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

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

PROVIDER: PRJNA945059 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23873911.fastq.gz	Fastqsanger.gz
	SRR23873912.fastq.gz	Fastqsanger.gz
	SRR23873913.fastq.gz	Fastqsanger.gz
	SRR23873914.fastq.gz	Fastqsanger.gz
	SRR23873915.fastq.gz	Fastqsanger.gz

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

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

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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

Aging impairs cold-induced beige adipogenesis and adipocyte metabolic reprogramming [single-nucleus 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 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.

2023-08-07 | GSE227440 | GEO

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

M2 macrophages independently promote beige adipogenesis via blocking adipocyte Ets1

Project description:M2 macrophages independently promote beige adipogenesis via blocking adipocyte Ets1

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LncRNAs expression profiling in adipose tissues and during brown adipocyte differentiation

Project description:Brown and beige fats generate heat via uncoupled respiration to defend against cold, mechanistically, through the action of a network of transcription factors and cofactors. Here we globally profiled long noncoding RNAs (lncRNAs) gene expression during thermogenic adipocyte formation and identified Brown fat lncRNA 1 (Blnc1) as a novel nuclear lncRNA that promotes brown and beige adipocyte differentiation and function by forming a feedforward regulatory loop with EBF2 to drive adipogenesis toward thermogenic phenotype. LncRNAs expression were measured in BAT and WAT from mice injected saline/CL and during brown adipocyte differentiation with two replicates using Arraystar Mouse LncRNA microarray V2.0

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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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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.

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PdgfrB signaling alters the beige adipogenic niche

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