Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA293363 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Ambient temperature affects energy intake and expenditure to maintain homeostasis in a continuously fluctuating environment. Here, mice with an adipose-specific defect in fatty acid oxidation (Cpt2A-/-) were subjected to varying temperature to determine the role of adipose bioenergetics to environmental adaptation. Cpt2A-/- brown adipose tissue (BAT) failed to induce thermogenic genes such as Ucp1 and Pgc1α in response to adrenergic stimulation, which is exacerbated by increasing temperature. Thermoneutrality induced a mitochondrial DNA stress in Cpt2A-/- BAT that resulted in a loss of classical interscapular BAT, but did not affect body weight gain or glucose tolerance in response to a high-fat diet. In this dataset, we include the expression data obtained from dissected mouse interscapular brown adipose tissue from mice acclimatized to thermoneutrality (30C) with and without beta3adrenergic stimulation with and without the deletion of carnitine palmitoyltransferase 2 (i.e., adipose unable to beta-oxidize long chain fatty acids in mitochondria). WildType and Cpt2A KnockOut mice were treated either with or without beta3adrenergic stimulation, thus four classes. Three biologic replicates were compared per class, thus twelve mice.
2016-02-04 | E-GEOD-72210 | biostudies-arrayexpress
Project description:Ambient temperature affects energy intake and expenditure to maintain homeostasis in a continuously fluctuating environment. Here, mice with an adipose-specific defect in fatty acid oxidation (Cpt2A-/-) were subjected to varying temperature to determine the role of adipose bioenergetics to environmental adaptation. Cpt2A-/- brown adipose tissue (BAT) failed to induce thermogenic genes such as Ucp1 and Pgc1α in response to adrenergic stimulation, which is exacerbated by increasing temperature. Thermoneutrality induced a mitochondrial DNA stress in Cpt2A-/- BAT that resulted in a loss of classical interscapular BAT, but did not affect body weight gain or glucose tolerance in response to a high-fat diet. In this dataset, we include the expression data obtained from dissected mouse interscapular brown adipose tissue from mice acclimatized to thermoneutrality (30C) with and without beta3adrenergic stimulation with and without the deletion of carnitine palmitoyltransferase 2 (i.e., adipose unable to beta-oxidize long chain fatty acids in mitochondria).
2016-02-04 | GSE72210 | GEO
Project description:We performed transcriptomic profiling for two models of adipose browning, the classical mouse model and our newly described great roundleaf bat (H. armiger) model. Transcriptomes were generated from subcutaneous adipose tissue (sWAT), intra-abdominal adipose tissue (aWAT) and interscapular BAT (iBAT) from male and female bats, as well as sWAT and iBAT from male and female mice, which were acclimatized to 10°C and 30°C. These 20 trascriptomes allowed us to identity genes, GO terms, and pathways that show significant expression changes and are shared by both species during the browning process.
2018-07-12 | GSE72603 | GEO
Project description:Adrenergic stimulation of brown adipose tissue (BAT) activates thermogenesis, by uncoupling oxidative phosphorylation and enabling high rates of substrate oxidation. Moreover, adrenergic stimulation signals to the nucleus, inducing gene expression changes that increase BAT thermogenic and oxidative capacity. The purpose of this study was to determine the role of two orphan nuclear receptors, ERRα and ERRγ, in adipose tissue function in response to adrenergic stimulation. Here we identify ERRα and ERRγ as collectively critical effectors of the adrenergic induced transcriptional program in BAT. Mice lacking adipose ERRs (ERRαγAd-/-) have diminished oxidative and thermogenic capacity, and become rapidly hypothermic when exposed to cold. Notably, the ability of the β3-adrenergic agonist CL316,243 to expand BAT oxidative and thermogenic capacity, increase energy expenditure, promote weight loss, and improve glucose tolerance is lost in ERRαγAd-/-. At the transcriptional level, RNA sequencing experiments show that the bulk of the response of BAT to CL316,243 (>80% of CL316,243-induced genes) relies on ERRs. These findings establish ERRα and ERRγ as essential BAT regulators that act coordinately to relay adrenergic signals and expand the capacity for thermogenesis and energy expenditure.
2018-03-19 | GSE104285 | 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:Brown adipose tissue (BAT) is a key thermogenic organ, whose activation in response to cold environmental temperatures and β-adrenergic stimulation requires the proper function of the NCOR/HDAC3 corepressor complex in brown adipocytes. The NCOR/HDAC3 complex is large, and multi-component, including the transducin beta-like 1 (TBL1) and TBL1-related 1 (TBLR1) proteins. Loss of TBL1 in the hepatocytes and TBLR1 in the white adipocytes has been shown to impair fasting- and β-adrenergic-induced lipolysis. However, their roles in BAT thermogenesis remain unknown. Here, we report that deletion of TBLR1 alone in brown adipocytes does not impair the adaptive thermogenic response to prolonged cold exposure. In contrast, simultaneous deletion of TBL1 and TBLR1 dampens β-adrenergic-induced lipolysis and mitochondrial respiration in cultured mouse brown adipocytes. Transgenic mice with UCP1-Cre mediated double deletion of TBLR1 and TBL1 exhibit reduced whole-body energy expenditure during prolonged cold exposure, lower core body temperature, increased appearance of unilocular adipocytes in BAT, and suppressed expression of metabolic and myogenic PRDM16 target genes. Also, we found that TBLR1 and TBL1 interact with HDAC3 and PRDM16 in brown adipocytes, suggesting a direct involvement in PRDM16-controlled transcriptional program. These findings identify TBLR1/TBL1 complex as a critical regulator of BAT adaptation to prolonged cold and systemic energy homeostasis, shedding light on the context-dependent functions of corepressor complexes.
