Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A novel GPR120-dependent pathway of control brown fat activation mediated by FGF21

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE77534 | GEO | 2016/12/12

SECONDARY ACCESSION(S): PRJNA310747

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-sequence analysis of immortalized, differentiated preadipocytes derived from inguinal subcutaneous white adipose tissue.

Project description:In acute cold stress in mammals, JMJD1A, an H3K9 demethylase, up-regulates thermogenic gene expressions through β-adrenergic signaling in brown adipose tissue (BAT). Aside BAT-driven thermogenesis, mammals also have another mechanism to cope with long-term cold stress by inducing the browning of subcutaneous white adipose tissue (scWAT). Here, we show that this occurs through a two-step process that requires both β-adrenergic dependent phosphorylation of S265 and demethylation of H3K9me2 by JMJD1A. The histone demethylation independent acute Ucp1 induction in BAT and demethylation dependent chronic Ucp1 expression in beige-scWAT provide complementary molecular mechanisms to ensure an ordered transition between acute and chronic adaptation to cold stress. JMJD1A mediates two major signaling pathways, namlely β-adrenergic receptor and PPARγ activation, via PRDM16-PPARγ-P-JMJD1A complex for beige adipogenesis.

2018-02-16 | GSE107900 | GEO

Genome-wide analysis of JMJD1A and PPARγ binding in immortalized, differentiated preadipocytes derived from inguinal subcutaneous white adipose tissue.

2018-02-16 | GSE107899 | GEO

RNA-Sequencing of wild type and UCP1-null beige adipose tissue

Project description:Since brown adipose tissue (BAT) dissipates energy through UCP1, BAT has garnered attention as a therapeutic intervention for obesity and metabolic diseases including type 2 diabetes. As we better understand the roles of classical brown and beige adipocytes, increased beige fat mass in response to a variety of external/internal cues is associated with significant improvements in glucose and lipid homeostasis that may not be entirely mediated by UCP1. We aim to analyze transcriptome of wild type and UCP1-null beige adipocyte to identify the UCP1-independent function.

2017-10-28 | E-MTAB-4085 | biostudies-arrayexpress

Impact of UCP1 and FGF21 for the development of diet-induced obesity at standard housing temperatures

Project description:Global RNA sequencing analysis of brown fat (BAT), inguinal white fat (iWAT), liver and muscle (quadriceps) of high-fat diet fed WT, FGF21 KO, UCP1 KO and UCP1/FGF21 double KO mice.

2019-11-05 | GSE122167 | GEO

Integrated proteome and phosphoproteome analysis of interscapular brown adipose and subcutaneous white adipose tissues upon high fat diet feeding in mouse

Project description:Thermogenesis is a promising approach to limit weight gain in response to excess nutrition. In contrast to cold-induced thermogenesis, the molecular and cellular mechanisms of diet-induced thermogenesis (DIT) have not been fully characterized. Here, we explored the response of brown adipose tissue (BAT) and beige adipose tissue to high fat diet (HFD) using proteome and phosphoproteome analysis. We observed that after HFD, DIT was only activated in BAT. Furthermore, fatty acid oxidation, tricarboxylic acid cycle, and oxidative phosphorylation were also activated in BAT. Nevertheless, most metabolic pathways downregulated in beige adipose tissue. Strikingly, we found that these metabolic changes accompanied with different variation of mitochondria between BAT and beige adipose tissue as well. HFD treatment impaired mitochondrial functions and mitochondrial protein synthesis in beige adipose tissue while it stimulated mitochondrial autophagy in BAT. Together, in BAT, HFD caused increased mitochondrial activity,

2022-04-01 | PXD032888 |

Transcriptome analysis in adipose tissues of BAF60a knockout mice

Project description:Brown and beige fat share a remarkably similar transcriptional program that supports fuel oxidation and thermogenesis. The chromatin-remodeling machinery that governs genome accessibility and renders adipocytes poised for thermogenic activation remains elusive. BAF60a serves an indispensable role in cold-induced thermogenesis in brown fat. Surprisingly, fat-specific BAF60a inactivation triggers more pronounced browning of inguinal white adipose tissue. These results suggest a dichotomous role of BAF60a-mediated chromatin remodeling in transcriptional control of brown and beige gene programs. To elucidate the mechanism, we performed microarray annalysis in inguinal white adipose tissues from mice after chronic cold exposure.

2020-02-19 | GSE145498 | GEO

Actomyosin-mediated tension orchestrates uncoupled respiration in adipose tissues

Project description:The activation of brown/beige adipose tissue (BAT) metabolism and the induction of uncoupling protein-1 (UCP1) expression are essential for BAT-based strategies to improve metabolic homeostasis. Adrenergic signaling is viewed as a key regulator of thermogenesis and UCP1-expression in BAT, while also operating as a potent contractile stimulator in muscle. The muscle-like gene expression patterns of UCP1+ adipocytes have previously been utilized as tissue specific markers, but have not been attributed with any functional role. Here, we demonstrate that BAT utilizes actomyosin machinery to generate tensional responses following adrenergic stimulation, similar to muscle tissues. We show that activation of actomyosin mechanics are critical for the acute induction of oxidative metabolism and uncoupled respiration in UCP1+ adipocytes. Additionally, actomyosin-mediated elasticity regulates mechanosensitive transcriptional co-activators, YAP/TAZ, that facilitate the thermogenic capacity of adipocytes. These unappreciated signaling and mechanical mechanisms may inform future strategies to promote the expansion and activation of brown/beige adipocytes.

2018-03-01 | GSE109829 | GEO

Exosomal Proteins and Brown Fat Activation

Project description:Brown adipose tissue (BAT) is a promising weapon to combat obesity and metabolic disease. BAT is thermogenic and consumes substantial amounts of glucose and fatty acids as fuel for thermogenesis and energy expenditure. To study BAT function in large human longitudinal cohorts, safe and precise detection methodologies are needed. Although regarded a gold standard, the foray of PET-CT into BAT research and clinical applications is limited by its high ionizing radiation doses. Here, we show that brown adipocytes release exosomes in blood plasma which can be utilized to assess BAT activity. In this study, we investigated circulating protein biomarkers that can accurately and reliably reflect BAT activation triggered by cold exposure, capsinoids ingestion and thyroid hormone excess in humans.

2022-06-09 | PXD023909 | Pride

RNA-seq comparison of CD81 positive and negative cells in subcutaneous and visceral white fat and brown fat tissues in mouse

Project description:Subcutaneous white adipose tissue (scWAT) is known to undergo browning in response to cold exposure. The goal of this study is to identify elusive precursors found within scWAT that possess the ability to differentiate into beige adipocytes. A single cell transcriptomics experiment conducted by us identified the tetraspanin CD81 as a marker of adipose precursor cells (APC) that can convert to beige upon cold exposure. However, what distinguishes a CD81 positive APC from its CD81 negative counterpart in the same tissue, or in a different tissue remains unknown. Therefore, we applied bulk RNA-seq to sorted populations of Lineage negative Sca1+, CD81+/ CD81- cells from subcutaneous and visceral WAT, and brown adipose tissue to decipher the molecular underpinnings that render a CD81+ APC residing in scWAT, beige in response to browning.

2020-04-24 | E-MTAB-8435 | biostudies-arrayexpress

EPAC1 enhances energy expenditure by selectively inducing brown and beige adipose tissue growth

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data