Metabolomics Workbench ST000662 - GNPS - Lipidomics of hormone-sensitive lipase variants
Ontology highlight
ABSTRACT:
INSTRUMENT(S): QTOF - NEGATIVE, QTOF - POSITIVE
ORGANISM(S): Homo Sapiens
SUBMITTER: 
Maureen Kachman
PROVIDER: MSV000082691 | GNPS | Thu Aug 02 17:04:00 BST 2018
REPOSITORIES: GNPS
Dataset's files
primary
| Action | DRS | |||
|---|---|---|---|---|
| MSV000082691 | Other | |||
| params.xml | Xml | |||
| 20140614_309_Negative_01.mzXML | Mzxml | |||
| 20140614_336_Negative_01.mzXML | Mzxml | |||
| 20140614_341_Negative_01.mzXML | Mzxml |
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Project description:The samples are frozen biopsies of whilte subcutaneous adipose tissues (50 mg). Samples were collected from 4 hormone-sensitive lipase (HSL) WT patients (adipose insulin sensitive), 3 HSL heterozygote patients and 1 HSL KO patient.
2017-06-05 | ST000662 | MetabolomicsWorkbench
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Project description:Obesity is a risk factor for numerous metabolic disorders; however, not all obese individuals are prone to insulin resistance. The central aim of this study was to identify molecular pathways directly related to insulin resistance independent of BMI in obesity. We sought to determine the gene expression signature of adipose tissue in a body mass index (BMI)-matched obese cohort of patients that are either insulin sensitive or insulin resistant. Overall design: We determined the global gene expression signatures of omental and subcutaneous adipose tissue samples obtained from insulin-sensitive obese and insulin-resistant obese patients undergoing gastric bypass surgery. The SQ sample for Insulin Resistant Patient 6 has been removed from the study.
2010-03-25 | GSE20950 | GEO
Project description:Abatract Obesity is known to be associated with adipose tissue inflammation and insulin resistance. Importantly, in obesity, the accumulation of proinflammatory macrophages in adipose tissue correlates with insulin resistance. We hypothesized that the receptor for advanced glycation end products (RAGE) and associated ligands are involved in adipose tissue insulin resistance, and that the activation of the AGE–RAGE axis plays an important role in obesity-associated inflammation. C57BL/6J mice (WT) and RAGE deficient (RAGE−/−) mice were fed a high fat diet (HFD) and subjected to glucose and insulin tolerance tests. Epdidymal adipose tissue (eAT) was collected and adipose stromal vascular cells isolated using flow cytometry. Visceral adipose tissue macrophage polarization was assessed by quantitative real time PCR. Immunoblotting was performed to evaluate the insulin signaling in adipose tissues. In additional studies, cell trafficking was assessed by injecting labeled blood monocytes into recipient mice. RAGE−/− mice displayed improved insulin sensitivity and glucose tolerance, accompanied by decreased body weight and eAT mass. Exogenous methylglyoxal (MGO) impaired insulin-stimulated AKT signaling in adipose tissues from WT mice fed a normal chow diet, but not in RAGE−/− mice. In contrast, in obese mice, treatment with MGO did not reduce insulin-induced phosphorylation of AKT in WT-HFD mice. Moreover, insulin-induced AKT phosphorylation was found to be impaired in adipose tissue from RAGE−/−-HFD mice. RAGE−/− mice displayed improved inflammatory profiles and evidence for increased adipose tissue browning. This observation is consistent with the finding of reduced plasma levels of FFA, glycerol, IL-6, and leptin in RAGE−/− mice compared to WT mice. Collectively the data demonstrate that RAGE-mediated adipose tissue inflammation and insulin-signaling are potentially important mechanisms that contribute to the development of obesity-associated insulin resistance.
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Project description:<h4>Background</h4>Obesity is a strong risk factor for resistance to insulin-mediated glucose disposal, a precursor of type 2 diabetes and other disorders. However, not all obese individuals are insulin resistant. We sought to identify the molecular pathways that might cause obesity-associated insulin resistance in humans by studying the morbidly obese who were insulin sensitive versus insulin resistant, thereby eliminating obesity as a variable.<h4>Methods</h4>Combining gene expression profiling with computational approaches, we determined the global gene expression signatures of omental and subcutaneous adipose tissue samples obtained from similarly obese patients undergoing gastric bypass surgery.<h4>Results</h4>Gene sets related to chemokine activity and chemokine receptor binding were identified as most highly expressed in the omental tissue from insulin-resistant compared with insulin-sensitive subjects, independent of the body mass index. These upregulated genes included chemokines (C-C motif) ligand 2, 3, 4, and 18 and interleukin-8/(CC-X motif) ligand 8 and were not differentially expressed in the subcutaneous adipose tissues between the 2 groups of subjects. Insulin resistance, but not the body mass index, was associated with increased macrophage infiltration in the omental adipose tissue, as was adipocyte size, in these morbidly obese subjects.<h4>Conclusion</h4>Our findings have demonstrated that inflammation of the omental adipose tissue is strongly associated with insulin resistance in human obesity even in subjects with similar body mass index values.
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