Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-70562E-GEOD-68382E-GEOD-68429
PROVIDER: PRJNA282723 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [BAT]
2016-01-08 | E-GEOD-68429 | ExpressionAtlas
Project description:Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [IWAT]
2016-01-08 | E-GEOD-68382 | ExpressionAtlas
Project description:Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity
| PRJNA282744 | ENA
Project description:Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [IWAT]
| PRJNA282719 | ENA
Project description:Brown adipose tissue (BAT) dissipates energy and promotes cardio-metabolic health4. However, loss of BAT during obesity and aging is a principal hurdle for BAT-centered obesity therapies. So far not much is known about BAT apoptosis and signals released by apoptotic brown adipocytes. Here, untargeted metabolomics demonstrated that apoptotic brown adipocytes release a specific pattern of metabolites with purine metabolites being highly enriched. Interestingly, this apoptotic secretome enhances expression of the thermogenic program in healthy adipocytes to maintain tissue functionality. This effect is mediated by the purine inosine which stimulates energy expenditure (EE) in brown adipocytes. Phosphoproteomic analysis demonstrated activation of the cAMP/protein kinase A signaling pathway and of pro-thermogenic transcription factors by inosine.
2022-05-31 | PXD032153 | Pride
Project description:The preoptic area (POA) of the hypothalamus is a key neural hub for thermoregulation, yet its role in modulating energy expenditure during caloric excess remains poorly defined. Here, we characterize prepronociceptin (PNOC)-expressing neurons in the medial POA (PNOCmPOA) that inhibit brown adipose tissue (BAT) thermogenesis and systemic energy expenditure. Chemogenetic activation of PNOCmPOA neurons reduced BAT activity, core temperature, energy expenditure, and glucose tolerance through inhibitory projections to the dorsomedial hypothalamus (DMH). In contrast, silencing or ablation of PNOCmPOA neurons increased BAT thermogenesis. Furthermore, PNOCmPOA activation promoted non-REM sleep, coupling thermoregulatory and arousal states. These findings define a hypothalamic circuit that limits postprandial arousal, thermogenesis, and energy dissipation, contributing to the pathophysiology of obesity. Targeting the PNOCmPOA→DMH pathway may provide a new therapeutic strategy to enhance BAT function in metabolic disease.
2026-06-02 | GSE306829 | GEO
Project description:The preoptic area (POA) of the hypothalamus is a key neural hub for thermoregulation, yet its role in modulating energy expenditure during caloric excess remains poorly defined. Here, we characterize prepronociceptin (PNOC)-expressing neurons in the medial POA (PNOCmPOA) that inhibit brown adipose tissue (BAT) thermogenesis and systemic energy expenditure. Chemogenetic activation of PNOCmPOA neurons reduced BAT activity, core temperature, energy expenditure, and glucose tolerance through inhibitory projections to the dorsomedial hypothalamus (DMH). In contrast, silencing or ablation of PNOCmPOA neurons increased BAT thermogenesis. Furthermore, PNOCmPOA activation promoted non-REM sleep, coupling thermoregulatory and arousal states. These findings define a hypothalamic circuit that limits postprandial arousal, thermogenesis, and energy dissipation, contributing to the pathophysiology of obesity. Targeting the PNOCmPOA→DMH pathway may provide a new therapeutic strategy to enhance BAT function in metabolic disease.
2026-06-02 | GSE292387 | GEO
Project description:Coenzyme Q is an essential component of mitochondrial function and required for thermogenic activity in brown adipose tissues (BAT). BAT CoQ deficiency (50-75%) by genetic or pharmacological means does not interfere with basal or maximal mitochondrial respiration in brown adipocytes but increases mitochondrial oxidants and induces UPRmt, ISR, and repression of UCP1 expression. ATF4, the master regulator of ISR, is required for UCP1 suppression in BAT CoQ deficiency. In animals, BAT CoQ deficiency causes cold intolerance but activates compensatory thermogenic mechanisms in BAT and other tissues via greatly induced BAT FGF21 expression resulting in paradoxically upregulated whole-body respiration rates and protection from obesity at room temperature and thermoneutrality. BAT-specific loss of either ATF4 or FGF21 abolishes these metabolic benefits demonstrating a central role for CoQ in the modulation of whole-body energy expenditure and thus for the etiology of primary and secondary CoQ deficiencies.
2022-02-01 | GSE165940 | GEO
Project description:Increasing energy expenditure through activation of brown adipose tissue (BAT) thermogenesis is an attractive approach to counteract obesity. Thus, it is essential to understand molecular mechanisms that control BAT functions. Here, we describe signal transducer and activator of transcription (STAT) 5 as key regulator of BAT functionality. We found that STAT5 is necessary for acute cold-induced temperature maintenance and stimulated lipid breakdown in BAT using mice that harbour an adipocyte-specific deletion of Stat5a/b genes. In addition, the mitochondrial respiratory capacity of primary differentiated brown adipocytes from STAT5 deficient mice was diminished. We show that increased sensitivity to cold stress upon STAT5 deficiency was associated with reduced expression of thermogenic key player uncoupling protein 1, while decreased stimulated lipolysis of STAT5-deficient BAT explants was linked to decreased protein kinase A activity. In addition, brown remodeling of white fat was diminished following chronic β-adrenergic stimulation. This impairment was linked to a decrease in mitochondrial functionality. We conclude that STAT5 is essential for the β-adrenergic responsiveness of brown adipose tissue and the physiologic function of thermogenic adipose tissue.
2020-05-28 | GSE137678 | GEO
Project description:Obesity has become a global health problem. Brown adipose tissue (BAT), specialized for energy expenditure through thermogenesis, potently counteracts obesity. Recently, BAT is also identified in human adults. We found that Lgr4 homozygous mutant (Lgr4m/m) mice display reduced adiposity and exhibit brown-like adipocytes in their WAT depots with higher expression of uncoupling protein 1 (Ucp1). Furthermore, Lgr4 ablation potentiates brown adipocyte differentiation from stromal vascular fraction (SVF) of epididymal WAT (eWAT) in vitro. We used microarrays to emxamine the gene expression profiles of the brown-like adipocytes differentiated from SVF of wild-type and Lgr4 mutant mice. We identified distinct gene expression profiles of these two groups.
2013-11-07 | GSE47760 | GEO