ABSTRACT: We conducted expression profiling of white adipose tissue isolated from WT and miR-22 KO animals. The main work is analysis of the miR-22 function in striated muscle. White adipose tissue (WAT) was analyzed to look at effects in WAT, as that might be induced by metabolic changes in skeletal muscle.
Project description:To explore the role of miR-22 targeting in different tissues in adult mice, we generated a miR-22 null mouse model and profiled expression in muscle, heart, liver, kidney and white adipose tissue.
Project description:Microarray analysis of white adipose tissue (WAT) and bone marrow adipose tissue (BMAT) from 22-week-old or 13-week-old male New Zealand White rabbits. From both cohorts, BMAT was sampled from the distal tibia (dBMAT) and the radius and ulna (ruBMAT), while WAT was sampled from the inguinal (iWAT) and gonadal (gWAT) depots. From the 13-week-old cohort, BMAT was also sampled from the proximal tibia (pBMAT). Sufficient RNA could not be isolated from all tissues for all rabbits, so for some rabbits only a subset of tissues is included.
Project description:Compare miRNA expression profiles in epididymal white adipose tissue (WAT), interscapular brown adipose tissue (BAT) and skeletal muscle from wild-type C57BL/6J mice
Project description:The effect of a short-term calorie restricted diet was evaluated in epididymal white adipose tissue (WAT) in seven strains of mice The dietary intervention was initiated at 8 weeks of age and continued until 22 weeks of age
Project description:To investigate the effect of miR-503 in aging associated type 2 diabetes, target genes of miR-503 need to be investigated. The global miR-322-503-351 deletion (KO) mouse was constructed, and RNA-seq was then performed on aged mouse liver and white adipose tissue (WAT).
Project description:The gut microbiota is a key environmental determinant of mammalian metabolism. Regulation of white adipose tissue (WAT) by the gut microbiota is a critical process that maintains metabolic fitness, while dysbiosis contributes to the development of obesity and insulin resistance (IR). However, how the gut microbiota controls WAT functions remain largely unknown. Herein, we show that tryptophan-derived metabolites produced by the microbiota control the expression of the miR-181 family in white adipocytes to regulate energy expenditure and insulin sensitivity. Moreover, we show that dysregulation of the microbiota-miR-181 axis is required for the development of obesity, IR, and WAT inflammation. Thus, our results indicate that regulation of miRNA levels in WAT by microbiota-derived cues is a central mechanism by which host metabolism is tuned in response to dietary and environmental changes. As MIR-181 is dysregulated in WAT from obese human individuals, the MIR-181 family may represent a potential therapeutic target to modulate WAT function in the context of obesity.
Project description:Transcriptome analysis of epididymal white adipose tissue (WAT) depots in Ercc1 animals: To further elucidate the role of ERCC1 in WAT we scanned the transcriptome of 15 day old wt and Ercc1 epididymal WAT.
Project description:To identify candidates of interest that were more highly expressed in BAT than WAT, we conducted RNAseq in human primary brown and white adipocytes. Adipose tissue was obtained from the central compartment of the neck, superior to the clavicle and deep to the lateral thyroid lobe either adjacent to the longus colli muscle or to the oesophagus (brown adipose tissue) and more superficially from the subcutaneous neck tissue (white adipose tissue). The stromal vascular fraction was isolated and cultured as described (Ramage, Akyol et al. 2016 doi: 10.1016/j.cmet.2016.06.011). Following differentiation, cells were cultured in serum-stripped medium for 48 hours prior to RNA extraction and subsequent bulk RNA-seq.
Project description:The popularity of high fat foods in modern society has been associated with epidemic of various metabolic diseases characterized by insulin resistance, the pathology of which involves complex interactions between multiple tissues such as liver, skeletal muscle and white adipose tissue (WAT). To uncover the mechanism by which excessive fat impairs insulin sensitivity, we conducted a multi- tissue study by using TMT-based quantitative proteomics. 3-week-old ICR mice were fed with high fat diet (HFD) for 19 weeks to induce insulin resistance. Liver, skeletal muscle and epididymal fat were collected for proteomics screening. Additionally, PRM was used for validating adipose differential proteins. By comparing tissue-specific protein profiles of HFD mice, multi-tissue regulation of glucose and lipid homeostasis and corresponding underlying mechanisms was systematically investigated and characterized.