Dataset Information

Adverse Effects of Bisphenol A and its substitute compounds on human SGBS preadipocytes

ABSTRACT: Bisphenol A (BPA), which is used in a variety of consumer-related plastic products, was reported to cause metabolic disruption. Substitute compounds are increasingly emerging, but are not sufficiently investigated. In this study, we aimed to investigate the mode of action of BPA and four of its substitutes during the differentiation of human preadipocytes. Human preadipocytes were exposed to BPA, BPS, BPB, BPF, and BPAF, as well as the PPARγ-antagonist GW9662. After 12 days of differentiation, global protein profiles were assessed using LC-MS/MS-based proteomics.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Preadipocyte Cell Line, Cell Culture, Preadipocyte, Adipose Tissue

SUBMITTER: Alexandra Schaffert

LAB HEAD: Kristin Schubert

PROVIDER: PXD023227 | Pride | 2021-08-05

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	20190306_Uniprot_HomoSapiens_Refset_IK.fasta	Fasta
	20200212_SGBS_Bisph_10_1.raw	Raw
	20200212_SGBS_Bisph_10_2.raw	Raw
	20200212_SGBS_Bisph_11_1.raw	Raw
	20200212_SGBS_Bisph_11_2.raw	Raw

Items per page:

1 - 5 of 27

Publications

Alternatives for the worse: Molecular insights into adverse effects of bisphenol a and substitutes during human adipocyte differentiation.

Schaffert Alexandra A Krieg Laura L Weiner Juliane J Schlichting Rita R Ueberham Elke E Karkossa Isabel I Bauer Mario M Landgraf Kathrin K Junge Kristin M KM Wabitsch Martin M Lehmann Jörg J Escher Beate I BI Zenclussen Ana C AC Körner Antje A Blüher Matthias M Heiker John T JT von Bergen Martin M Schubert Kristin K

Environment international 20210627

Bisphenol A (BPA), which is used in a variety of consumer-related plastic products, was reported to cause adverse effects, including disruption of adipocyte differentiation, interference with obesity mechanisms, and impairment of insulin- and glucose homeostasis. Substitute compounds are increasingly emerging but are not sufficiently investigated.We aimed to investigate the mode of action of BPA and four of its substitutes during the differentiation of human preadipocytes to adipocytes and their ...[more]

PMID: 34186270

Similar Datasets

Project description:Background: Exposure to the endocrine-disrupting chemical bisphenol A (BPA) is correlated with obesity and promotes adipogenesis of human preadipocytes into mature adipocytes. However, the mechanism of action of BPA-induced human adipogenesis in vitro remains to be fully characterized. Methods: In this study, potential mechanisms of BPA-induced adipogenesis in primary human preadipocytes were evaluated using gene expression microarray analysis. Preadipocytes from donors with normal body mass indexes were differentiated in the presence of 50 M-BM-5M BPA or 1 M-BM-5M dexamethasone (DEX) for 48 hours. Results: Microarray analysis revealed 235 up-regulated and 138 down-regulated genes following BPA treatment, including sterol regulatory element binding factor 1 (SREBF1), a key transcription factor known to regulate many components of lipid metabolism and adipogenesis. For DEX treated preadipocytes, 1136 genes were up-regulated, including the adipogenic marker lipoprotein lipase, while 1031 genes were down-regulated. Ingenuity Pathway Analysis was used to identify functional annotations of the gene expression changes associated with response to BPA and DEX treatments. BPA exposure was associated with expression changes in the genes involved in the accumulation of triacylglycerol while DEX was linked to metabolism of triacylglycerol and cleavage of fatty acids. The analysis also revealed enrichment of genes in pathways known to be associated with BPA exposure including thyroid-receptor/retinoic X receptor (TR/RXR) activation, mammalian target of rapamycin (mTOR) signaling and cholesterol biosynthesis, whereas DEX treatment was linked to cholesterol biosynthesis and ethanol degradation. Interestingly, alterations in the mTOR pathway in response to BPA did not occur in DEX-treated preadipocytes. Conclusions: Our data suggest that potential mechanisms of action of BPA-induced adipogenesis involve SREBF1, the TR/RXR and the mTOR pathways. The study used 40 samples in total which included 5 replicates (cells from 5 unique donors) of 8 different treatments. The 8 treatments were as follows: 1) untreated (negative) control for 48 hours, 2) 25 uM BPA treated for 48 hours, 3) 50 uM BPA treated for 48 hours, 4) untreated (negative) control + insulin for 48 hours, 5) 25 uM BPA + insulin treated for 48 hours, 6) 50 uM BPA + insulin treated for 48 hours, 7) 1uM Dexamethasone + insulin treated for 48 hours, 8) 1uM Dexamethasone + insulin treated for 96 hours.