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Transcriptome profiling of cold exposure induced browning of white fat

ABSTRACT: We revealed the common alterations and highlighted the differential effects between cold and β-AR agonists exposure on beige fat

ORGANISM(S): Mus musculus

PROVIDER: GSE164219 | GEO | 2021/05/25

REPOSITORIES: GEO

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Methylation profiling of cold exposure induced browning of white fat

Project description:We set two groups of 2-month-old C57BL6/J male mice at either thermoneutral temperature of 30℃ or under cold stimulation at 4℃ for one week. To identify events vital to beige fat activation, we performed MeRIP-seq using mice subcutaneous adipose tissue (iWAT) and focused on differentially-expressed genes characterized significant upregulation.

2023-08-20 | GSE222425 | GEO

Tanscriptome profiling of cold exposure induced browning of white fat

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2023-08-20 | GSE222424 | GEO

BAF60a deficiency uncouples chromatin accessibility and cold sensitivity from white fat browning

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. Here we found that BAF60a, a subunit of the SWI/SNF chromatin-remodeling complexes, serves an indispensible role in cold-induced thermogenesis in brown fat. BAF60a maintains chromatin accessibility for key thermogenic genes in close proximity to PPARg and EBF2 binding sites. Surprisingly, fat-specific BAF60a inactivation triggers more pronounced browning of inguinal white adipose tissue that is linked to induction of MC2R, a receptor for the pituitary hormone ACTH. Elevated MC2R expression sensitizes adipocytes and BAF60a-deficient adipose tissue to thermogenic activation in response to ACTH stimulation. These observations reveal an unexpected dichotomous role of BAF60a-mediated chromatin remodeling in transcriptional control of brown and beige gene programs and illustrate a pituitary-adipose signaling axis in the control of thermogenesis.

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Project description:Adipose tissue beiging refers to a process through which beige adipocytes emerge in classical white adipose tissue depots. Beige adipocytes dissipate chemical energy and secrete adipokines like classical brown adipocytes to improve systemic metabolism, which offers benefits for people with obesity and metabolic diseases. Cold exposure and β3-adrenergic receptor (AR) agonist treatment are two commonly used stimuli for increasing beige adipocytes in mice, but their underlying biological processes are different. Transcriptional analysis of inguinal white adipose tissue (iWAT) has revealed that changes in extracellular matrix (ECM) pathway genes are specific to cold exposure. Hyaluronic acid (HA), a non-sulfated linear polysaccharide produced by nearly all cells, is one of the most common components of ECM. We found that cold exposure significantly increases iWAT HA levels while β3-AR agonist CL316,243 fails to do so. Increasing HA level in iWAT by Has2 overexpression significantly increases cold-induced adipose tissue beiging; in contrast, decreasing HA by Spam1 overexpression, which encodes a hyaluronidase that digests HA, significantly decreases cold-induced iWAT beiging. All of these data implicate a role of HA in promoting adipose tissue beiging that is unique to cold exposure. Given the failure of β3-AR agonists in clinical trials for obesity and metabolic diseases, increasing HA could serve as a new approach to recruiting more beige adipocytes to combat metabolic diseases.

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Profiling of cold exposure induced browning of white fat

Project description:Profiling of cold exposure induced browning of white fat

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Profiling of cold exposure induced browning of white fat

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-20 | GSE222426 | GEO

Transcriptome profiling of cold exposure induced browning of white fat

Project description:Transcriptome profiling of cold exposure induced browning of white fat

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Methylation profiling of cold exposure induced browning of white fat

Project description:Methylation profiling of cold exposure induced browning of white fat

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Tanscriptome profiling of cold exposure induced browning of white fat

Project description:Tanscriptome profiling of cold exposure induced browning of white fat

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Neuregulin 4 mediates the metabolic benefits of mild cold exposure by promoting beige fat thermogenesis

Project description:Interorgan crosstalk via secreted hormones and metabolites is a fundamental aspect of mammalian metabolic physiology. Beyond the highly specialized endocrine cells, peripheral tissues are emerging as an important source of metabolic hormones that influence energy and nutrient metabolism and contribute to disease pathogenesis. Neuregulin 4 (Nrg4) is a fat-derived hormone that protects mice from nonalcoholic steatohepatitis (NASH) and NASH-associated liver cancer by shaping hepatic lipid metabolism and the liver immune microenvironment. Despite its enriched expression in brown fat, whether NRG4 plays a role in thermogenic response and mediates the metabolic benefits of cold exposure remain unexplored. Here we show that Nrg4 expression in inguinal white adipose tissue (iWAT) is highly responsive to chronic cold exposure. Nrg4 deficiency impairs beige fat induction and renders mice more susceptible to diet-induced metabolic disorders under mild cold conditions. Using mice with adipocyte and hepatocyte-specific Nrg4 deletion, we reveal that adipose tissue-derived NRG4, but not hepatic NRG4, is essential for beige fat induction following cold acclimation. Furthermore, treatment with recombinant NRG4-Fc fusion protein promotes beige fat induction in iWAT and improves metabolic health in diet-induced obese mice. These findings highlight a critical role of NRG4 in mediating beige fat induction and preserving metabolic health under mild cold conditions.

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