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双F通过ER介导的PI3K/AKT通路促进了前脂细胞的分化

Yanchao Zhang¹, Jingyi Cao¹, Yiwa Liu¹

¹Dongguan Key Laboratory of Environmental Medicine, The First Dongguan Affiliated Hospital, School of Public Health, Guangdong Medical University, Guangdong Province, Dongguan, 523808, China.

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

|August 2, 2025

概括

双F (BPF) 是BPA的替代品,促进脂肪细胞 (脂肪细胞) 的分化和甘油三积累. 这通过雌激素受体 (ER) 和PI3K/AKT通路发生,这表明BPF可能会导致肥胖.

科学领域:

内分泌学在内分泌学.
环境健康环境健康
分子生物学分子生物学

背景情况:

双是用于塑料和树脂的工业化学品.
双A (BPA) 是一种内分泌干扰化学物质 (EDC),被怀疑是致肥的.
双F (BPF) 是一种BPA的替代品,对其肥胖潜在的研究有限.

研究的目的:

为了研究BPF对脂肪生成的影响,使用3T3-L1预adipocytes.
为了阐明BPF诱导的脂肪生成的潜在分子机制.

主要方法:

3T3-L1前脂质细胞暴露于不同剂量的BPF.
通过测量细胞内脂质滴和甘油三含量来评估脂肪生成.
分析了阿迪波基因标记物的基因和蛋白质表达 (PPARγ,C/EBPα,阿迪波内克丁,FABP4).
使用特定的抑制剂检查了雌激素受体 (ER) 和PI3K/AKT通路的作用.

主要成果:

在3T3-L1细胞中,BPF显著增加了脂质滴积和甘油三含量.
在BPF上调节了关键的脂肪生成基因和蛋白质,包括PPARγ,C/EBPα,氨酸和FABP4.
由BPF诱导的脂肪生成是由ER-PI3K/AKT信号通路调解的.

结论:

BPF促进了前脂肪细胞的分化成为成熟的脂肪细胞.
该ER-PI3K/AKT通路对于BPF的肥胖效应至关重要.
血压可能导致肥胖,凸显了人们对环境化学肥胖因子的担忧.

关键词:

3T3-L1 预脂细胞亚原体的分化差异化双二醇 F 是一种双二醇雌激素受体的受体是什么在PI3K/AKT信号通路中.

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