Expression data from human omental and subcutaneous adipose tissue taken from volunteers undergoing bariatric surgery
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE29411 | GEO | 2012/01/01
SECONDARY ACCESSION(S): PRJNA141549
REPOSITORIES: GEO
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE29409: Subcutaneous and omental white adipose tissue biopsies analysed from five obese patients GSE29410: Subcutaneous and omental white adipose tissue biopsies analysed from three obese patients Refer to individual Series
2012-01-01 | E-GEOD-29411 | biostudies-arrayexpress
Project description:BackgroundObesity plays a major role in the development of insulin resistance (IR) and diabetes (T2DM). Increased adipose tissue (AT) is particularly of interest because it activates a chronic inflammatory response in adipocytes and other tissues. AT plays key endocrine and metabolic functions, acting in the regulation of insulin sensitivity and energy homeostasis. Additionally, it can be easily collected during bariatric surgery. The purpose of this pilot study was to explore the potential differences in AT metabolism, through comparing the untargeted metabolomic profiles of diabetic and non-diabetic obese patients undergoing bariatric surgery.MethodsFor this exploratory study, samples were collected from 17 subjects. Subcutaneous AT (SAT) samples from obese-diabetic (n = 8) and Obese-non-Diabetic (n = 9) subjects were obtained from the Human Metabolic Tissue Bank. Untargeted metabolomic profiling was performed by Metabolon® Inc. Statistical analysis was performed using the MetaboAnalyst 4.0 platform.ResultsAmong the 421 metabolites identified and analyzed there were no significant differences between the Obese-Diabetics and the Obese-non-Diabetics. Small changes were observed by fold change analysis mainly in lipid (n = 12; e.g. NEFAs) and amino acid (n = 8; e.g. BCAAs) metabolic pathways. Dysregulation of these metabolites has been associated with IR and other T2DM-related pathophysiological processes.ConclusionObesity may influence SAT metabolism masking T2DM-dependent dysregulation. Better understanding the metabolic differences within SAT in diabetic populations may help identify potential biomarkers for diagnosis and monitoring of T2DM in patients undergoing bariatric surgery.
| S-EPMC7874365 | biostudies-literature
Project description:We investigated interindividual variability in gene expression in abdominal subcutaneous (SC) and omental (OM) adipose tissue of 10 massively obese men. Affymetrix human U133A microarrays were used to measure gene expression levels. A total of 6811 probesets generated significant signal in both depots in all samples. Interindividual variability in gene expression was rather low, with more than 90% of transcripts showing a coefficient of variation (CV) lower than 23.6% and 21.7% in OM and SC adipose tissues, respectively. The distributions of CV were similar between the two fat depots. A set of highly variable genes was identified for both tissues on the basis of a high CV and elevated gene expression level. Among the set of highly regulated genes, 18 transcripts were involved in lipid metabolism and 28 transcripts were involved in cell death for SC and OM samples, respectively. In conclusion, gene expression interindividual variability was rather low and globally similar between fat compartments, and the adipose tissue transcriptome appeared as relatively stable, although specific pathways were found to be highly variable in SC and OM depots.
| S-EPMC6042019 | biostudies-literature
Project description:Bariatric surgery (BS) is the most effective treatment for obesity and has a positive impact on cardiometabolic risk and in the remission of type 2 diabetes. Following BS, the majority of fat mass is lost from the subcutaneous adipose tissue depot (SAT). However, the changes in this depot and functions and as well as its relative contribution to the beneficial effects of this surgery are still controversial. With the aim of studying altered proteins and molecular pathways in abdominal SAT (aSAT) after body weight normalization induced by BS, we carried out a proteomic approach sequential window acquisition of all theoretical mass spectra (SWATH-MS) analysis. These results were complemented by Western blot, electron microscopy and RT-qPCR. With all of the working tools mentioned, we confirmed that after BS, up-regulated proteins were associated with metabolism, the citric acid cycle and respiratory electron transport, triglyceride catabolism and metabolism, formation of ATP, pyruvate metabolism, glycolysis/gluconeogenesis and thermogenesis among others. In contrast, proteins with decreased values are part of the biological pathways related to the immune system. We also confirmed that obesity caused a significant decrease in mitochondrial density and coverage, which was corrected by BS. Together, these findings reveal specific molecular mechanisms, genes and proteins that improve adipose tissue function after BS characterized by lower inflammation, increased glucose uptake, higher insulin sensitivity, higher de novo lipogenesis, increased mitochondrial function and decreased adipocyte size.
