Expression data from the visceral adipose tissues of Lgr4 mutant (KO) and wild-type (WT) mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE195570 | GEO | 2022/01/28
REPOSITORIES: GEO
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Project description:Obesity has become a global health problem. Brown adipose tissue (BAT), specialized for energy expenditure through thermogenesis, potently counteracts obesity. Recently, BAT is also identified in human adults. We found that Lgr4 homozygous mutant (Lgr4m/m) mice display reduced adiposity and exhibit brown-like adipocytes in their WAT depots with higher expression of uncoupling protein 1 (Ucp1). Furthermore, Lgr4 ablation potentiates brown adipocyte differentiation from stromal vascular fraction (SVF) of epididymal WAT (eWAT) in vitro. We used microarrays to emxamine the gene expression profiles of the brown-like adipocytes differentiated from SVF of wild-type and Lgr4 mutant mice. We identified distinct gene expression profiles of these two groups. To demonstrate Lgr4 ablation can potentiate the differentiation of SVF from eWAT toward brown-like adipocytes in vitro, we isolated SVF from epididymal white adipose tissue (eWAT) of wild-type (WT) and Lgr4 mutant mice. We then plated SVF cells in 12-well plate, and differentiated them to brown adipocytes, followed by RNA extraction and hybridization with Affymetrix microarrays.
2013-11-07 | E-GEOD-47760 | biostudies-arrayexpress
Project description:Obesity has become a global health problem. Brown adipose tissue (BAT), specialized for energy expenditure through thermogenesis, potently counteracts obesity. Recently, BAT is also identified in human adults. We found that Lgr4 homozygous mutant (Lgr4m/m) mice display reduced adiposity and exhibit brown-like adipocytes in their WAT depots with higher expression of uncoupling protein 1 (Ucp1). Furthermore, Lgr4 ablation potentiates brown adipocyte differentiation from stromal vascular fraction (SVF) of epididymal WAT (eWAT) in vitro. We used microarrays to emxamine the gene expression profiles of the brown-like adipocytes differentiated from SVF of wild-type and Lgr4 mutant mice. We identified distinct gene expression profiles of these two groups.
2013-11-07 | GSE47760 | 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:White fat browning is a highly variable genetic trait in mice (Guerra et al., 1998). To gain an overview of strain variations in browning capacities, we performed transcriptome analysis of white fat browning in (1) 5 inbred mouse strains (C57BL/6J, 129S6sv/ev, A/J, AKR/J, and SWR/J) with distinct browning propensities in WAT, and (2) F1 hybrids derived from a high (129S6sv/ev) and low browning strain (C57BL/6J) cross. White fat browning is a highly variable genetic trait in mice (Guerra et al., 1998). To gain an overview of strain variations in browning capacities, we performed transcriptome analysis of white fat browning in three genetic models (Figure 1A), including (1) 5 inbred mouse strains (C57BL/6J, 129S6sv/ev, A/J, AKR/J, and SWR/J) with distinct browning propensities in WAT, (2) F1 hybrids derived from a high (129S6sv/ev) and low browning strain (C57BL/6J) cross.
2019-11-01 | E-MTAB-8344 | biostudies-arrayexpress
Project description:White fat browning is a highly variable genetic trait in mice (Guerra et al., 1998). To gain an overview of strain variations in browning capacities, we performed transcriptome analysis of white fat browning in (1) 5 inbred mouse strains (C57BL/6J, 129S6sv/ev, A/J, AKR/J, and SWR/J) with distinct browning propensities in WAT, and (2) F1 hybrids derived from a high (129S6sv/ev) and low browning strain (C57BL/6J) cross. From our analyses, several transcription factors emerged as novel regulators of white fat browning, including the TFs Zfp521, Fhl1, and Mxd1. We further validated the role of these TFs and performed 3' RNA-seq experiments upon their knockdown, in order to characterize their mechanism of action.
2019-11-01 | E-MTAB-8343 | biostudies-arrayexpress
Project description:Brown adipose tissue (BAT) thermogenesis and the browning of white adipose tissue are important components of energy expenditure. An RNAseq-based analysis of the mouse BAT transcriptome led us to identify GPR120 as a gene induced by thermogenic activation. GPR120, a G protein-coupled receptor binding unsaturated long-chain fatty acids, is known to mediate some beneficial metabolic actions of polyunsaturated fatty acids. We show that pharmacological activation of GPR120 induces BAT activity and promotes the browning of white fat in mice, whereas GRP120-null mice show impaired browning in response to cold. n-3 polyunsaturated fatty acids induce brown and beige adipocyte differentiation and thermogenic activation, and these effects require GPR120. GPR120 activation induces the release of fibroblast growth factor-21 (FGF-21) by brown and beige adipocytes and increases blood FGF21 levels. The effects of GPR120 activation are impaired in FGF21-null mice and cells. Thus, the lipid sensor GPR120 constitutes a novel pathway of brown fat activation and involves FGF21.
