Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE91081
PROVIDER: PRJNA356837 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5091940_1.fastq.gz | Fastqsanger.gz | |||
| SRR5091940_2.fastq.gz | Fastqsanger.gz | |||
| SRR5091941_1.fastq.gz | Fastqsanger.gz | |||
| SRR5091941_2.fastq.gz | Fastqsanger.gz | |||
| SRR5091942_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
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2024-03-21 | E-MTAB-12834 | biostudies-arrayexpress
Project description:Brown adipose tissue (BAT) has in recent times been rediscovered in adult humans, and together with work from preclinical models, shown to have the potential of providing a variety of positive metabolic benefits. These include improved insulin sensitivity and reduced susceptibility to obesity and its various co-morbidities. As such, its continued study could offer insights to therapeutically modulate this tissue to improve metabolic health. It has been reported that adipose-specific deletion of the gene for protein kinase D1 (Prkd1) enhances mitochondrial respiration and improves whole-body glucose homeostasis. We sought to determine whether these effects were mediated specifically through brown adipocytes using a Prkd1 brown adipose tissue (BAT) Ucp1-Cre-specific knockout mouse model, Prkd1BKO. We unexpectedly observed that upon both cold exposure and beta-3-AR agonist administration, Prkd1 loss in BAT did not alter canonical thermogenic gene expression or adipocyte morphology. We took an unbiased approach to assess whether other signaling pathways were altered. RNAs from cold-exposed control and Prkd1BKO were subjected to RNA-Seq analysis. These studies revealed that myogenic gene expression is altered in Prkd1BKO BAT after both acute (8 hr) and extended (4 day) cold exposure. Given that brown adipocytes and skeletal myocytes share a common precursor cell lineage expressing myogenic factor 5 (Myf5), these data suggest that loss of Prkd1 in BAT may alter the biology of preadipocytes in this depot. The data presented herein clarify the role of Prkd1 in BAT thermogenesis and present new avenues for the further study of Prkd1 function in BAT.
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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.
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Project description:miRNA expression during differentiation of white and brown adipocytes
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Project description:PKGI KO vs. WT brown adipocytes and brown adipose tissues
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Project description:We used microarrays to detail the gene expression profile during WAT -beige transition by treatment of beta adrenergic receptor agonist .
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