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Abstract Title:

Curcumin inhibits adipogenesis induced by benzyl butyl phthalate in 3T3-L1 cells.

Abstract Source:

Toxicol Appl Pharmacol. 2017 Aug 15 ;329:158-164. PMID: 28595985

Abstract Author(s):

Satoru Sakuma, Maki Sumida, Yukiko Endoh, Ayaka Kurita, Ayana Yamaguchi, Tomoki Watanabe, Tetsuya Kohda, Yui Tsukiyama, Yohko Fujimoto

Article Affiliation:

Satoru Sakuma

Abstract:

Phthalates are a group of endocrine disrupting chemicals and may have contributed to the recent global obesity health crisis. Increased adipogenesis via the peroxisome proliferator-activated receptorγ (PPARγ)-CCAAT-enhancer binding protein α (C/EBPα) pathway could be one critical mechanism responsible for phthalate-induced weight gain. On the other hand, curcumin has been shown to inhibit adipogenesis in cells and animal models. The present study was undertaken to evaluate, for the first time, whether curcumin could reduce adipogenesis induced by benzyl butyl phthalate (BBP) via downregulation of the PPARγ-C/EBPα pathway. 3T3-L1 preadipocytes were differentiated by treating them with insulin, dexamethasone, and 3-isobutyl-1-methylxanthine in the presence of BBP, with or without curcumin. Cells that were grown in the presence of BBP alone showed a significant increase in triacylglycerol (TG) levels. In addition, the number of Oil Red O-stained cells and the mRNA expression levels of PPARγ, C/EBPα, adiponectin, and tumor necrosis factor-α (TNFα) were significantly increased.However, treatment with BBP in combination with curcumin resulted in major reductions in TG levels, the numbers of Oil Red O-stained cells, and the mRNA expression levels of the four proteins. These results suggest that curcumin might be an inhibitor of BBP-induced weight gain and inflammation viastimulation of adipocyte differentiation and TNFα generation. Curcumin may, therefore, be a potential medication for preventing the harmful effects of phthalates.

Study Type : In Vitro Study

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Sayer Ji
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