Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25318399_1.fastq.gz | Fastqsanger.gz | |||
| SRR25318399_2.fastq.gz | Fastqsanger.gz |
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Project description:Gene expression profiling in 6 tissues (white adipose tissue (WAT), brown adipose tissue (BAT), cardiac muscle (CM), liver (LIV), kidney (KID), skeletal muscle (SM)) from ATGL(-/-) mice versus wildtype (ATGL+/+) mice.
2008-02-03 | E-MARS-8 | biostudies-arrayexpress
Project description:Compare miRNA expression profiles in epididymal white adipose tissue (WAT), interscapular brown adipose tissue (BAT) and skeletal muscle from wild-type C57BL/6J mice
2010-12-01 | E-MEXP-2553 | biostudies-arrayexpress
Project description:The activation of brown/beige adipose tissue (BAT) metabolism and the induction of uncoupling protein-1 (UCP1) expression are essential for BAT-based strategies to improve metabolic homeostasis. Adrenergic signaling is viewed as a key regulator of thermogenesis and UCP1-expression in BAT, while also operating as a potent contractile stimulator in muscle. The muscle-like gene expression patterns of UCP1+ adipocytes have previously been utilized as tissue specific markers, but have not been attributed with any functional role. Here, we demonstrate that BAT utilizes actomyosin machinery to generate tensional responses following adrenergic stimulation, similar to muscle tissues. We show that activation of actomyosin mechanics are critical for the acute induction of oxidative metabolism and uncoupled respiration in UCP1+ adipocytes. Additionally, actomyosin-mediated elasticity regulates mechanosensitive transcriptional co-activators, YAP/TAZ, that facilitate the thermogenic capacity of adipocytes. These unappreciated signaling and mechanical mechanisms may inform future strategies to promote the expansion and activation of brown/beige adipocytes.
2018-03-01 | GSE109829 | GEO
Project description:Brown adipose tissue (BAT) plays an essential role in metabolic homeostasis by dissipating energy via thermogenesis through uncoupling protein 1 (Ucp1). Previously, we reported that the TATA-binding protein Associated Factor 7L (Taf7l) is an important regulator of white adipose tissue (WAT) differentiation. Here, we show that Taf7l also serves as a molecular switch between brown fat and muscle lineages in vivo and in vitro. In adipose tissue, Taf7l containing TFIID complexes associate with PPAR to mediate DNA looping between distal enhancers and core promoter elements. Our findings suggest that presence of the tissue-specific Taf7l subunit in TFIID functions to promote long-range chromatin interactions during BAT lineage specification. mRNA-seq expression profiling wild type and Taf7l knockout interscapular brown adipose tissue (BAT)
2014-06-03 | E-GEOD-55797 | biostudies-arrayexpress
Project description:Differential gene expression in a wide range of tissues including brown adipose tissue (BAT), liver, heart, hypothalamus, and skeletal muscle in hibernating arctic ground squirrels during multiple stages in torpor-arousal cycles compared to non-hibernating (post-reproductive) animals with illumina beadarray technology. Arctic Ground Squirrels were sampled at four stages of hibernation: early arousal denoted as EA (1-2 hrs after Tb cross 30¡C, n=4), late arousal denoted as LA (7-8 hrs after Tb cross 30¡C, n=4), early torpor denoted as ET (10-20% of torpid episode, n=4) and late torpor denoted as LT (80-90% of torpid episode, n=5), where Tb is the body temperature and the length of torpid episode is estimated from the previous torpor bout. Post-reproductive animals denoted as PR (n=7) were used as non-hibernating control. Five tissue types: brown adipose tissue (BAT), liver, heart, hypothalamus, and skeletal muscle were hybridized on two customized 700-gene beadarray platforms: 1A and 2A on 96-sample Illumina ArrayMatrix. The data of a pilot study involving brown adipose tissue (BAT), liver, and skeletal muscle on 16-sample Illumina BeadChip denoted as 16chip are also included in this series.
