The omentum of obese girls harbors small adipocytes and browning transcrips
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA606603 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11085132_1.fastq.gz | Fastqsanger.gz | |||
| SRR11085132_2.fastq.gz | Fastqsanger.gz | |||
| SRR11085133_1.fastq.gz | Fastqsanger.gz | |||
| SRR11085133_2.fastq.gz | Fastqsanger.gz | |||
| SRR11085134_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 48 |
Similar Datasets
Project description:Severe obesity (SO) affects about 6% of youth in US, augmenting the risks for cardiovascular disease and Type 2 diabetes. Herein, we obtained paired omental (omVAT) and abdominal subcutaneous (SAT) adipose tissue biopsies from obese girls with SO, undergoing sleeve gastrectomy (SG), to test whether differences in cellular and transcriptomic profiles between omVAT and SAT depots affect insulin sensitivity differentially. Following weight loss, these analyses were repeated in a subgroup of subjects having a second SAT biopsy. We found that omVAT displayed smaller adipocytes compared to SAT, increased lipolysis through adipose triglyceride lipase (ATGL) phosphorylation, reduced inflammation and increased expression of browning/beige markers. Contrary to omVAT, SAT adipocyte diameter correlated with insulin resistance. Following SG, both weight and insulin sensitivity improved markedly in all subjects. SAT adipocytes size became smaller showing an increased lipolysis through perilipin-1 phosphorylation, decreased inflammation and increased expression in browning/beige markers. In summary, in adolescent girls with SO, both omVAT and SAT depots showed distinct cellular and transcriptomic profiles. Following weight loss, the SAT depot changed its cellular morphology and transcriptomic profiles into a more favorable one. These changes in the SAT depot may play a fundamental role in the resolution of insulin resistance.
2020-05-19 | GSE145284 | GEO
Project description:Severe obesity (SO) affects about 6% of youth in the United States, augmenting the risks for cardiovascular disease and type 2 diabetes. Herein, we obtained paired omental adipose tissue (omVAT) and abdominal subcutaneous adipose tissue (SAT) biopsies from girls with SO undergoing sleeve gastrectomy (SG), to test whether differences in cellular and transcriptomic profiles between omVAT and SAT depots affect insulin sensitivity differently. Following weight loss, these analyses were repeated in a subgroup of subjects having a second SAT biopsy. We found that omVAT displayed smaller adipocytes compared with SAT, increased lipolysis through adipose triglyceride lipase phosphorylation, reduced inflammation, and increased expression of browning/beiging markers. Contrary to omVAT, SAT adipocyte diameter correlated with insulin resistance. Following SG, both weight and insulin sensitivity improved markedly in all subjects. SAT adipocytes' size became smaller, showing increased lipolysis through perilipin 1 phosphorylation, decreased inflammation, and increased expression in browning/beiging markers. In summary, in adolescent girls with SO, both omVAT and SAT depots showed distinct cellular and transcriptomic profiles. Following weight loss, the SAT depot changed its cellular morphology and transcriptomic profiles into more favorable ones. These changes in the SAT depot may play a fundamental role in the resolution of insulin resistance.
| S-EPMC7213797 | biostudies-literature
Project description:To investigate the profiles of mRNAs, lncRNAs and circRNAs in browning of human adipose derived stem cells (hADSCs), we obtained hADSCs from omentum adipose tissues of 5 patients on who were performed abdominal operation and derived them into brown adipocytes. Then we employed microarray profiling the expression of lncRNAs, circRNAs and mRNA of hADSCs and their derived brown adipocytes.
