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.
Adiponectin; Adipoq protein, mouse; Anti-Inflammatory Agents; Anti-Obesity Agents; CCAAT-Enhancer-Binding Proteins; CEBPA protein, mouse; Endocrine Disruptors; PPAR gamma; Phthalic Acids; RNA, Messenger; Triglycerides; Tumor Necrosis Factor-alpha; Curcumin; IT942ZTH98; butylbenzyl phthalate; YPC4PJX59M; Index Medicus; Benzyl butyl phthalate; 3T3-L1 cell; Adipocyte differentiation; Tumor necrosis factor-α; PPAR gamma -- drug effects; Adiponectin -- metabolism; 3T3-L1 Cells; CCAAT-Enhancer-Binding Proteins -- metabolism; Dose-Response Relationship, Drug; RNA, Messenger -- metabolism; PPAR gamma -- genetics; Tumor Necrosis Factor-alpha -- metabolism; Animals; PPAR gamma -- metabolism; RNA, Messenger -- genetics; CCAAT-Enhancer-Binding Proteins -- genetics; Adiponectin -- genetics; Tumor Necrosis Factor-alpha -- genetics; Triglycerides -- metabolism; Gene Expression Regulation -- drug effects; Cytoprotection; Adipocytes -- drug effects; Anti-Obesity Agents -- pharmacology; Endocrine Disruptors -- toxicity; Anti-Inflammatory Agents -- pharmacology; Adipocytes -- metabolism; Phthalic Acids -- toxicity; Adipogenesis -- drug effects; Adipocytes -- pathology; Curcumin -- pharmacology