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.
Project description:One-pot enrichment and label-free quantification of protein acetylation and protein succinylation in mouse brown adipose tissue (BAT) in response to cold-acclimation and/or BAT-specific Sirt5 KO.
Project description:Histones were isolated from brown adipose tissue and liver from mice housed at 28, 22, or 8 C. Quantitative top- or middle-down approaches were used to quantitate histone H4 and H3.2 proteoforms. See published article for complimentary RNA-seq and RRBS datasets.
Project description:We report the application of sequencing technology for high-throughput profiling of PPARα/γ in mammalian cells. By obtaining over 3 billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of mouse brown adipose tissue. We find that PPARα binds to a subset of PPARγ sites, suggesting a potential redundancy in which PPARα function may not be necessary in brown adipose tissue.While PPARα may not itself be necessary for BAT function, shared targets regulation by PPARα and PPARγ may nonetheless reveal relevant biology in this tissue.This study provides a framework for the application of comprehensive chromatin profiling towards characterization of PPARα/γ regulation in mouse brown adipose tissue.
Project description:Two types of adipose tissues, white and brown, are found in mammals. Increasingly novel strategies are being proposed for the treatment of obesity and its associated complications by altering amount and/or activity of BAT using mouse models. We used microarrays to detail the global programme of gene expression in subcutaneous white adipose tissue and brown adipose tissue. White adipose tissue (Subcutaneous region) and brown adipose tissue (intrascapular) were isolated from LACA mice (male, 25 ± 3g ) for RNA extraction and hybridization on Affymetrix microarrays.
Project description:Brown adipose tissue (BAT) is a thermogenic organ that protects animals against hypothermia and obesity. BAT derives from the multipotent paraxial mesoderm; however, the identity of embryonic brown fat progenitor cells and regulators of adipogenic commitment are unclear. Here, we performed single cell gene expression analyses of mesenchymal cells during mouse embryogenesis with a focus on BAT development.
Project description:Brown adipose tissue (BAT) is a thermogenic organ that protects animals against hypothermia and obesity. BAT derives from the multipotent paraxial mesoderm; however, the identity of embryonic brown fat progenitor cells and regulators of adipogenic commitment are unclear. Here, we performed single cell gene expression analyses of mesenchymal cells during mouse embryogenesis with a focus on BAT development.
Project description:Using high throughput sequencing we report chromatin accessibility(ATAC-seq) and transcriptome profiling (RNA-seq)and in mouse brown adipose tissue (BAT) upon cold exposure in wildtype and Dot1L-BAT specific KO mice.
Project description:Two types of adipose tissues, white and brown, are found in mammals. Increasingly novel strategies are being proposed for the treatment of obesity and its associated complications by altering amount and/or activity of BAT using mouse models. We used microarrays to detail the global programme of gene expression in subcutaneous white adipose tissue and brown adipose tissue.
Project description:We performed a genome-wide deep sequencing analysis of the microRNAs abundant in mesenchymal stem cells (MSCs) derived from murine brown adipose tissue and in in vitro differentiated mature brown adipocytes. Several microRNAs were identified as differentially regulated when comparing datasets from MSCs vs. mature fat cells. These microRNAs may have an implication in the regulation of adipogenesis as well as thermogenesis in brown adipose tissue (BAT). Examination of BAT-derived MSCs (BAT-MSC; 1 sample) and in vitro differentiated mature brown fat cells (BAT-DIFF; 1 sample) vertis biotechnologie AG, D-85354 Freising, Germany (library construction and sequencing)