Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Obesity modifies cell fate plasticity of Pdgfrα-expressing adipocyte progenitors to promote an aberrant mammary microenvironment

ABSTRACT: The cellular basis of increased breast cancer risk linked to obesity is poorly understood. Using single-cell RNA sequencing (scRNA-seq), we investigated the cell fate dynamics of Pdgfra+ mammary adipocyte progenitors which we found were elevated in obesity.

ORGANISM(S): Mus musculus

PROVIDER: GSE254670 | GEO | 2025/10/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Obesity modifies cell fate plasticity of Pdgfrα-expressing adipocyte progenitors to promote an aberrant mammary microenvironment

Project description:Obesity modifies cell fate plasticity of Pdgfrα-expressing adipocyte progenitors to promote an aberrant mammary microenvironment

| PRJNA1071498 | ENA

Time Restricted Feeding Mitigates Obesity Through Adipocyte Thermogenesis

Project description:In obesity, misalignment of feeding time with the light/dark environment results in disruption of peripheral circadian clocks. Conversely, restricting feeding to the active period mitigates metabolic syndrome through mechanisms that remain unknown. Here we show that adipocyte thermogenesis is essential for the healthful metabolic response to time restricted feeding. Genetic enhancement of adipocyte thermogenesis through ablation of Zfp423 attenuates obesity caused by circadian mistimed high fat diet feeding through a mechanism involving creatine metabolism. Circadian control of adipocyte creatine metabolism underlies timing of diet-induced thermogenesis, and enhancement of adipocyte circadian rhythms through overexpression of the clock activator Bmal1 ameliorates metabolic complications during diet induced obesity. These findings establish creatine mediated diet-induced thermogenesis as a bioenergetic mechanism driving metabolic benefits during time-restricted feeding.

2022-10-24 | GSE181443 | GEO

Defective Olfactomedin-2 connects adipocyte dysfunction to obesity

Project description:Olfactomedin-2 (OLFM2) is a pleiotropic glycoprotein emerging as a regulator of energy homeostasis. We here show the expression of OLFM2 to be adipocyte-specific and inversely associated with obesity. OLFM2 levels increase during adipocyte differentiation and are suppressed in inflamed adipocytes. Functionally, OLFM2 deficiency impairs adipogenesis, while its over-production enhances the transformation of fat cell progenitors. Loss and gain of function experiments revealed that OLFM2 modulates key metabolic and structural pathways, including PPAR signaling, citrate cycle, fatty acid degradation, axon guidance and focal adhesion. On the molecular level, OLFM2 deficiency in adipocytes predominantly downregulates genes involved in cell cycle. Extending these findings in vivo, both whole-body Olfm2 knockout and adipose-specific Olfm2 depletion resulted in impaired adipose cell cycle gene expression, with the latter also displaying fat mass accretion and metabolic dysfunction. Collectively, our results underscore a critical role for OLFM2 in adipocyte biology, and support a causative link between reduced adipose OLFM2 and the pathophysiology of obesity.

2025-06-24 | MSV000098300 | MassIVE

LMO3 reprogramms viseral adipocyte metabolism during obesity

Project description:LMO3 reprogramms viseral adipocyte metabolism during obesity

| PRJNA578670 | ENA

The obesity-linked human lncRNA AATBC regulates adipocyte plasticity by stimulating mitochondrial dynamics and respiration [II]