| S-EPMC7019912 | biostudies-literature
Project description:BackgroundAdipose tissue dysfunction contributes to obesity-associated chronic diseases. In the first year after bariatric surgery, obese patients significantly improve their metabolic status upon losing weight. We aimed to investigate whether changes in subcutaneous adipose tissue gene expression reflect a restoration of a healthy lean phenotype after bariatric surgery.MethodsThirty-one severely obese patients (BMI ≥ 40 kg/m2) were examined before and after surgery. subcutaneous adipose tissue (SAT) was collected during and 1 year after bariatric surgery. SAT from 20 matched lean and overweight patients (BMI < 30 kg/m2) was collected during elective abdominal surgery. Baseline characteristics and SAT gene expression relevant to glucose and lipid metabolism, inflammation, and apoptosis were analyzed.ResultsAfter surgery, mean BMI decreased from 46.1 ± 6.3 to 31.1 ± 5.7 kg/m2 and homeostasis model assessment of insulin resistance from 5.4 ± 5.3 to 0.8 ± 0.8. SAT expression of most analyzed inflammatory cytokines, growth factors, and metabolic and cell surface markers was greatly downregulated even compared to the lean cohort. In contrast, gene expression of TNF and CASP3 was significantly upregulated. Elastic net regression analysis showed that fasting glucose levels and CASP3 predicted increased TNF expression in the post-obese group.ConclusionsGene expression patterns in SAT 1 year after bariatric surgery point to a reduced inflammation. The unexpected high TNF expression in SAT of post-obese subjects is most likely not an indicator for inflammation, but rather an indicator for increased lipolysis and adipose tissue catabolism. Notably, after bariatric surgery SAT gene expression reflects a cachexia-like phenotype and differs from the lean state.
| S-EPMC5423994 | biostudies-literature
Project description:CONTEXT:The mechanisms mediating the short- and long-term improvements in glucose homeostasis following bariatric/metabolic surgery remain incompletely understood. OBJECTIVE:To investigate whether a reduction in adipose tissue inflammation plays a role in the metabolic improvements seen after bariatric/metabolic surgery, both in the short-term and longer-term. DESIGN:Fasting blood and subcutaneous abdominal adipose tissue were obtained before (n=14), at one month (n=9), and 6-12months (n=14) after bariatric/metabolic surgery from individuals with obesity who were not on insulin or anti-diabetes medication. Adipose tissue inflammation was assessed by a combination of whole-tissue gene expression and flow cytometry-based quantification of tissue leukocytes. RESULTS:One month after surgery, body weight was reduced by 13.5±4.4kg (p<0.001), with improvements in glucose tolerance reflected by a decrease in area-under-the-curve (AUC) glucose in 3-h oral glucose tolerance tests (-105±98mmol/L * min; p=0.009) and enhanced pancreatic ?-cell function (insulinogenic index: +0.8±0.9pmol/mmol; p=0.032), but no change in estimated insulin sensitivity (Matsuda insulin sensitivity index [ISI]; p=0.720). Furthermore, although biomarkers of systemic inflammation and pro-inflammatory gene expression in adipose tissue remained unchanged, the number of neutrophils increased in adipose tissue 15-20 fold (p<0.001), with less substantial increases in other leukocyte populations. By the 6-12month follow-up visit, body weight was reduced by 34.8±10.8kg (p<0.001) relative to baseline, and glucose tolerance was further improved (AUC glucose -276±229; p<0.001) along with estimated insulin sensitivity (Matsuda ISI: +4.6±3.2; p<0.001). In addition, improvements in systemic inflammation were reflected by reductions in circulating C-reactive protein (CRP; -2.0±5.3mg/dL; p=0.002), and increased serum adiponectin (+1358±1406pg/mL; p=0.003). However, leukocyte infiltration of adipose tissue remained elevated relative to baseline, with pro-inflammatory cytokine mRNA expression unchanged, while adiponectin mRNA expression trended downward (p=0.069). CONCLUSION:Both the short- and longer-term metabolic improvements following bariatric/metabolic surgery occur without significant reductions in measures of adipose tissue inflammation, as assessed by measuring the expression of genes encoding key mediators of inflammation and by flow cytometric immunophenotyping and quantification of adipose tissue leukocytes.
