Gene expression profile in visceral-pancreatic adipose tissue from control rats fed a standard chow diet and obese rats fed a high-caloric cafeteria diet for 30 days.
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ABSTRACT: Changes in the secretion profile of visceral-pancreatic white adipose tissue due to diet-induced obesity are partially responsible for increased beta cell replication, suggesting that a crosstalk between pWAT and beta cells may play a role in regulating beta cell plasticity. The molecular mechanisms underlying this cross-talk are still not fully understood. The aim of this study was to integrate transcriptomic, proteomic and metabolomic data to unravel the cross-talk between adipose tissue and pancreatic islets during evolution of obesity. Adipose tissue from control lean and obese rats were obtained. RNA was extracted and processed for further hybridization on Affymetrix microarrays (GeneChip Rat Genome 230 2.0 (Affymetrix, Santa Clara, CA)).
Project description:Changes in the secretion profile of visceral-pancreatic white adipose tissue (pWAT) due to diet-induced obesity are partially responsible for increased beta cell replication, suggesting that a crosstalk between pWAT and beta cells may play a role in regulating beta cell plasticity. The molecular mechanisms underlying this cross-talk are still not fully understood. The aim of this study was to integrate transcriptomic, proteomic and metabolomic data to unravel the cross-talk between adipose tissue and pancreatic islets during evolution of obesity. Pancreatic islets from control lean and cafeteria diet fed obese rats were obtained. RNA was extracted and processed for further hybridization on Affymetrix microarrays (GeneChip Rat Genome 230 2.0 (Affymetrix, Santa Clara, CA)).
Project description:Changes in the secretion profile of visceral-pancreatic white adipose tissue (pWAT) due to diet-induced obesity are partially responsible for increased beta cell replication, suggesting that a crosstalk between pWAT and beta cells may play a role in regulating beta cell plasticity. The molecular mechanisms underlying this cross-talk are still not fully understood. The aim of this study was to integrate transcriptomic, proteomic and metabolomic data to unravel the cross-talk between adipose tissue and pancreatic islets during evolution of obesity.
Project description:Changes in the secretion profile of visceral-pancreatic white adipose tissue due to diet-induced obesity are partially responsible for increased beta cell replication, suggesting that a crosstalk between pWAT and beta cells may play a role in regulating beta cell plasticity. The molecular mechanisms underlying this cross-talk are still not fully understood. The aim of this study was to integrate transcriptomic, proteomic and metabolomic data to unravel the cross-talk between adipose tissue and pancreatic islets during evolution of obesity.
Project description:To identify novel Peroxisome Proliferator-Activated Receptor gamma (PPARg) responsive secretory and/or transmembrane genes that is related to obesity, we integrated the expression data from the adipose tissue derived from obese mice with the other two data sets: expression profiling of adipocyte differentiation using ST2 cells and siRNA-mediated knockdown of Pparg during ST2 cell adipogenesis. We used microarrays to detect the up-regulated genes in adipose tissue derived from mice fed a high fat diet compared to a control. Total RNA from adipose tissue was obtained and from mice fed a high fat diet HFD32 (MOUSE_HFD) from 6 week-old to 18 week-old, or a normal diet CE-2 (MOUSE_ND) as a control. Pooled RNAs of each three animals were analyzed by the Affymetrix GeneChip microarray system.
Project description:This SuperSeries is composed of the following subset Series: GSE25401: Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity [gene expression] GSE25470: Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity [miRNA data] GSE25910: Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity [differentiation data] Refer to individual Series
Project description:Obesity is characterised by increased adipocyte size and number. Analysis of altered gene expression gives better understading about the mechanisms involved/alterted in the development of obesity in this new obese rat model. We used Microarrays to delinate the alted gene expression in adipose tissue of WNIN/Ob obese rats Retroperitioneal adipose tissue was collected from 4 month old WNIN/Ob lean and obese rats (n=2 per phenotype) for RNA extraction and hybridization on Affymatrix Rat gene 1ST arrays.
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:Adipose tissues play an important role in the pathophysiology of obesity-related disease including type 2 diabetes. To describe gene expression patterns and functional pathways in obesity-related type 2 diabetes, we performed global transcript profiling of omental adipose tissue in morbidly obese individuals with or without diabetes. Fourteen (14) morbidly obese diabetics (cases) and 6 morbidly obese non-diabetics (reference) were included in this study.
Project description:Obesity is a known risk factor for breast cancer. To identify genes and underlying pathways in human triple-negative breast cancer cells affected by interaction with adipose tissue, MDA-MB-231 breast cancer cells were cultivated in a co-culture system with or without adipose tissue explants from mice for the purpose of a microarray gene expression analysis. Co-culture of MDA-MB-231 breast cancer cells was performed with adipose tissue explants obtained from C57BL/6J mice that were fed a high-fat diet (HFD, 58%Kcal from fat) or normal chow diet (NC; 11%Kcal from fat) ad libitum for 16 weeks. For co-cultivation analyses of breast cancer cells and adipose tissue explants, we set up a two-dimensional transwell system, which enables intercellular communication through soluble factors secreted into the medium but inhibits intermixture of the different cell types. Following 72 hours of co-culture with or without adipose tissue, total RNA was isolated from the breast cancer cells and subjected to microarray gene expression analyses.
Project description:Inflammasome activation in adipose tissue has been implicated in obesity-associated insulin resistance and type 2 diabetes. However, when and how inflammasome is activated in adipose tissue remains speculative. Here we test the hypothesis that extracellular ATP, a potent stimulus of inflammasome in macrophages via purinergic receptor P2X, ligand-gated ion channel, 7 (P2X7), may play a role in inflammasome activation in adipose tissue in obesity. Our data show that inflammasome is activated in adipose tissue upon 8-week feeding of 60% HFD, coinciding with the onset of hyperglycemia and hyperinsulinemia as well as the induction of P2X7 in adipose tissue. Unexpectedly, P2X7-deficient animals on HFD exhibit no changes in metabolic phenotypes, nor in inflammatory responses or inflammasome activation when compared to the wildtype controls. Similar observations have been obtained in hematopoietic cell-specific P2X7-deficient animals generated by bone marrow transplantation. Thus, we conclude that inflammasome activation in adipose tissue in obesity coincides with the onset of hyperglycemia and hyperinsulinemia, but unexpectedly, is not mediated by the ATP-P2X7 signaling axis. The nature of the inflammasome-activating danger signal(s) in adipose tissue in obesity remains to be characterized. Wild type and P2X7 knockout mice were fed a low fat diet (chow) or high fat diet for 12 weeks. After the diet intervention period, the animals were killed and epididymal white adipose tissue was removed. Total RNA was isolated and subjected to gene expression profiling.