Summary of Study ST002922

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001814. The data can be accessed directly via it's Project DOI: 10.21228/M87D9M This work is supported by NIH grant, U2C- DK119886.

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This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002922
Study TitleEffects of DINCH and MINCH on adipocyte metabolism of human SGBS cells.
Study SummaryIn the first part of the project, we investigated the effects of DINCH and MINCH on central carbon metabolism. For this purpose, the human SGBS preadipocyte cell line (Wabitsch et al., 2001) was exposed to DINCH and MINCH at concentrations ranging from 10 nM to 10 µM and compared with cells differentiated with rosiglitazone (adipogenic reference) and without rosiglitazone (undifferentiated control). Analysis of central carbon metabolism showed that MINCH, similar to rosiglitazone, induces lipid accumulation mainly through PPARG-mediated upregulation of the pyruvate cycle. In addition, increased lactate production suggests altered glucose homeostasis induced by MINCH-treatment. Our results suggest that MINCH could potentially lead to a weight-promoting effect, as observed with thiazolidinediones, because of the similarity of the observed changes to the effects of the thiazolidinedione rosiglitazone.
Institute
Helmholtz Centre for Environmental Research
DepartmentMolecular Systems Biology
Last NameEngelmann
First NameBeatrice
AddressPermoserstraße 15, Leipzipg, Saxony, 03418, Germany
Emailbeatrice.engelmann@ufz.de
Phone00493412351099
Submit Date2023-10-04
Raw Data AvailableYes
Raw Data File Type(s)wiff
Analysis Type DetailLC-MS
Release Date2023-11-03
Release Version1
Beatrice Engelmann Beatrice Engelmann
https://dx.doi.org/10.21228/M87D9M
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR001814
Project DOI:doi: 10.21228/M87D9M
Project Title:MINCH causes metabolic rewiring towards lipid accumulation and adipogenesis
Project Summary:Humans are ubiquitously exposed to plastic additives, including plasticizers. There is growing evidence that exposure to certain plasticizers is associated with the development of obesity due to their metabolism-disrupting properties. Following the restriction of the use of the phthalate plasticizer di-(2-ethylhexyl) phthalate (DEHP) due to its adverse health effects, it has been replaced by new substitutes such as the plasticizer diisononylcyclohexane-1,2-dicarboxylate (DINCH). Despite recent studies suggesting that the primary metabolite monoisononylcyclohexane-1,2-dicarboxylic acid ester (MINCH) promotes human adipocyte differentiation, the adipogenic properties of MINCH remain controversial. Because the metabolome largely reflects the molecular phenotype and is sensitive to perturbation by external factors, we used targeted metabolomics to investigate the effects of DINCH and MINCH on key metabolic pathways of adipocytes. Analysis of central carbon metabolism is particularly relevant because it provides cellular energy through the degradation of organic compounds and metabolic precursors for anabolic functions that are critical for adipocyte function, such as de novo lipogenesis. The project consists of three main studies: analysis of the effects of DINCH and MINCH on central carbon metabolism of human SGSB cells, analysis of the insulin response of DINCH- and MINCH-treated SGSB cells, and analysis of the effects of DINCH and MINCH on central carbon metabolism of human SGSB cells in the presence of the PPARG inhibitor GW9662.
Institute:Helmholtz Centre for Environmental Research
Last Name:Engelmann
First Name:Beatrice
Address:Permoserstr. 15
Email:beatrice.engelmann@ufz.de
Phone:00493412351099
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