| S-EPMC5407411 | biostudies-literature
Project description:Obesity is associated with extensive expansion and remodeling of the adipose tissue architecture, including its microenvironment and extracellular matrix (ECM). Although obesity has been reported to induce adipose tissue fibrosis, the composition of the ECM under healthy physiological conditions has remained underexplored and debated. Here, we used a combination of three established techniques (picrosirius red staining, a colorimetric hydroxyproline assay, and sensitive gene expression measurements) to evaluate the status of the ECM in metabolically healthy lean (MHL) and metabolically unhealthy obese (MUO) subjects. We investigated ECM deposition in the two major human adipose tissues, namely the omental and subcutaneous depots. Biopsies were obtained from the same anatomic region of respective individuals. We found robust ECM deposition in MHL subjects, which correlated with high expression of collagens and enzymes involved in ECM remodeling. In contrast, MUO individuals showed lower expression of ECM components but elevated levels of ECM cross-linking and adhesion proteins, e.g., lysyl oxidase and thrombospondin. Our data suggests that subcutaneous fat is more prone to express proteins involved in ECM remodeling than omental adipose tissues. We conclude that a more dynamic ability to deposit and remodel ECM may be a key signature of healthy adipose tissue, and that subcutaneous fat may adapt more readily to changing metabolic conditions than omental fat.
| S-EPMC8745535 | biostudies-literature
Project description:BackgroundBariatric surgery, especially Roux-en-Y gastric bypass (RYGB), is the most effective and durable treatment option for severe obesity. The mechanisms involving adipose tissue may be important to explain the effects of surgery.MethodsWe aimed to identify the genetic signatures of adipose tissue in patients undergoing RYGB. We evaluated 13 obese, non-diabetic patients (mean age 37 years, 100% women, Body mass index (BMI) 42.2 kg/m2) one day before surgery, 3 and 6 months (M) after RYGB.ResultsAnalysis of gene expression in adipose tissue collected at surgery compared with samples collected at 3 M and 6 M Post-RYGB showed that interleukins [Interleukin 6, Tumor necrosis factor-α (TNF-α), and Monocyte chemoattractant protein-1(MCP1)] and endoplasmic reticulum stress (ERS) genes [Eukaryotic translation initiation factor 2 alpha kinase 3 (EIF2AK3) and Calreticulin (CALR)] decreased during the follow-up (P ≤ 0.01 for all). Otherwise, genes involved in energy homeostasis [Adiponectin and AMP-activated protein kinase (AMPK)], cellular response to oxidative stress [Sirtuin 1, Sirtuin 3, and Nuclear factor erythroid 2-related factor 2 (NRF2)], mitochondrial biogenesis [Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α)] and amino acids metabolism [General control nonderepressible 2 (GCN2)] increased from baseline to all other time points evaluated (P ≤ 0.01 for all). Also, expression of Peroxisome proliferator-activated receptor gamma (PPARϒ) (adipogenesis regulation) was significantly decreased after RYGB (P < 0.05). Additionally, we observed that PGC1α, SIRT1 and AMPK strongly correlated to BMI at 3 M (P ≤ 0.01 for all), as well as ADIPOQ and SIRT1 to BMI at 6 M (P ≤ 0.01 for all).ConclusionsOur findings demonstrate that weight loss is associated with amelioration of inflammation and ERS and increased protection against oxidative stress in adipose tissue. These observations are strongly correlated with a decrease in BMI and essential genes that control cellular energy homeostasis, suggesting an adaptive process on a gene expression level during the caloric restriction and weight loss period after RYGB. Trial registration CAAE: 73,585,317.0.0000.5440.
| S-EPMC7887793 | biostudies-literature
Project description:We generated single nucleus transcriptomic atlas for human subcutaneous and omental white adipose tissue (WAT).
2023-02-23 | GSE225700 | GEO
Project description:The genomic landscape of hepatic tissue affected by nonalcoholic steatohepatitis (NASH) in severely obese adolescents undergoing bariatric surgery is unknown. Our purpose here was to uncover genomic profiles of obese controls, and obese cases with nonalcoholic fatty liver disease (NAFLD), borderline nonalcoholic steatohepatitis, and definite nonalcoholic steatohepatitis, in order to clarify molecular functions, biological processes, and pathways that are dysregulated in nonalcoholic steatohepatitis in the severely obese adolescent. In a prospective observational cohort study, we have intra-operatively obtained 165 liver samples; of these 67 were submited for microarray analysis. Through ANOVA, we found 8648 genes with differential regulation between the four histologies; from these, we uncovered gene signatures shared between borderline and definite nonalcoholic steatohepatitis, and gene sets with differential effects between borderline and definite.
2017-07-21 | GSE66676 | GEO