2016-12-12 | GSE77534 | GEO
Project description:Brown adipose tissue (BAT) is a central thermogenic organ that enhances energy expenditure (EE) and cardiometabolic health. However, regulators that specifically increase the number of thermogenic adipocytes are still an unmet need. Here, we show by phosphoproteomics that cAMP activates distinct signaling pathways in brown progenitors, with the cAMP-EPAC1 axis enhancing proliferation and differentiation of thermogenic but not white adipocytes. Further analysis revealed that a specific subpopulation of preadipocytes that are PDGFRα-positive express EPAC1. In vivo, pharmacological activation of EPAC1 enhances BAT growth and browning of white fat, leading to increased EE and reduced diet-induced adiposity. In contrast, mice lacking EPAC1 in PDGFRα-positive preadipocytes show the opposite phenotype. Importantly, EPAC1 activation enhances proliferation and differentiation of human brown adipocytes and human brown fat organoids. Interestingly, a coding variant in EPAC1 that positively correlates with BMI abolishes norepinephrine-induced proliferation of brown adipocytes. Thus, EPAC1 might be an attractive target to enhance thermogenic adipocyte number and EE to combat metabolic diseases.
2023-11-11 | PXD046709 | Pride
Project description:Brown adipose tissue (BAT) protects against obesity by promoting energy expenditure via uncoupled respiration. To uncover BAT-specific long non-coding RNAs (lncRNAs), we used RNA-seq to reconstruct de novo transcriptomes of mouse brown, inguinal white, and epididymal white fat and identified ~1500 lncRNAs, including 127 BAT-restricted loci induced during differentiation and often targeted by key regulators PPARγ, C/EBPα and C/EBPβ. One of them, lnc-BATE1, is required for establishment and maintenance of BAT identity and thermogenic capacity. lnc-BATE1 inhibition impairs concurrent activation of brown fat and repression of white fat genes, and is partially rescued by exogenous lnc-BATE1 with mutated siRNA-targeting sites, demonstrating a function in trans. We show that lnc-BATE1 binds heterogeneous nuclear ribonucleoprotein U and that both are required for brown adipogenesis. Our work provides an annotated catalog for the study of fat depot-selective lncRNAs, available online, and establishes lnc-BATE1 as a novel regulator of BAT development and physiology. Total RNA profiles of BAT, iWAT and eWAT samples were sequenced on the Illumina HiSeq2000 platform
2015-04-23 | E-GEOD-66686 | biostudies-arrayexpress
Project description:We identify fibroblast growth factor 1 (FGF1) as a critical transducer in adipose tissue remodeling and link its regulation to peroxisome proliferator activated-receptor ? (PPAR?), the adipocyte master regulator and target of the thiazolidinedione (TZD) class of insulin sensitizing drugs. We show that FGF1 is highly induced in adipose tissue in response to high-fat diet (HFD) and that mice lacking FGF1 develop an aggressive diabetic phenotype coupled to aberrant adipose expansion when challenged with HFD. Mechanistically, we show that transcription of FGF1 is directly regulated by an adipocyte-selective proximal PPAR response element, and that this PPAR?-FGF1 axis is evolutionarily conserved in mammals. This work describes the first phenotype of the FGF1 knockout mouse and establishes FGF1 as a new member of the NR-FGF axis critical for maintaining metabolic homeostasis and insulin sensitization. Total RNA was obtained from epidydimal white adipose tissue (eWAT) and livers from 6 month old wild-type and FGF1-/- mice after 16 weeks on normal chow or high-fat diets.
2012-04-22 | E-GEOD-31692 | biostudies-arrayexpress
Project description:Enhancing brown fat activity and promoting white fat browning are attractive therapeutic strategies for obesity and its associated metabolic disorders. To provide a comprehensive picture of the regulatory network in these processes, we conducted a series of transcriptome studies by RNA-seq and quantified the mRNA and lncRNA changes during white fat browning induced by chronic cold exposure, beta-adrenergic agonist and intensive exercises, brown fat activation by acute cold exposure and inactivation by thermoneutrality.
2017-08-01 | GSE86338 | GEO