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Aging impairs cold-induced beige adipogenesis and adipocyte metabolic reprogramming [single-nucleus RNA-seq]

ABSTRACT: The energy-burning capability of beige adipose tissue is a potential therapeutic tool for reducing obesity and metabolic disease, but this capacity is decreased by aging. Here, we evaluate the impact of aging on the profile and activity of adipocytes during the beiging process through single nucleus gene expression analysis of inguinal white adipose tissue of young and aged mice in response to cold exposure.

ORGANISM(S): Mus musculus

PROVIDER: GSE227440 | GEO | 2023/08/07

REPOSITORIES: GEO

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Aging impairs cold-induced beige adipogenesis and adipocyte metabolic reprogramming [single-cell RNA-seq]

Project description:The energy-burning capability of beige adipose tissue is a potential therapeutic tool for reducing obesity and metabolic disease, but this capacity is decreased by aging. Here, we evaluate the impact of aging on the profile and activity of adipogenic precursor cells (APCs) through single cell gene expression analysis of inguinal white adipose tissue of young and aged mice through in response to cold exposure.

2023-08-07 | GSE227439 | GEO

Hyaluronan mediates cold-induced adipose tissue beiging

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.

2024-08-01 | GSE268781 | GEO

A non-cell autonomous mechanism of beige adipocyte renaissance in subcutaneous adipose tissue

Project description:Two types of UCP1 positive cells-brown and beige adipocytes exist in mammals. Beige adipocytes are very plastic, and can be dynamically regulated by environment.Beige adipocytes formed postnatally in subcutaneous inguinal white adipose tissue (iWAT) lost thermogenic gene expression and multilocular morphology at adult stage, but cold could restore their “beigeing” characteristics, a phenomenon termed as beige adipocyte renaissance. Our results showed that beige cell maintenance and renaissance in adult mice were regulated by cAMP and HDAC4 signaling in white adipocytes non-cell autonomously. Genetic modulations of various components of this cAMP-HDAC4 cascade (e.g. LKB1) led to persistent browning and reduced adiposity independent of thermogenesis. To further study the mechanisms of beige adipocytes maintenance, we performed RNA-seq with samples from inguinal white adipose tissues of WT, AdipoqCre LKB1 F/F, and AdipoqCre LKB1 F/F; HDAC4 F/F mice.Our studies will move the beige adipocyte field forward and attract clinical applications to target beige adipocyte renaissance.

2018-02-14 | GSE85335 | GEO

Naa10p Inhibits Beige Adipocyte-mediated Thermogenesis through N-α-acetylation of Pgc1α

Project description:We reported that both conventional and adipose-specific Naa10p deletions in mice result in increased energy expenditure, thermogenesis, beige adipocyte differentiation and activation. Mechanistically, Naa10p acetylates the N-terminus of Pgc1α and prevents it from interacting with Ppar to activate key genes, such as Ucp1, involved in beige adipocyte function. We used microarrays to profile the gene expression changes by Naa10p KO in inguinal white adipose tissues (iWATs) derived from mice fed with high fat diet for 15 weeks.

2019-08-16 | GSE133865 | GEO

Aging impairs cold-induced beige adipogenesis and adipocyte metabolic reprogramming

Project description:Aging impairs cold-induced beige adipogenesis and adipocyte metabolic reprogramming

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snRNA-seq of Beiging Inguinal Adipose Tissue from UCP1-KO and WT mice under cold-stress and mice treated with Beta-Blocker and mild cold exposure.

Project description:Atlas of UCP1-KO Beiging inguinal adipose tissue and tissue in which beta adrenergic signaling is blocked provides further insight into UCP1-independent mechanisms of beiging.

2021-05-17 | GSE174497 | GEO

M2 macrophages independently promote beige adipogenesis via blocking adipocyte Ets1

Project description:Beige adipocytes accumulates mitochondria and alleviates metabolic disorder via activating energy expenditure. Whether the opposing process of mitochondrial biogenesis and clearance are integrated regulated in beige adipocytes is beyond known. Here we show that DNA binding protein Ets1 suppresses beige adipocyte formation via bidirectional regulation of mitochondrial biogenesis and clearance. The expression level of Ets1 was down-regulated in browning adipocytes, and up-regulated in the subcutaneous fat of obese mice. Adipocyte Ets1 heterozygous knock-in mice showed suppressed beige adipocytes formation under cold stress, while the homozygous knock-in mice are cold intolerance. On the other hand, knocking out Ets1 in adipocytes enhanced energy expenditure and protect the mice from high fat diet induced metabolic disorders. Mechanical assay suggests Ets1 binds to the promoter region of mitochondria complex coding genes and autophagy related genes, transcriptionally suppresses mitochondrial biogenesis and activates its clearance. Our results indicate that Ets1 integrally regulates the balance of mitochondria generation and degradation, hence acts as a pivotal governor of mitochondria content and negatively regulates beige adipocyte formation.

2023-07-01 | GSE234879 | GEO

RNA-seq of cold stimulated inguinal fat of wild type and Rarres2-/- mice

Project description:Although various stimuli and mediators have been identified to promote thermogenic beige fat development, less is known about the negative regulator of cold-induced beiging. We here show that lack of chemerin that is highly expressed in white adipose tissue or its receptor CMKLR1 in adipocytes enhances cold-induced beiging and thermogenesis. Our results reveal a previously unrecognized beige-inhibitory role of chemerin-CMKLR1 axis, and suggests CMKLR1 as a therapeutic target for obesity-related metabolic disorders.

2019-12-31 | GSE133978 | GEO

Genome-wide binding sites of Foxp4 in beige adipocyte

Project description:We found deletion of Foxp4 in mature adipocytes would augment juvenile and mature beige adipocyte thermogenesis.In order to investage the binding site of Foxp4 in the genome of beige adipocytes, we did Foxp4 ChIP-Seq with differentiated SVF cells derived from ingunal adipose tissues.

2022-04-06 | GSE199559 | GEO

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.

2024-01-01 | GSE246993 | GEO

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