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

ORGANISM(S): Mus musculus

PROVIDER: GSE227439 | GEO | 2023/08/07

REPOSITORIES: GEO

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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

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.

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

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Project description:Adipocyte progenitor cells (APCs) provide the reservoir of regenerative cells to produce new adipocytes, although their identity in humans remains elusive. Using FACS analysis, gene expression profiling and metabolic and proteomic analyses, we identified three APCs subtypes in human white adipose tissues. The APC subtypes are molecularly distinct but possess similar proliferative and adipogenic capacities. Adipocytes derived from APCs with high CD34 expression exhibit exceedingly high rates of lipid flux compared with APCs with low or no CD34 expression, while adipocytes produced from CD34- APCs display beige-like adipocyte properties and a unique endocrine profile. APCs were more abundant in gluteofemoral compared with abdominal subcutaneous and omental adipose tissues, and the distribution of APC subtypes varies between depots and in patients with type 2 diabetes. These findings provide a mechanistic explanation for the heterogeneity of human white adipose tissue and a potential basis for dysregulated adipocyte function in type 2 diabetes.

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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.

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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.

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Transcriptomic Characterization of Human Beige Adipocyte Differentiated From Adipose Mesenchymal Stem Cells

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2018-04-24 | E-MTAB-6029 | biostudies-arrayexpress

Thermogenic differentiation of adipocyte progenitors

Project description:FACS-purified adipocyte progenitors from murine subcutaneous adipose tissue were cultured under conditions promoting general adipogenic differentiation or beige/brite adipocyte differentiation (treatment with cPGI2). Time course expression profiling was performed during differentiation. In addition, some cultures of differentiated adipocytes were stimulated with norepinephrine for 3 hours. In parallel, differentiation and norepinephrine stimulation of progenitors from interscapular brown fat was performed and profiled.

2015-08-20 | E-MTAB-3693 | biostudies-arrayexpress

Preweaning β-hydroxybutyrate elevation attenuates predisposition to metabolic dysregulation and impairs beige fat biogenesis in offspring of parents with high-fat diet-induced obesity

Project description:Parental obesity (PO) predisposes offspring to an increased risk of obesity and type 2 diabetes in adulthood. We demonstrated that exogenous ketosis enhances blood ketone body β-hydroxybutyrate (βHB) concentration, regulating the adipogenic activity of parental obesity (PO) offspring and promoting beige adipogenesis to counteract obesity. Bulk RNA-seq analysis was performed on inguinal white adipose tissue-derived stromal vascular cells (iWAT-SVCs) obtained from offspring of control mice (Ln-F1) and obese mice (parental obesity; Ob-F1) induced with ketosis using 1,3-butanediol during the pre-weaning period (P2 to P21).

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