Ontology highlight
ABSTRACT:
PROVIDER: PRJNA851270 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19761300.fastq.gz | Fastqsanger.gz | |||
| SRR19761301.fastq.gz | Fastqsanger.gz | |||
| SRR19761302.fastq.gz | Fastqsanger.gz | |||
| SRR19761303.fastq.gz | Fastqsanger.gz | |||
| SRR19761295.fastq.gz | Fastqsanger.gz |
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Project description:Excess weight is associated with an increased risk of insulin resistance and type 2 diabetes. Activating thermogenic mechanisms is a potentially powerful means to reduce excess weight and achieve metabolic benefits. Recent studies show that cold stimuli trigger the conversion of white fat into beige fat, which can mediate non-shivering thermogenesis. The purpose of this study is to determine effect of chronic cold exposure on gene expression in iWAT. To this end, we performed RNA-sequencing of iWAT from mice at 30 ˚C or 7 ˚C for 3 weeks and identified significantly regulated genes under chronic cold in iWAT.
2021-12-14 | GSE133619 | GEO
Project description:Adipocytes deficient in fatty acid synthase (iAdFASNKO) emit signals that mimic cold exposure to enhance the appearance of thermogenic beige adipocytes in mouse inguinal white adipose tissues (iWAT). Both cold- and iAdFASNKO-induced iWAT “browning” pathways upregulate the sympathetic nerve fiber (SNF) modulator Nrg4 and activate SNFs adjacent to beige adipocytes. Adipocyte cAMP/protein kinase A signaling is necessary for beige adipocyte appearance, as we show here it is blocked in Gsa deficient cold exposed or iAdFASNKO mice. Surprisingly however, denervation of iWAT failed to block adipocyte browning in iAdFASNKO mice, as it does in cold-exposed mice. Similarly, Nrg4 deficiency markedly reduced iWAT UCP1 in the cold, but not in double FASN/Nrg4 KO mice. Single-cell transcriptomic analysis of iWAT stromal cells revealed increased macrophages displaying gene expression signatures of the alternately activated type in iAdFASNKO mice, and their depletion abrogated iWAT beiging. Altogether, these findings reveal divergent cellular pathways are sufficient to cause adipocyte browning. Importantly, adipocyte signaling to enhance alternatively activated macrophages in iAdFASNKO mice is associated with enhanced adipose thermogenesis independent of the sympathetic neuron involvement this process requires in the cold.
2020-08-18 | GSE154047 | GEO
Project description:We applied a deep-sequencing based method – digital gene expression profiling (DGEP), to investigate gene expression in interscapular brown adipose tissue (iBAT), inguinal white adipose tissue (iWAT) and epididymal white adipose tissue (eWAT) in acute cold exposure Examination of gene expression level in 3 different adipose tissues in 3 time points, day0, day2 and day4 in cold exposure.
2014-12-19 | E-GEOD-63031 | biostudies-arrayexpress
Project description:We found the mPRAT adipose undergoes a whitning process which differs from iBAT and iWAT. The whitened adipocytes can still respond to cold exposure, which has cellular and molecular differences compared with iBAT and iWAT.
2024-02-22 | GSE241800 | GEO
Project description:We applied a deep-sequencing based method – digital gene expression profiling (DGEP), to investigate gene expression in interscapular brown adipose tissue (iBAT), inguinal white adipose tissue (iWAT) and epididymal white adipose tissue (eWAT) in acute cold exposure
2014-12-19 | GSE63031 | GEO
Project description:There is a regional preference around lymph nodes (LNs) for adipose beiging upon cold exposure. However, the importance of this unique anatomical location remains poorly understood. In this study, the potential role of Lymph nodes in iWAT was investigated. to elucidate functional outcomes, we performed RNA-sequencing analysis using littermate sham and lymph nodes removal (LNR) mice upon cold exposure
2023-10-23 | GSE245718 | GEO
Project description:Adipose tissue beiging refers to a process through which beige adipocytes emerge in classical white adipose tissue depots. Beige adipocytes dissipate chemical energy and secrete adipokines like classical brown adipocytes to improve systemic metabolism, which offers benefits for people with obesity and metabolic diseases. Cold exposure and β3-adrenergic receptor (AR) agonist treatment are two commonly used stimuli for increasing beige adipocytes in mice, but their underlying biological processes are different. Transcriptional analysis of inguinal white adipose tissue (iWAT) has revealed that changes in extracellular matrix (ECM) pathway genes are specific to cold exposure. Hyaluronic acid (HA), a non-sulfated linear polysaccharide produced by nearly all cells, is one of the most common components of ECM. We found that cold exposure significantly increases iWAT HA levels while β3-AR agonist CL316,243 fails to do so. Increasing HA level in iWAT by Has2 overexpression significantly increases cold-induced adipose tissue beiging; in contrast, decreasing HA by Spam1 overexpression, which encodes a hyaluronidase that digests HA, significantly decreases cold-induced iWAT beiging. All of these data implicate a role of HA in promoting adipose tissue beiging that is unique to cold exposure. Given the failure of β3-AR agonists in clinical trials for obesity and metabolic diseases, increasing HA could serve as a new approach to recruiting more beige adipocytes to combat metabolic diseases.
2024-08-01 | GSE268781 | GEO
Project description:Beige adipocyes are compromised with aging even upon cold exposure. Besides, estrogen levels, which have metabolic benefit ,are also decreased with aging. However, the relationship between beige adipocyte and estrogen in aging remains poorly understood. In this study, the potential role of estrogen in iWAT of old aged mice was investigated. To elucidate functional outcomes, we performed RNA-sequencing analysis using vehicle treated group and estrogen treated group upon cold exposure
2024-03-18 | GSE261481 | GEO
Project description:Our study represents the detailed analysis of whole-genome DNA-binding sites of linker histone variant H1.2 in iWAT of male C57BL/6 mice under normal conditions or upon cold exposures, with biologic replicates, generated by ChIP-seq technology
2023-06-15 | GSE232530 | GEO
Project description:Obesity causes insulin resistance, and PPARγ ligands like rosiglitazone (rosi) are insulin-sensitizing, yet mechanisms remain unclear. High fat diet (HFD) induced obesity has major effects on visceral epididymal adipose tissue (eWAT) of C57BL/6 (B6) mice, and here we report altered activity of gene regulatory elements with changes in PPARγ genome-wide occupancy. Treatment with rosi restored insulin sensitivity, yet surprisingly had little effect on eWAT, leading us to consider the subcutaneous inguinal fat (iWAT). In this depot, rosi markedly induced molecular signatures of brown fat including the key thermogenic gene Ucp1. Obesity-resistant 129S1/SvImJ (129) mice showed this degree of iWAT browning even in the absence of rosi. Remarkably, the 129 Ucp1 locus had increased PPARγ binding and gene expression that was preserved in B6x129 F1 intercross iWAT, with imbalance favoring the 129-derived alleles showing a cis-acting genetic difference. Thus, B6 mice have a genetic defect in Ucp1 expression. However, imbalanced expression favoring 129 over B6 was nearly lost when Ucp1 was activated by rosi, or by iWAT browning in cold-exposed or young mice. These results provide a novel framework for understanding how environmental influences like drugs can rescue genetically determined disease phenotypes by affecting the epigenome.
2017-02-27 | GSE92606 | GEO