Project description:ob/ob mice is an obese mice. CIDE family proteins including Cidea, Cideb and Cidec play important role in lipid metabolism. Cidea is mainly expressed in the brown adipose tissue (BAT). Cidec is mainly expressed in the BAT and white adipose tissue (WAT). We generated ob/ob/Cidea-/-/Cidec-/- mice to investigate the phenotype of fat tissue. ob/ob/Cidea-/-/Cidec-/- mice are lean when compared with ob/ob mice. The tissue weight and TAG content of BAT and WAT was extreamly decreased in ob/ob/Cidea-/-/Cidec-/- mice compared with that in ob/ob mice. We next extract the total RNA from the BAT and WAT of ob/ob and ob/ob/Cidea-/-/Cidec-/- mice, to perform microarray analysis using Mouse Gene 1.0 ST array system, Affymetrix. We then analysised the up-regulated and down regulated pathways.
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 used microarrays to detail the gene expression profile during WAT -beige transition by treatment of beta adrenergic receptor agonist .
Project description:Background: Brown and white adipose tissues (BAT and WAT) play critical roles in controlling energy homeostasis and in the development of obesity and diabetes. Fsp27 is expressed in both BAT and WAT and promotes lipid storage and the development of obesity and diabetes. In addition, Fsp27-deficient white adipocytes acquired certain BAT-like properties including reduced lipid droplet size and increased mitochondrial activity. Using microarray and semi-quantitative real-time PCR analyses, we systematically analyzed the gene expression profile in Fsp27-deficient WAT and BAT. Results: We observed that BAT-selective genes were significantly up-regulated, whereas WAT-selective genes were down-regulated in the WAT of Fsp27-/- mice. Expression levels of BAT-selective genes were also dramatically up-regulated in the WAT of leptin and Fsp27 double deficient mice. Furthermore, we observed that expression levels of genes in multiple metabolic pathways including oxidative phosphorylation, the TCA cycle and fatty acid synthesis and oxidation were increased in the Fsp27-/- WAT. In contrast, expression levels for extracellular matrix remodeling, the classic complement pathway and TGF-β signaling"were down-regulated in the WAT of Fsp27-/- mice. Most importantly, regulatory factors that determine BAT identity such as CEBPα/β, PRDM16 and major components in the cAMP pathway were markedly up-regulated in the WAT of Fsp27-/- mice. Interestingly, we observed distinct gene expression profiles in the BAT of Fsp27-/- mice. Conclusion: Our data suggest that Fsp27 acts at upstream to control gene expression of diverse pathways, in particular the expression of regulatory factors that determine the identity of BAT and WAT. Therefore, Fsp27 is an important molecular determinant for the identity of WAT, and loss of Fsp27 leads to the conversion of WAT to a BAT-like tissue. Total RNAs were extracted from individual gonadal WAT of five pairs of 3-month-old wild-type and Fsp27-null male mice. Equal amounts of RNA from five pairs of mice with each genotype were pooled to form RNA pools (total 45 μg). Duplicate experiments were carried out.
Project description:To study the gene expression profiles of brown (BAT) and white (WAT) adipose tissues in wild type and LR11-deficeint mice. The four RNA sources, WT scWAT, Lr11 -/- scWAT, WT BAT and Lr11 -/- BAT, were prepared from subcutaneous WAT and BAT from wild-type mice and Lr11 -/- mice, respectively (n=3 each).
Project description:Background: Brown and white adipose tissues (BAT and WAT) play critical roles in controlling energy homeostasis and in the development of obesity and diabetes. Fsp27 is expressed in both BAT and WAT and promotes lipid storage and the development of obesity and diabetes. In addition, Fsp27-deficient white adipocytes acquired certain BAT-like properties including reduced lipid droplet size and increased mitochondrial activity. Using microarray and semi-quantitative real-time PCR analyses, we systematically analyzed the gene expression profile in Fsp27-deficient WAT and BAT. Results: We observed that BAT-selective genes were significantly up-regulated, whereas WAT-selective genes were down-regulated in the WAT of Fsp27-/- mice. Expression levels of BAT-selective genes were also dramatically up-regulated in the WAT of leptin and Fsp27 double deficient mice. Furthermore, we observed that expression levels of genes in multiple metabolic pathways including oxidative phosphorylation, the TCA cycle and fatty acid synthesis and oxidation were increased in the Fsp27-/- WAT. In contrast, expression levels for extracellular matrix remodeling, the classic complement pathway and TGF-β signaling"were down-regulated in the WAT of Fsp27-/- mice. Most importantly, regulatory factors that determine BAT identity such as CEBPα/β, PRDM16 and major components in the cAMP pathway were markedly up-regulated in the WAT of Fsp27-/- mice. Interestingly, we observed distinct gene expression profiles in the BAT of Fsp27-/- mice. Conclusion: Our data suggest that Fsp27 acts at upstream to control gene expression of diverse pathways, in particular the expression of regulatory factors that determine the identity of BAT and WAT. Therefore, Fsp27 is an important molecular determinant for the identity of WAT, and loss of Fsp27 leads to the conversion of WAT to a BAT-like tissue.
Project description:Med13 cardiac over-expression regulates obesity. Liver, WAT and BAT from alphaMHC-Med13 TG mice was analyzed Liver, WAT and BAT from Med13 alphaMHC transgenic mice and wild type littermates
Project description:To identify the target genes of integrated stress reponse (ISR) in WAT and BAT, we have employed whole genome microarray expression in WAT and BAT specific Fv2E-PERK transgenic mice. The mAP::Fv2E-PERK transgenic mice were injected by AP20187 or mock.