2024-12-24 | GSE192634 | GEO
Project description:Here we have characterized the transcriptional processes underlying the formation of human brown in white (i.e. brite) adipocytes using a genome-wide approach. We show that the browning process is associated with reprogramming of peroxisome proliferator-activated receptor γ (PPARγ) binding to form brite adipocyte-selective PPARγ super-enhancers that appear to play a key role in activation of brite adipocyte-selective genes. We identify the KLF11 gene based on its association with a PPARγ super-enhancer and show that KLF11 is a novel browning factor directly induced by rosiglitazone and required for the activation of brite adipocyte-selective gene program by rosiglitazone. Genome-wide profiling of Dnase I hypersenstive (DHS) sites, epigenomic marks, transcription factor and co-factor binding, and gene expression in hMADS white and brite adipocytes
2014-12-12 | E-GEOD-59703 | biostudies-arrayexpress
Project description:Adipose tissue is one of the main regulative sites for energy metabolism. Excess lipid storage and expansion of white adipose tissue (WAT) is the primary contributor to obesity, a strong predisposing factor for development of insulin resistance. Sentrin-specific protease (SENP) 2 has been shown to play a role in metabolism in murine fat and skeletal muscle cells, and we have previously demonstrated its role in energy metabolism of human skeletal muscle cells. In the present work, we have investigated the impact of SENP2 on fatty acid and glucose metabolism in primary human fat cells by using cultured primary human adipocytes to knock down the SENP2 gene. Glucose uptake and oxidation, as well as accumulation and distribution of oleic acid into complex lipids were decreased while oleic acid oxidation was increased in SENP2-knockdown cells compared to control cells. Furthermore, de novo lipogenesis was reduced by SENP2-knockdown in the adipocytes and expression of several metabolically important regulators and markers of browning of WAT were upregulated both on gene and protein level. In conclusion, SENP2 is an important regulator of energy metabolism in primary human adipocytes, and the results indicates a potential role in browning of the cells as well.
2023-02-10 | PXD033508 | Pride
Project description:Here we have characterized the transcriptional processes underlying the formation of human brown in white (i.e. brite) adipocytes using a genome-wide approach. We show that the browning process is associated with reprogramming of peroxisome proliferator-activated receptor γ (PPARγ) binding to form brite adipocyte-selective PPARγ super-enhancers that appear to play a key role in activation of brite adipocyte-selective genes. We identify the KLF11 gene based on its association with a PPARγ super-enhancer and show that KLF11 is a novel browning factor directly induced by rosiglitazone and required for the activation of brite adipocyte-selective gene program by rosiglitazone.
2014-12-12 | GSE59703 | GEO
Project description:Canonical WNT pathway in mature adipocytes exacerbates obesity. In this study, we constructed UCP1-positive adipocytes-specific Ctnnb1 knockout mice (UBKO) and observed increased “browning” of white adipose tissue (WAT) following cold exposure or CL-316,243 administration compared to controls. UBKO mice also displayed increased energy expenditure. Furthermore, β-catenin (encoded by Ctnnb1) inhibited thermogenic genes expression in differentiated beige adipocytes and repressed Ucp1 expression at transcription level. Transcriptome analysis revealed UBKO mice treated with CL-316,243 had enhanced mitochondrial function and downregulated immunerelated genes in WAT. Improved glucose tolerance and insulin sensitivity were observed in 50-week-old UBKO mice. Public datasets indicated CTNNB1 expression inversely correlated with several thermogenic genes expression in human adipose/adipocytes, and positively correlated with body mass index (BMI) or waist-hip ratio (WHR). We proposed that intervention of β-catenin in adipocytes could be an effective strategy to enhance energy expenditure and improve age-related metabolic performance.
2023-03-31 | GSE227415 | GEO
Project description:We report mRNA seq during time course of white preadipocyte browning from WT and HMGN1 and HMGN2 double knockout (DKO) mice . Moreover, we support our finding that loss of HMGN promotes white adipocyte browning with RNA seq of WT and DKO MEFs transdifferentiation into brown-like adipocytes.
2022-10-19 | GSE193338 | GEO
Project description:We report single-cell RNA seq (scRNA seq) at day 0 and day 6 of white preadipocyte browning from WT and HMGN1 and HMGN2 double knockout (DKO) mice. This supports our finding that loss of HMGN promotes white adipocyte browning with RNA seq of WT and DKO MEFs transdifferentiation into brown-like adipocytes.
2022-10-19 | GSE193462 | GEO
Project description:Differentiation of brown adipocytes is a crucial process for adaptive thermogenesis, which is stimulated by various factors. We found robust browning of inguinal white adipose tissue in UCP1/ApoE-DKO mice, but not in ApoE-KO mice, under high-fat diet condition. We used microarray to determine the genes specifically regulated in the browning white adipose tissue in UCP1/ApoE-DKO mice.
2018-10-01 | GSE95273 | GEO