Dataset Information

In-vitro and in-vivo effects of an environmental PPARγ metabolic disruptor, triphenyl phosphate, on adipogenic differentiation and metabolic functions

ABSTRACT: Comparison of TPhP and Rosi exposure to adipocytes.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture

SUBMITTER: Benjamin Blum

LAB HEAD: Andrew Emili

PROVIDER: PXD012337 | Pride | 2021-09-08

REPOSITORIES: Pride

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Publications

Triphenyl phosphate is a selective PPARγ modulator that does not induce brite adipogenesis in vitro and in vivo.

Kim Stephanie S Rabhi Nabil N Blum Benjamin C BC Hekman Ryan R Wynne Kieran K Emili Andrew A Farmer Stephen S Schlezinger Jennifer J JJ

Archives of toxicology 20200718 9

Triphenyl phosphate (TPhP) is an environmental PPARγ ligand, and growing evidence suggests that it is a metabolic disruptor. We have shown previously that the structurally similar ligand, tributyltin, does not induce brite adipocyte gene expression. Here, using in vivo and in vitro models, we tested the hypothesis that TPhP is a selective PPARγ ligand, which fails to induce brite adipogenesis. C57BL/6 J male mice were fed either a low or very high-fat diet for 13 weeks. From weeks 7-13, mice wer ...[more]

PMID: 32683515

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Project description:Metabolic syndrome is an important public concern and demand for effective therapeutic strategies. Abdominal obesity, especially an increase in the visceral adipose tissue, is the main cause of this syndrome. Flavonoids are expected to improve risk factors for metabolic syndrome. Bilberry, original species of blueberry containing anthocyanidin flavonoids have been used for centuries in Europe to ameliorate the symptoms of diabetes, but their effects and the mechanisms on lipid accumulation of adipocyte cells are not well defined. In the present study, we investigated effects of the Bilberry extract on differentiation of adipocytes using 3T3-L1 adipocyte cell line. Exposure to Bilberry extract during the early period of adipogenesis (6 days) was significantly inhibited adipocyte differentiation of 3T3-L1. During this period, Bilberry extract greatly down-regulated the mRNA levels of the key adipogenesis-associated markers peroxisome proliferator-activated receptor-γ (PPARγ). Furthermore, Bilberry extract significantly decreased expression of the transcription factor Sterol Regulatory Element Binding Protein 1c (SREBP1c), which plays a central role in adipocyte differentiation including the induction of PPARγ. The expression of SREBP1c is remarkably enhanced in response to insulin, thus raises the possibility that Bilberry extract might inhibit the Insulin pathway. So, We investigated whether Billberry extract and anthocyanidines turned the insulin signaling pathway using microarray. As a result, Gene Set Enrichment Analysis (GSEA) shows that these additives turned insulin signaling pathway certainly. We quantified expression profiles of whole mRNAs by microarray in the adipocyte from 3T3-L1 with or without additives. 3T3-L1 preadipocytes (American Type Culture Collection, Manassas, VA) were grown to confluence in DMEM media (Sigma Aldrich, Tokyo, Japan) with 10% calf serum and penicillin (100 U/ml)/streptomycin (100 ug/ml). Adipogenesis was induced using an adipogenesis assay kit (Chemicon International, Temecula, CA). On day 0, cells were induced with initiation media (10 ug/ml insulin, 1 uM dexamethasone and 0.5 uM IBMX in DMEM media added with 1: 0.1% DMSO, 2: 100 ug/ml Bilberry extract, 3: 100 nM Delphinidin or 4: 100 nM Cyanidin (total 4 samples). On day 2, harvested the cells, extracted total RNA and did microarray experiments.

Dataset Information

In-vitro and in-vivo effects of an environmental PPARγ metabolic disruptor, triphenyl phosphate, on adipogenic differentiation and metabolic functions

Publications

Triphenyl phosphate is a selective PPARγ modulator that does not induce brite adipogenesis in vitro and in vivo.

Similar Datasets

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