Perfluorobutanesulfonic acid (PFBS) is used as the replacement of perfluorooctanesulfonic acid (PFOS) since 2000 because of the concern on PFOS’ persistence in the environment and the bioaccumulation in animals. Accumulating evidence has shown the correlation between the exposure to perfluorinated compounds and enhanced adipogenesis. There is no report, however, of the effect of PFBS on adipogenesis. Therefore, the present work aimed to investigate the role of PFBS in adipogenesis using 3T3-L1 adipocytes. PFBS treatment for 6 days extensively promoted the differentiation of 3T3-L1 preadipocytes to adipocytes, resulting in significantly increased triglyceride levels. In particular, the treatments of PFBS at the early adipogenic differentiation period (day 0–2) were positively correlated with increased the triglyceride accumulation on day 6. PFBS treatments significantly increased the protein and mRNA levels of the master transcription factors in adipocyte differentiation; CCAAT/enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ), along with acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), the key proteins in lipogenesis. PFBS significantly activated the phosphorylation of extracellular signal-regulated kinase1/2 (ERK1/2) after 4-h treatment, and PFBS′ effect on triglyceride was abolished by U0126, a specific MAPK/ERK kinase (MEK) inhibitor. In conclusion, PFBS increased the adipogenesis of 3T3-L1 adipocytes, in part, via MEK/ERK-dependent pathway.

自2000年以来，由于对全氟辛烷磺酸在环境中的持久性和动物体内生物蓄积性的担忧，全氟丁烷磺酸（PFBS）被用作全氟辛烷磺酸（PFOS）的替代品。越来越多的证据表明，暴露于全氟化合物与增强脂肪形成之间存在相关性。但是，没有关于PFBS对脂肪形成的影响的报道。因此，本工作旨在研究PFBS在使用3T3-L1脂肪细胞的脂肪形成中的作用。PFBS治疗6天广泛促进了3T3-L1前脂肪细胞向脂肪细胞的分化，从而导致甘油三酸酯水平显着提高。特别是，在成脂分化早期（第0-2天）的PFBS治疗与第6天甘油三酯积累的增加呈正相关。PFBS处理可显着增加脂肪细胞分化过程中主转录因子的蛋白质和mRNA水平。CCAAT /增强子结合蛋白α（C /EBPα）和过氧化物酶体增殖物激活受体γ（PPARγ），以及脂肪形成中的关键蛋白乙酰辅酶A羧化酶（ACC）和脂肪酸合酶（FAS）。PFBS在4 h处理后显着激活了细胞外信号调节激酶1/2（ERK1 / 2）的磷酸化作用，而特异性MAPK / ERK激酶（MEK）抑制剂U0126取消了PFBS对甘油三酸酯的作用。总之，PFBS部分通过MEK / ERK依赖性途径增加了3T3-L1脂肪细胞的脂肪生成。CCAAT /增强子结合蛋白α（C /EBPα）和过氧化物酶体增殖物激活受体γ（PPARγ），以及脂肪形成中的关键蛋白乙酰辅酶A羧化酶（ACC）和脂肪酸合酶（FAS）。PFBS在4 h处理后显着激活了细胞外信号调节激酶1/2（ERK1 / 2）的磷酸化作用，而特异性MAPK / ERK激酶（MEK）抑制剂U0126取消了PFBS对甘油三酸酯的作用。总之，PFBS部分通过MEK / ERK依赖性途径增加了3T3-L1脂肪细胞的脂肪生成。CCAAT /增强子结合蛋白α（C /EBPα）和过氧化物酶体增殖物激活受体γ（PPARγ），以及脂肪形成中的关键蛋白乙酰辅酶A羧化酶（ACC）和脂肪酸合酶（FAS）。PFBS在4 h处理后显着激活了细胞外信号调节激酶1/2（ERK1 / 2）的磷酸化作用，而特异性MAPK / ERK激酶（MEK）抑制剂U0126取消了PFBS对甘油三酸酯的作用。总之，PFBS部分通过MEK / ERK依赖性途径增加了3T3-L1脂肪细胞的脂肪生成。特异的MAPK / ERK激酶（MEK）抑制剂U0126消除了PFBS对甘油三酸酯的作用。总之，PFBS部分通过MEK / ERK依赖性途径增加了3T3-L1脂肪细胞的脂肪生成。特异的MAPK / ERK激酶（MEK）抑制剂U0126消除了PFBS对甘油三酸酯的作用。总之，PFBS部分通过MEK / ERK依赖性途径增加了3T3-L1脂肪细胞的脂肪生成。