2010-07-01 | E-GEOD-5414 | biostudies-arrayexpress
Project description:Background: The prevalence of type 2 diabetes has increased dramatically in recent decades. Increasing brown adipose tissue (BAT) mass and activity has recently emerged as an interesting approach to not only increase energy expenditure, but also improve glucose homeostasis. BAT can be recruited by prolonged cold exposure in lean, healthy humans. Here, we tested whether cold acclimation could have therapeutic value for patients with type 2 diabetes by improving insulin sensitivity. Methods: Eight type 2 diabetic patients (age 59.3±5.8 years, BMI 29.8±3.2 kg/m2) followed a cold acclimation protocol, consisting of intermittent cold exposure (6 hours/day, 14-14.5 °C) for 12 consecutive days. Before and after cold acclimation, cold-induced BAT activity was assessed by [18F]FDG-PET/CT scanning, insulin sensitivity at thermoneutrality by a hyperinsulinemic-euglycemic clamp, and muscle and WAT biopsies were taken. Results: Cold-induced BAT activity was low, but increased in all patients upon cold acclimation (SUV from 0.40±0.29 to 0.63±0.78, p<0.05). Interestingly, insulin sensitivity showed a very pronounced 40% increase upon cold acclimation (glucose rate of disappearance from 14.9±4.1 to 20.5±6.9 μmol kg-1 min-1, p<0.05). A 40% increase in insulin sensitivity cannot be explained by BAT glucose uptake, in fact basal skeletal muscle GLUT4 content and translocation was markedly increased after cold acclimation, without effects on insulin signaling or AMPk activation. Conclusions: Regular mild cold exposure has marked effects on insulin sensitivity, which are accompanied by small increases in BAT activity and more pronounced effects on skeletal muscle. These data suggest a novel therapeutic option for the treatment of type 2 diabetes. Microarray analysis was performed on abdominal subcutaneous white adipose tissue samples from human type 2 diabetic patients before, and after 10 days of cold acclimation. A total of 14 samples, from 7 subjects, were used for the microarray analysis.
2015-07-05 | E-GEOD-67297 | biostudies-arrayexpress
Project description:Myostatin (MSTN) has been discovered as a critical regulator of muscle mass. Recently, there has been an increasing interest in its functions in metabolism. Here, we specific knocked out MSTN in brown adipose tissue (BAT) (MSTNΔUCP1), and found that the MSTNΔUCP1 mice gained more weight than controls on high-fat diet, with progressive hepatosteatosis, and impaired skeletal muscle activity. RNA-seq analysis indicated signatures of mitochondrial dysfunction and inflammation in MSTN-ablation BAT. Further studies demonstrated that KLF4 is required for the metabolic phenotypes and FGF21 contributes to the microenvironment communication between adipocytes and macrophages induced by loss of MSTN in BAT. Moreover, MSTN-SMAD2/3-p38 signaling pathway mediated the expression of KLF4 and FGF21 in adipocytes. Taken together, brown adipocytes-derived MSTN governs metabolic niche in BAT and regulates systemic energy homeostasis.
2024-07-23 | GSE249029 | GEO
Project description:Myostatin (MSTN) has been discovered as a critical regulator of muscle mass. Recently, there has been an increasing interest in its functions in metabolism. Here, we specific knocked out MSTN in brown adipose tissue (BAT) (MSTNΔUCP1), and found that the MSTNΔUCP1 mice gained more weight than controls on high-fat diet, with progressive hepatosteatosis, and impaired skeletal muscle activity. RNA-seq analysis indicated signatures of mitochondrial dysfunction and inflammation in MSTN-ablation BAT. Further studies demonstrated that KLF4 is required for the metabolic phenotypes and FGF21 contributes to the microenvironment communication between adipocytes and macrophages induced by loss of MSTN in BAT. Moreover, MSTN-SMAD2/3-p38 signaling pathway mediated the expression of KLF4 and FGF21 in adipocytes. Taken together, brown adipocytes-derived MSTN governs metabolic niche in BAT and regulates systemic energy homeostasis.
2024-07-23 | GSE249028 | GEO
Project description:Glucocorticoids (GCs) are widely applied anti-inflammatory drugs that are associated with adverse metabolic effects including insulin resistance and weight gain. Previous research indicated that GCs may negatively impact brown adipose tissue (BAT) in rodents and humans. Here, we demonstrate that treatment of human volunteers with high doses of GCs increases resting energy expenditure (REE) but does not reduce BAT activity. In line with the physiological results, gene expression in human BAT was not significantly altered by GCs in vivo. However, the RNA-sequencing of skeletal muscle revealed that GCs increase the expression of enzymes involved in calcium cycling as well as the respiratory chain. Collectively, these data suggest that the raise of EE after GCs exposure is mediated by skeletal muscle rather than a change in BAT activity.
2023-09-04 | GSE220158 | GEO
Project description:Mitochondria are the provider of cellular energy from aerobic respiration in all tissues. However, only brown adipose tissue (BAT) mitochondria are able to convert chemical energy in the form triglycerides into heat (thermogenesis). To ask if cellular respiration or thermogenic function require a specific lipidomic environment, we investigated the lipid species composition of brown adipose tissue mitochondria, and compared it those purified from liver, skeletal muscle and white adipose tissue. We emplyed mass spectrometry-based proteomics to evalaute the purity of the mitochondia fractions isolated from murine BAT and liver tissue by differential centrifugation, by comparison of its full proteome with endoplasmatic reticulum, mitochondrial-associated membrane, and mitochondria fractions isolated by density gradient centrifugation.
2024-05-24 | PXD028128 | Pride