ABSTRACT: Genome-wide analysis of brown adipose tissue gene expression of IL15-depleted mice under normal diet or diet enriched with the beta3-adrenergic agonist CL 316243
Project description:Chronic inflammation is one of the major players in the obesity related metabolic syndrome. However the various inflammatory mediators appear to promote insulin resistance directly or indirectly through their ability to induce the inflammatory cascade. Interleukin-15 (IL-15) is a pro-inflammatory cytokine that is involved in the pathogenesis of different autoimmune diseases such as rheumatoid arthritis, inflammatory bowel disease and type 1 diabetes. We postulated that as a pro-inflammatory cytokine, IL-15 promotes obesity during fat excess by promoting insulin resistance from tissues involved in energy metabolism. We used microarrays to characterize the gene expression profile of the brown adipose tissue of IL-15 mice under normal diet or diet enriched with the beta3-adrenergic agonist CL 316243 Total RNA obtained from adipose tissue of wt- or IL15-KO mice under normal diet or diet enriched with the beta3-adrenergic agonist CL 316243
Project description:Chronic inflammation is one of the major players in the obesity related metabolic syndrome. However the various inflammatory mediators appear to promote insulin resistance directly or indirectly through their ability to induce the inflammatory cascade. Interleukin-15 (IL-15) is a pro-inflammatory cytokine that is involved in the pathogenesis of different autoimmune diseases such as rheumatoid arthritis, inflammatory bowel disease and type 1 diabetes. We postulated that as a pro-inflammatory cytokine, IL-15 promotes obesity during fat excess by promoting insulin resistance from tissues involved in energy metabolism. We used microarrays to characterize the gene expression profile of the brown adipose tissue of IL-15 mice under normal diet or diet enriched with the beta3-adrenergic agonist CL 316243
Project description:We used microarrays to detail the gene expression profile during WAT -beige transition by treatment of beta adrenergic receptor agonist . Stromal vascular fractions (SVF) from mice (n = 3/group) that received vehicle or beta3 adrenergic receptor agonist, CL, treatment were served for RNA extraction and hybridization on Affymetrix microarrays. We are trying to find out angiogenic factors genes dynamics during white adipose tissues (WAT) - beige transition.
Project description:We performed RT-PCR panels analysis of microRNAs expression in exosomes from the serum of wt mice, cold exposed mice or beta3 Adrenergic receptor agonist (CL-316.243) treated mice, and in exosomes from culture medium of mature brown adipocytes with or without cAMP treatment. Several microRNAs were identified as indicator correlated to brown adipocytes activity. The selected microRNAs may become potential biomarkers of brown fat activation in vivo
Project description:Experiment designed to identify differences in gene expression profile in white adipose tissue upon stimulation by beta 3 adrenergic receptor agonist. This series compares 2 groups of C57BL/6J acutely treated with CL-316,243 or Saline for 3 hours.
Project description:Experiment designed to identify differences in gene expression profile in white adipose tissue upon stimulation by beta 3 adrenergic receptor agonist. This series compares 2 groups of C57BL/6J acutely treated with CL-316,243 or Saline for 3 hours. Keywords: parallel sample
Project description:A single cell suspension was generated from B3-adrenergic agonist (CL; 1 mg/kg/day) for 4 days and saline mouse SVF, and single-cell mRNAseq libraries were generated with Drop-Seq. A single cell suspension was generated from mouse mature adipocyte nuclei under the following conditions: RT, 24hrs @ 4 °C , 48hrs @ 4 °C, 4days @ 4 °C and B3-adrenergic agonist (CL; 1 mg/kg/day) and single-cell mRNAseq libraries were generated with 10X genomics.
Project description:Insufficient mitochondrial quantity in brown adipose tissue (BAT) causes defective thermogenesis and positive energy balance, which is coupled with the development of obesity. Whether disturbance of mitochondrial quality affects BAT function remains unknown. Here, we describe that the brown adipocyte-specific Leucine-rich PPR motif-containing protein knockout mice (LrpprcBKO) exhibited mitochondrial electron transport chain (ETC) proteome imbalance and a complete loss of the -adrenergic-stimulated thermogenesis at room temperature (RT), due to specific reduction of mtDNA-encoded genes. However, the LrpprcBKO mice were lean at normal chow and were protected against high-fat-diet-induced metabolic abnormalities, such as obesity, insulin resistance, adipose inflammation, hepatic steatosis, and hypertriglyceridemia. The beige adipocytes in inguinal white adipose tissue were expanded in LrpprcBKO mice at RT, but not at thermoneutrality. However, BAT thermogenic defects and metabolic benefits were present in LrpprcBKO mice regardless of ambient temperatures. Collectively, our results reveal that a thermogenesis-incapable BAT with mitochondrial ETC proteome imbalance can improve systemic metabolism, suggesting BAT’s contributions to thermoregulation and systemic metabolism can be uncoupled.
Project description:Genome-scale analysis of the genetic factors that govern the development of white and brown adipose tissue is still far from complete. In order to identify the key genes that regulate the development of white and brown adipose tissue in mice, the transcriptome analysis was performed on adipose tissues Total RNA obtained from interscapular brown adipose tissue of C57BL/6J mice fed normal diet or high fat diet for 2, 4, 8, 20 and 24 weeks
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.
