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Ctnnb1/β-catenin inactivation in UCP1-positive adipocytes augments the browning of white adipose tissue

ABSTRACT: Ctnnb1/β-catenin inactivation in UCP1-positive adipocytes augments the browning of white adipose tissue

PROVIDER: PRJNA945003 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23869847_1.fastq.gz	Fastqsanger.gz
	SRR23869847_2.fastq.gz	Fastqsanger.gz
	SRR23869848_1.fastq.gz	Fastqsanger.gz
	SRR23869848_2.fastq.gz	Fastqsanger.gz
	SRR23869849_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Ctnnb1/β-catenin inactivation in UCP1-positive adipocytes augments the browning of white adipose tissue

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

<i>Ctnnb1</i>/β-catenin inactivation in UCP1-positive adipocytes augments the browning of white adipose tissue.

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 immune-related genes in epididymal WAT. Improved glucose tolerance and insulin sensitivity were observed in 50-week-old UBKO mice. Public datasets indicated that CTNNB1 expression was inversely correlated with several thermogenic genes expression in human adipose tissue/adipocytes and positively correlated with 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.

| S-EPMC10148125 | biostudies-literature

Expression data from browning inguinal white adipose tissue in UCP1/ApoE-DKO mice

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

Browning of White Adipose Tissue with Roscovitine Induces a Distinct Population of UCP1+ Adipocytes.

Project description:Analysis of FACS sorted UCP1+ adipocytes shows that the mRNA signature of brite adipocytes is distinct from beige adipocytes, which arise through catecholamine signaling.

2016-12-13 | GSE87191 | GEO

Browning of human adipocytes requires KLF11 and reprogramming of PPARγ super-enhancers

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

Epigenomic rescue of genetically defective Ucp1 expression in subcutaneous fat of C57BL/6 mice [RNA-Seq]

Project description:Obesity causes insulin resistance, and PPARγ ligands like rosiglitazone (rosi) are insulin-sensitizing, yet mechanisms remain unclear. High fat diet (HFD) induced obesity has major effects on visceral epididymal adipose tissue (eWAT) of C57BL/6 (B6) mice, and here we report altered activity of gene regulatory elements with changes in PPARγ genome-wide occupancy. Treatment with rosi restored insulin sensitivity, yet surprisingly had little effect on eWAT, leading us to consider the subcutaneous inguinal fat (iWAT). In this depot, rosi markedly induced molecular signatures of brown fat including the key thermogenic gene Ucp1. Obesity-resistant 129S1/SvImJ (129) mice showed this degree of iWAT browning even in the absence of rosi. Remarkably, the 129 Ucp1 locus had increased PPARγ binding and gene expression that was preserved in B6x129 F1 intercross iWAT, with imbalance favoring the 129-derived alleles showing a cis-acting genetic difference. Thus, B6 mice have a genetic defect in Ucp1 expression. However, imbalanced expression favoring 129 over B6 was nearly lost when Ucp1 was activated by rosi, or by iWAT browning in cold-exposed or young mice. These results provide a novel framework for understanding how environmental influences like drugs can rescue genetically determined disease phenotypes by affecting the epigenome.

2017-02-27 | GSE91067 | GEO

Epigenomic rescue of genetically defective Ucp1 expression in subcutaneous fat of C57BL/6 mice [ChIP-Seq]

2017-02-27 | GSE92606 | GEO

Transcriptome differences between primary brown adipocytes of wildtype and UCP1-KO mice

Project description:We analyzed coding transcript abundance in fully differentiated, primary brown adipocytes from murine, interscapular brown adipose tissue of wildtype and UCP1-KO mice.

2018-09-13 | GSE119873 | GEO

Browning of human adipocytes requires KLF11 and reprogramming of PPARγ super-enhancers

2014-12-12 | GSE59703 | GEO

Browning of White Adipose Tissue with Roscovitine Induces a Distinct Population of UCP1<sup>+</sup> Adipocytes.

Project description:Brown-like adipocytes exist in several adipose depots including white (WAT) as well as brown (BAT). Activation of these UCP1+ cells is a potential therapeutic strategy to combat obesity. Studies have shown that posttranslational modifications of PPARγ regulate select adipocyte programs. Deacetylation of K268 and K293 in the ligand-binding domain of PPARγ by Sirt1 induces browning of WAT. Phosphorylation of S273 of PPARγ by CDK5 or ERK stimulates a diabetogenic program of gene expression in WAT. Here, we report that roscovitine, a CDK inhibitor, prevents S273 phosphorylation and promotes formation of UCP1+ (brite) adipocytes in WAT. It also enhances energy expenditure as well as prevents diet-induced obesity and insulin resistance. Analysis of fluorescence-activated cell-sorted UCP1+ adipocytes shows that the mRNA signature of brite adipocytes is distinct from beige adipocytes, which arise through catecholamine signaling. These results suggest that brown-like adipocytes in WAT may arise from multiple origins.

| S-EPMC6674884 | biostudies-literature

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