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

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 receptor γ (PPARγ)-CCAAT-enhancer binding protein α (C/EBPα) pathway could be one critical mechanism responsi...

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Published in:	Toxicology and applied pharmacology Vol. 329; pp. 158 - 164
Main Authors:	Sakuma, Satoru, Sumida, Maki, Endoh, Yukiko, Kurita, Ayaka, Yamaguchi, Ayana, Watanabe, Tomoki, Kohda, Tetsuya, Tsukiyama, Yui, Fujimoto, Yohko
Format:	Journal Article
Language:	English
Published:	United States Elsevier Inc 15-08-2017
Subjects:	3T3-L1 cell 3T3-L1 Cells 60 APPLIED LIFE SCIENCES Adipocyte differentiation Adipocytes - drug effects Adipocytes - metabolism Adipocytes - pathology Adipogenesis - drug effects Adiponectin - genetics Adiponectin - metabolism Animals Anti-Inflammatory Agents - pharmacology Anti-Obesity Agents - pharmacology Benzyl butyl phthalate CCAAT-Enhancer-Binding Proteins - genetics CCAAT-Enhancer-Binding Proteins - metabolism CURCUMIN Curcumin - pharmacology Cytoprotection Dose-Response Relationship, Drug Endocrine Disruptors - toxicity Gene Expression Regulation - drug effects INHIBITION MESSENGER-RNA METABOLIC DISEASES Mice PHTHALATES Phthalic Acids - toxicity PPAR gamma - drug effects PPAR gamma - genetics PPAR gamma - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Triglycerides - metabolism Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-α C/EBP C/EBPα IBMX 3T3-L1 cell Tumor necrosis factor-α PPARγ BBP DMEM Benzyl butyl phthalate TG TNF-α FBS Curcumin Adipocyte differentiation
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Summary:	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 receptor γ (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 via stimulation of adipocyte differentiation and TNFα generation. Curcumin may, therefore, be a potential medication for preventing the harmful effects of phthalates. •3T3-L1 cells treated with BBP alone showed a significant increase in TG levels.•Curcumin reduced the mRNA levels of PPARγ, C/EBPα, adiponectin, and TNFα.•Curcumin might be an inhibitor of BBP-induced weight gain and inflammation.
ISSN:	0041-008X 1096-0333
DOI:	10.1016/j.taap.2017.05.036