脂肪生成
过氧化物酶体增殖物激活受体
受体
过氧化物酶体
化学
3T3-L1
脂蛋白脂酶
细胞生物学
脂肪组织
脂肪酸合酶
脂肪酸结合蛋白
报告基因
信号转导
生物
生物化学
脂肪酸
基因表达
基因
作者
Weijie Sun,Xiaoyu Duan,Hao Chen,Lianying Zhang,Hongwen Sun
标识
DOI:10.1016/j.scitotenv.2019.134810
摘要
Recent studies have shown that exposure to some organophosphates, such as triphenyl phosphate (TPHP) and diphenyl phosphate (DPHP), can affect adipogenesis in preadipocytes. 2-Ethylhexyl diphenyl phosphate (EHDPP), an organophosphate, is frequently detected in various environmental media. However, there is less information about the toxicity effects and the mechanism by which EHDPP affects preadipocytes. In the present study, we investigated whether EHDPP could induce differentiation in 3T3-L1 preadipocytes through the peroxisome proliferator-activated receptor γ (PPARγ) signaling pathway. The fluorescence competitive binding assay and the dual-luciferase reporter gene assay were used to assess the binding affinity and activation of PPARγ, and the results showed that EHDPP can bind to the ligand binding domain of PPARγ (PPARγ-LBD) and activate PPARγ in vitro. Exposure to EHDPP for 10 days extensively induced adipogenesis in 3T3-L1 preadipocytes as assessed by lipid accumulation and gene expression of adipogenic markers of fatty acid binding protein 4 (FABP4), lipoprotein lipase (Lpl), adiponectin (Adip), and fatty acid synthase (Fasn). Furthermore, the preadipocytes differentiation was blocked by the PPARγ-specific antagonist GW9662, indicating that the PPARγ signaling pathway plays an important part in 3T3-L1 cell differentiation induced by EHDPP. Taken together, EHDPP can bind to PPARγ-LBD, activate PPARγ receptor, and induce cell differentiation via the PPARγ signaling pathway in 3T3-L1 preadipocytes.
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