2025-08-02 | GSE298802 | GEO
Project description:Thoracic perivascular adipose tissue (PVAT) is a unique adipose depot that likely influences vascular function and susceptibility to pathogenesis in obesity and metabolic syndrome. Surprisingly, PVAT has been reported to share characteristics of both brown and white adipose, but a detailed direct comparison to interscapular brown adipose tissue (BAT) has not been performed. Here we show by full genome DNA microarray analysis that global gene expression profiles of PVAT are virtually identical to BAT, with equally high expression of Ucp-1, Cidea and other genes known to be uniquely or very highly expressed in BAT. PVAT and BAT also displayed nearly identical phenotypes upon immunohistochemical analysis, and electron microscopy confirmed that PVAT contained multilocular lipid droplets and abundant mitochondria. Compared to white adipose tissue (WAT), PVAT and BAT from C57BL/6 mice fed a high fat diet for 13 weeks had markedly lower expression of immune cell-enriched mRNAs, suggesting resistance to obesity-induced inflammation. Indeed, staining of BAT and PVAT for macrophage markers (F4/80, CD68) in obese mice showed virtually no macrophage infiltration, and FACS analysis of BAT confirmed the presence of very few CD11b+/CD11c+ macrophages in BAT (1.0%) in comparison to WAT (31%). In summary, murine PVAT from the thoracic aorta is virtually identical to interscapular BAT, is resistant to diet-induced macrophage infiltration, and thus may play an important role in protecting the vascular bed from thermal and inflammatory stress. 8-week-old male C57BL6/J mice were fed a normal (ND) or high fat diet (HFD) (Research Diets 12451, 45 kcal% fat) for 13 weeks. Mice were then euthanized and four different adipose depots were harvested for RNA analysis: perivascular fat from the lesser curvature of the aortic arch (PVAT), interscapular brown adipose (BAT), inguinal adipose tissue (SAT), and epididymal adipose tissue (VAT). 250 ng total RNA pooled from two mice was used for cDNA synthesis; 3 biological replicates per tissue and diet were performed for a total of 24 hybridizations.
2011-08-22 | E-GEOD-28440 | biostudies-arrayexpress
Project description:Recent studies suggest that brown adipose tissue (BAT) plays a role in energy and glucose metabolism in humans. However, the physiological significance of human BAT in lipid metabolism remains unknown. To gain insight regarding the mechanisms of accelerated lipid metabolism in relation to the cold-activated BAT, we performed molecular (transcriptome) profiling of supraclavicular and subcutaneous abdominal adipose tissue samples collected from one subject during CE (cold exposure) and TN (thermoneutral) conditions.
2016-05-26 | E-MTAB-4031 | biostudies-arrayexpress
Project description:Rodents are commonly housed below thermoneutrality (~20°C) 1. Under these conditions there is a substantial effect on rodent physiology including the hyperactivation of brown (BAT) and beige adipose tissue 2. Here, we raised animals from weaning, on an obesogenic diet at thermoneutrality (28°C) to closer mimic human physiology and determine the impact of a) moderate cold exposure (i.e. 20°C, a temperature reduction of ~8°C) or b) treatment with YM-178, a highly-selective, clinically used β3-adrenoreceptor agonist on classical BAT or subcutaneous inguinal (IWAT) beige depots. Under these conditions, uncoupling protein 1 mRNA was undetectable in IWAT in all groups. Maintenance at 20°C drove weight gain and a 125% increase in subcutaneous fat, an effect not seen with YM-178 administration thus suggesting a direct effect of ambient temperature in promoting weight gain and adiposity in obese rats. Using exploratory adipose tissue proteomics we reveal novel processes and pathways associated with cold-induced weight gain in BAT (i.e. histone deacetylation and glycosphingolipid biosynthesis) and IWAT (i.e. NAD+ binding and retinol metabolism). Conversely, YM-178 had minimal metabolic-related effects on BAT and drove a pro-inflammatory phenotype in IWAT. Exercise training elicits diverse effects on brown (BAT) and white adipose tissue (WAT) physiology in rodents housed below their thermoneutral zone (i.e. 28-32°C). In these conditions, BAT is chronically hyperactive and, unlike human residence, closer to thermoneutrality. Therefore, we set out to determine the effects of exercise training in obese animals at 28°C (i.e. thermoneutrality) on BAT and WAT in its basal (i.e. inactive) state. Sprague-Dawley rats (n=12) were housed at thermoneutrality from 3 weeks of age and fed a high-fat diet. At 12 weeks of age half these animals were randomised to 4-weeks of swim-training (1 hour/day, 5 days per week). Following a metabolic assessment interscapular and perivascular BAT and inguinal (I)WAT were taken for analysis of thermogenic genes and the proteome. Exercise attenuated weight gain but did not affect total fat mass or thermogenic gene expression. Proteomics revealed an impact of exercise training on2-oxoglutarate metabolic process, mitochondrial respiratory chain complex IV, carbon metabolism and oxidative phosphorylation. This was accompanied by an upregulation of multiple proteins involved in skeletal muscle physiology suggesting an adipocyte to myocyte switch in BAT. UCP1 mRNA was undetectable in IWAT with proteomics highlighting changes to DNA binding, the positive regulation of apoptosis, HIF-1 signalling and cytokine-cytokine receptor interaction.
2020-04-09 | PXD017306 | Pride
Project description:We identified Letm1 domain containing 1 (Letmd1) as a candidate regulator of BAT thermogenesis. We generated Letmd1 KO mice, raised at thermoneutral or cold conditions, and performed RNA-sequencing in BAT.
2021-12-14 | GSE162907 | GEO