard protocol with rosiglitazone. For plasticizer treatments, differentiation was conducted without rosiglitazone and cells were continuously exposed from day 0 – day 16 to the plasticizers or their transformation products. As for plasticizer treatments, the negative control was differentiated with rosiglitazone-free medium containing equivalent amounts of solvent (0.01 MeOH, v/v) for 16 days, resulting in minimal differentiation. All media were renewed every second day to mimic continuous exposure.
2022-06-20 | PXD031041 | Pride
Project description:Enlarged white adipose tissue (WAT) is a feature of obesity and leads to changes in its paracrine and endocrine function. Dysfunction of WAT cells is associated with obesity associated disorders like type 2 diabetes and cardiovascular diseases. Resveratrol (RSV) a natural polyphenolic compound mimics beneficial effects of calorie restriction. As such, RSV seems a promising therapeutic target for obesity-associated disorders. The effect of RSV on the human adipokine profile is still elusive. Therefore, a proteomic study together with bioinformatical analysis was performed to investigate the effect of RSV on the secretion profile of mature human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes. RSV incubation resulted in elevated basal glycerol release and reduced intracellular TG content. This increased intracellular lipolysis was accompanied by profound changes in the adipocyte secretion profile. Extracellular matrix proteins were down-regulated while processing proteins were mostly up-regulated after RSV treatment. Interestingly, RSV induced secretion of proteins protective against cellular stress and proteins involved in the regulation of apoptosis. Furthermore, we found a RSV-induced up-regulation of adiponectin and ApoE accompanied by a down-regulation of PAI-1 and PEDF secretion which may improve anti-inflammatory processes and increased insulin sensitivity. These effects are beneficial to alleviate obesity-induced metabolic complications. In addition, two novel RSV-regulated adipocyte-secreted proteins were identified.
2012-08-31 | PXD000012 | Pride
Project description:Promoter capture Hi-C of human SGBS (Simpson-Golabi-Behmel syndrome preadipocyte) cells and iPSC-derived hypothalamic cells
| PRJEB43592 | ENA
Project description:Most information on molecular processes accompanying and driving adipocyte differentiation are derived from rodent models. Here, a comprehensive analysis of combined transcriptomic and proteomic alterations during adipocyte differentiation in Simpson–Golabi–Behmel Syndrome (SGBS) cells is provided. The SGBS cells are a well-established and the most widely applied cell model to study human adipocyte differentiation and cell biology. However, the molecular alterations during human adipocyte differentiation in SGBS cells have not yet been described in a combined analysis of proteome and transcriptome. Here a global proteomic and transcriptomic data set comprising relative quantification of a total of 14372 mRNA transcripts and 2641 intracellular and secreted proteins is presented. 1153 proteins and 313 genes are determined as differentially expressed between preadipocytes and the fully differentiated cells including adiponectin, lipoprotein lipase, fatty acid binding protein 4, fatty acid synthase, stearoyl-CoA desaturase, and apolipoprotein E and many other proteins from the fatty acid synthesis, amino acid synthesis as well as glucose and lipid metabolic pathways. Preadipocyte markers, such as latexin, GATA6, and CXCL6, are found to be significantly downregulated at the protein and transcript level. This multi-omics data set provides a deep molecular profile of adipogenesis and will support future studies to understand adipocyte function.
2020-05-25 | GSE123385 | GEO
Project description:Identifying the regulatory mechanisms of genome-wide association study (GWAS) loci affecting adipose tissue has been restricted due to limited characterization of adipose transcriptional regulatory elements. We profiled chromatin accessibility in three frozen human subcutaneous adipose tissue needle biopsies and preadipocytes and adipocytes from the Simpson Golabi-Behmel Syndrome (SGBS) cell strain using an assay for transposase-accessible chromatin (ATAC-seq). We identified 68,571 representative accessible chromatin regions (peaks) across adipose tissue samples (FDR<5%). GWAS loci for eight cardiometabolic traits were enriched in these peaks (p<0.005), with the strongest enrichment for waist-hip ratio. Of 110 recently described cardiometabolic GWAS loci colocalized with adipose tissue eQTLs, 59 loci had one or more variants overlapping an adipose tissue peak. Annotated variants at the SNX10 waist-hip ratio locus and the ATP2A1-SH2B1 body mass index locus showed allelic differences in regulatory assays. These adipose tissue accessible chromatin regions elucidate genetic variants that may alter adipose tissue function to impact cardiometabolic traits.
2019-01-01 | GSE110734 | GEO
Project description:Human pluripotent stem cell (hPSC)-derived cardiomyocytes (CMs) hold great promise for the repair of the injured heart, but optimal cell production in a fully chemically defined and cost-effective system is essential for the efficacy and safety of cell transplantation therapies. In this study, we provided a simple and efficient strategy for cardiac differentiation from hPSCs and performed functional evaluation in a rat model of myocardial infarction. Using a chemically defined medium including four components, recombinant human albumin, ascorbic acid, human transferrin, and RPMI 1640, we developed a manageable and cost-effective protocol for robust generation of CMs from hPSCs. Interestingly, the addition of transferrin helped hPSCs to transit from TeSR-E8 medium to the simple cardiac differentiation medium and successfully initiated mesoderm differentiation without significant cell death. The CM generation efficiency was up to 85% based on cTnT expression. We performed transcriptome profiling from differentiation day 0 to 35, and characterized interesting dynamic change of cardiac genes. CMs derived from transferrin supplemented simple medium have similar transcriptome and the maturation level compared to cardiomyocytes generated in B27 minus insulin medium as well as their in vivo counterparts. Importantly, after transplantation, hPSC derived CMs survived in the infarcted rat heart, significantly improved the physiological function and reduced fibrosis. Our study offers an easy-to-use and cost-effective method for cardiac differentiation and facilitates the translational application of hPSC-derived CMs for heart repair.
2021-01-13 | GSE154294 | GEO