Project description:Adipocytes are critical regulators of metabolism and energy balance. While white adipocyte dysfunction is a hallmark of obesity-associated disorders, the activation of thermogenic brown and beige adipocytes is linked to improved cardiometabolic health. As adipocytes dynamically adapt to environmental cues by functionally switching between white and thermogenic phenotypes, a molecular understanding of this adipocyte plasticity could help improving energy balance and weight loss. Here, we show that the long non-coding RNA (lncRNA) Apoptosis associated transcript in bladder cancer (AATBC) is a human-specific regulator of adipocyte plasticity. Searching for new human lncRNAs implicated in adipocyte biology we compared transcriptional profiles of human adipose tissues and cultured adipocytes and discovered that AATBC was enriched in thermogenic conditions. Using primary human adipocytes and immortalized human adipocytes we found that gain-of-function of AATBC enhanced the thermogenic phenotype whereas loss-of-function diminished this effect. The AATBC-mediated increase in mitochondrial respiration was linked to a more fragmented mitochondrial network and vice versa. While we found that AATBC is predominantly located in the nucleus, its effect on global transcription was only marginal. As AATBC is specific to humans, we expressed AATBC in adipose tissue of mice to study its systemic impact, which led to lower plasma leptin levels. Interestingly, this association was also present in human subjects, as AATBC in adipose tissue was inversely correlated with plasma leptin levels, body mass index and other measures of metabolic health. In conclusion, AATBC is a novel obesity-linked regulator of adipocyte plasticity and mitochondrial function in humans.

2023-08-29 | GSE239671 | GEO

The obesity-linked human lncRNA AATBC regulates adipocyte plasticity by stimulating mitochondrial dynamics and respiration [1]

2023-08-29 | GSE236966 | GEO

Adipocyte autophagy-mediated signals in the control of macrophage phenotype during diet-induced obesity

Project description:A hallmark of obesity is a pathological expansion of white adipose tissue that is accompanied by an increase in local inflammation and fibrosis. Autophagy is increased during obesity in adipose tissue, however, its role remains incompletely understood. Here, we report that autophagy is a critical regulator of pathological white adipose tissue remodelling and inflammation in diet-induced obese mice. The absence of adipocyte autophagy substantially exacerbates pericellular fibrosis specifically in gonadal white adipose tissue, ameliorating metabolic syndrome. Notably, changes in tissue architecture correlate with increased infiltration of macrophages and autophagy-dependent rewiring of adipocyte metabolism.

2025-09-26 | PXD052894 | Pride

YAP and TAZ protect against white adipocyte cell death during obesity

Project description:Investigation of the effect of YAP/TAZ on white adipocyte survival during obesity

2020-09-25 | GSE138911 | GEO

Secretory kinase FAM20C triggers adipocyte dysfunction inciting insulin resistance and inflammation in obesity

Project description:Obesity is a major driver of type 2 diabetes (T2D) and related metabolic disorders, characterized by chronic inflammation and adipocyte dysfunction. However, the molecular triggers initiating these processes remain poorly understood. We identify FAM20C, a serine/threonine kinase, as an early obesity-induced mediator of adipocyte dysfunction. Fam20c expression is substantially upregulated in adipocytes in response to obesity, correlating with a proinflammatory transcriptional signature. Forced expression of Fam20c in adipocytes promotes robust upregulation of proinflammatory cytokines and induces insulin resistance that is dependent on its kinase activity. Conversely, deletion of adipocyte Fam20c after established obesity and hyperglycemia improves glucose tolerance, augments insulin sensitivity, and reduces visceral adiposity, without altering body weight. Phosphoproteomic studies reveal that FAM20C regulates phosphorylation of intracellular and secreted proteins, modulating pathways critical to inflammation, metabolism, and extracellular matrix remodeling. We identify FAM20C-dependent substrates, such as CNPY4, whose phosphorylation contributes to proinflammatory adipocyte signaling. Of translational relevance, we show that in humans visceral adipose FAM20C expression positively correlates with insulin resistance. Our findings establish FAM20C as an early regulator of obesity-induced adipocyte dysfunction and systemic metabolic impairment. Our studies provide proof of concept that inhibition of FAM20C may serve as a potential therapy for T2D by restoring adipocyte health.

2025-11-18 | GSE309948 | GEO

LMO3 reprogramms viseral adipocyte metabolism during obesity [Mouse]

Project description:LMO3 reprogramms viseral adipocyte metabolism during obesity [Mouse]

| PRJNA578677 | ENA