Project description:Purpose: To investigate the involvement of mTORC1 as a mediator of the actions of the PPARγ ligand rosiglitazone in subcutaneous inguinal white adipose tissue transcriptome; Methods: Mice bearing regulatory associated protein of mTOR (Raptor) deletion and therefore mTORC1 deficiency exclusively in adipocytes (adiponectin Cre recombinase) and littermate controls were fed a high-fat diet supplemented or not with the PPARγ agonist rosiglitazone (30 mg/kg/day) for 8 weeks and evaluated for inguinal white adipose tissue transcriptome (Rnaseq); Results: 3,2425 genes had their correspondent mRNA levels altered by either adipocyte Raptor deficiency or rosiglitazone administration or their combination. Among those, 408 genes modulated by rosiglitazone required mTORC1. Conclusion: PPARγ and mTORC1 are essential partners in the regulation of a cluster of genes in inguinal white adipose tissue.
Project description:Here we provide scRNAseq data from the stromal vascular fraction of adult (8 weeks) and adolescent (2 weeks) murine inguinal subcutaneous white adipose tissue. This allows studying cellular composition and cellular heterogeneity within subcutaneous fat.
Project description:Comparing gene expression profiles of murine subcutaneous vs. visceral adipose tissue. Gene expression was analyzed in two subcutaneous depots (inguinal and axillary) and two visceral depots (epididymal and mesenteric) from male C57Bl/6 mice. 4 samples were analyzed as two groups: inguinal and axillary (subcutaneous) and epididymal and mesenteric (visceral). Each sample was derived by pooling RNA from the relevant fat depot from 3 age-matched, male C57Bl6 mice.
Project description:Lgr4 acts as a key factor to regulate energy expenditure and body weight. Visceral fat (epidydimal white adipose tissue, eWAT) show a significant reduction in Lgr4 mutant mice than littermate controls, especially in high-fat diet (HFD) condition. A white-to-brown fat switch of eWAT in Lgr4 mice was reported by our group. However, the whole-genome expression profile of eWAT has not been comphrehensively studied. We used microarrays to reveal the potential novel factors underlying browning process.
Project description:Mice were kept at RT, thermoneutrality (humanized condition) and thermoneutrality plus high fat diet. Inter scapular brown adipose tissue and inguinal white adipose tissue were used for RNA seq. Illumina Truseq ribosomal RNA depletion protocol was used.
Project description:The brain renin-angiotensin system (RAS) stimulates resting metabolic rate in part through a mechanism involving suppression of the circulating RAS. This effect appears to be mediated through a reduction in angiotensin AT2 receptor (AT2R) signaling within inguinal fat. To examine the molecular mechanisms underlying this effect, mice with hyperactivity of the brain RAS (“sRA” mice, expressing human renin via the synapsin promoter and human angiotensinogen via its own promoter) and littermate controls were chronically infused with vehicle or the AT2R specific agonist, CGP-42112a (CGP, 90 ng/hr, 8 wk, sc). To identify altered signaling pathways, total RNA was isolated from inguinal adipose tissue and transcript abundance was quantitated by RNA-Seq.
Project description:Global RNA sequencing analysis of brown fat (BAT), inguinal white fat (iWAT), liver and muscle (quadriceps) of high-fat diet fed WT, FGF21 KO, UCP1 KO and UCP1/FGF21 double KO mice.
Project description:We report RNA-seq data from the brown fat and vastus muscles of mice lacking IRF4 in brown fat (BATI4KO) vs floxed littermate controls
