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首页> 外文期刊>Archives of Toxicology >Mono(2-ethylhexyl)phthalate accumulation disturbs energy metabolism of fat cells
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Mono(2-ethylhexyl)phthalate accumulation disturbs energy metabolism of fat cells

机译：单体（2-乙基己基）邻苯二甲酸盐积累脂肪细胞的能量代谢

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Phthalates are lipophilic and tend to accumulate in adipose tissue, an important regulator of energy balance and glucose homeostasis. The study aimed to determine whether cellular phthalate accumulation influenced fat cell energy metabolism. Following a 3-day treatment with adipogenesis-inducing medium and a 2-day treatment with adipogenesis-maintaining medium, 3T3-L1 cells differentiated into adipocytes in the presence of a phthalate at a clinically relevant concentration (30-300 mu M) for another 6 days. Two phthalates, di(2-ethylhexyl)phthalate and di-n-butylphthalate, and their metabolites, mono(2-ethylhexyl)phthalate (MEHP) and mono-n-butylphthalate, were used here. The phthalate treatments caused no marked effect on cytotoxicity and adipogenesis. Only the MEHP-treated adipocytes were found having smaller lipid droplets; MEHP accumulated in cells in a dose- and time-dependent manner. The MEHP-treated adipocytes exhibited significant increases in lipolysis and glucose uptake; quantitative real-time polymerase chain reaction (qPCR) analysis revealed correlated changes in expression of marker genes involved in adipogenesis, lipid metabolism, and glucose uptake. Analysis of oxygen consumption rate (a mitochondrial respiration indicator) and extracellular acidification rate (a glycolysis indicator) indicated a higher energy metabolism in the adipocytes. qPCR analysis of critical genes involved in mitochondrial biogenesis and/or energy metabolism showed that expression of peroxisome proliferator-activated receptor gamma coactivator-1 alpha, sirtuin 3, and protein kinase A were significantly enhanced in the MEHP-treated adipocytes. In vitro evidence of MEHP impacts on lipolysis, glucose uptake/glycolysis, and mitochondrial respiration/biogenesis demonstrates that MEHP accumulation disturbs energy metabolism of fat cells.
机译：邻苯二甲酸酯是亲脂性的，并且倾向于在脂肪组织中积聚，这是能量平衡和葡萄糖稳态的重要调节因子。该研究旨在确定细胞邻苯二甲酸盐累积是否影响了脂肪细胞能量代谢。在用脂肪发生诱导培养基治疗和用脂肪发生维持培养基治疗的治疗后，3T3-L1细胞在临床相关浓度（30-300μm）的邻苯二甲酸酯存在下分化成脂肪细胞6天。这里使用了两种邻苯二甲酸酯，二（2-乙基己基）邻苯二甲酸酯和二丁基苯二甲酸酯，以及它们的代谢物，单醇（2-乙基己基）邻苯二甲酸酯（MeHP）和单叔丁二醇酯。邻苯二甲酸酯治疗对细胞毒性和脂肪发生不显着影响。发现含有较小的脂质液滴的MeHP处理的脂肪细胞; MEHP以剂量和时间依赖的方式在细胞中累积。 MeHP处理的脂肪细胞表现出脂解和葡萄糖摄取的显着增加;定量实时聚合酶链反应（QPCR）分析揭示了参与脂肪发生，脂质代谢和葡萄糖摄取的标志物基因表达的相关变化。氧消耗率（线粒体呼吸指示剂）和细胞外酸化速率（糖酵解指示剂）分析表明脂肪细胞中的较高能量代谢。 QPCR分析参与线粒体生物发生和/或能量代谢的关键基因表明，在MeHP处理的脂肪细胞中，过氧化物组织增殖物激活受体γ-1α，Sirtuin 3和蛋白激酶A的表达显着提高。 MEHP对脂解，葡萄糖摄取/糖酵解和线粒体呼吸/生物发生的体外证据表明MEHP积累了脂肪细胞的能量代谢。

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