Project description:Mesenchymal stem/stromal cells (MSCs) were harvested from subcutaneous adipose tissue of patients with obesity or healthy controls and expanded for 3-4 passages, and 5hmC profiles were examined through hydroxymethylated DNA immunoprecipitation sequencing (hMeDIP-seq). We hypothesized that obesity and cardiovascular risk factors induce functionally-relevant, locus-specific changes in overall exonic coverage of 5hmC in human adipose-derived MSCs.
Project description:Genome wide DNA methylation in blood, subcutaneous and omental visceral adipose tissue from two-step surgical approach (N=9) was analysed in patients with severe obesity using Illumina 850K EPIC technology before and after metabolic surgery (Leipzig Obesity BioBank (LOBB) cohort). Additionally, a validation blood cohort of patients with obesity undergoing metabolic surgery was analyzed for results validation.
Project description:Our study seeked to identify changes in DNA methylation and gene expression that might underlie type 2 diabetes susceptibility. We investigated DNA methylation and gene expression in VAT biopsies from 19 women with obesity, without (n=9) or with T2D (n=10). We analyzed and compared the methylome and transcriptome of visceral adipose tissue biopsies of women with obesity, with and without type 2 diabetes. Differential methylation and expression where then paired to test for Pearson's correlation to measure their relationship.
Project description:Here, we evaluated the molecular effects of dietary DINCH exposure, on the proteome, phosphoproteome and acetylome profiles of visceral and subcutaneous adipose tissue in a model of diet-induced obesity in male and female C57BL/6N mice. This study includes data on visceral and subcutaneous adipose tissue of male and female mice that were either fed a standard high-fat diet (HFD) or two HFD diets including doses of DINCH (4,500 ppm and 15,000 ppm).
Project description:Macrophages are primary immune cells involved in obesity-triggered chronic low-grade inflammation in adipose tissues. Prostaglandin (PG) E2, mainly generated from macrophages, can regulate adipose tissue remodeling. Here, we observed that PGE2 receptor subtype 3 (EP3) was remarkably downregulated in adipose tissue macrophages from high-fat diet (HFD)-fed mice and patients with obesity. Notably, macrophage-specific deletion of EP3 exacerbated HFD-induced obesity in mice, whereas EP3α isoform overexpression in macrophages alleviated obesity phenotype in HFD-fed mice. EP3 deficiency suppressed anti-adipogenic secreted protein acidic and rich in cysteine (SPARC) secretion in macrophages. SPARC deletion in macrophages abrogated the protection of EP3α-overexpression against HFD-induced obesity in mice. Mechanistically, EP3 activation promoted SPARC expression by suppressing DNA methylation in macrophages through the PKA/Sp1/Dnmt1/3a signaling cascade. EP3 agonist treatment ameliorates HFD-induced obesity in mice. Thus, EP3 inhibits adipogenesis through promoting macrophage releasing SPARC and may serve as a therapeutic target for managing diet-induced obesity.
Project description:Visceral adipose tissue samples were obtained from severely obese individuals that underwent bariatric surgery. The goal of this study was to identify tissue specific methylation QTLs. Whole-transcriptome subcutaneous adipose tissue methylation levels were determined in 71 individuals with a BMI >35 kg/m2. Bisulphite converted DNA from the 71 visceral adipose tissue samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip.
