Department of Clinical and Experimental Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy.
Department of Medicine and Surgery, University of Salerno, Baronissi, Salerno, Italy.
Aliment Pharmacol Ther. 2018 Mar;47(6):826-837. doi: 10.1111/apt.14499. Epub 2018 Jan 11.
Bisphenol A is an endocrine disrupting chemical associated with type 2 diabetes mellitus (T2DM), cardiovascular disease and liver enzyme abnormalities.
To evaluate bisphenol A plasma and urine levels in non-alcoholic fatty liver disease (NAFLD) patients compared to healthy subjects. Furthermore, we evaluated, in human HepG2 cells, the effects of exposure to different concentrations of bisphenol A on both oxidative stress induction and cell proliferation.
We enrolled 60 patients with histological diagnosis of NAFLD with or without T2DM and sixty healthy subjects. In vitro, the proliferation of bisphenol A-exposed HepG2 cells at two different concentrations (0.025 and 0.05 μM) was evaluated, both at high (H-HepG2) and at low (L-HepG2) glucose concentrations for 48 h. Lipoperoxidation was assessed by thiobarbituric acid reactive substances (TBARS) assay.
Bisphenol A levels were significantly higher in 60 NAFLD subjects, both in urine and in plasma (P < 0.0001) when compared to controls and, in this group, it appeared to be higher in 30 non-alcoholic steatohepatitis patients compared to 30 simple steatosis subjects (P < 0.05), independently from the presence of T2DM. After a bisphenol A-free diet for 1 month, NAFLD patients showed a significant reduction in bisphenol A circulating levels (P < 0.05), without a significant reduction in urine levels. H-HepG2 cells treated with bisphenol A (0.05 μM) increased proliferation compared to controls at 48 h (P < 0.0001). Bisphenol A increased TBARS levels at 48 h versus controls.
Our study reveals a possible role of bisphenol A as an environmental factor involved in the promotion of NAFLD, particularly in T2DM patients.
双酚 A 是一种内分泌干扰化学物质，与 2 型糖尿病（T2DM）、心血管疾病和肝酶异常有关。
评估非酒精性脂肪性肝病（NAFLD）患者与健康受试者相比的双酚 A 血浆和尿液水平。此外，我们还在人 HepG2 细胞中评估了暴露于不同浓度双酚 A 对氧化应激诱导和细胞增殖的影响。
我们纳入了 60 例经组织学诊断为 NAFLD 的患者，其中包括有或无 T2DM 的患者，以及 60 例健康对照者。在体外，我们评估了在高（H-HepG2）和低（L-HepG2）葡萄糖浓度下，两种不同浓度（0.025 和 0.05 μM）的双酚 A 暴露对 HepG2 细胞增殖的影响，时间为 48 小时。通过硫代巴比妥酸反应物质（TBARS）测定法评估脂质过氧化。
与对照组相比，60 例 NAFLD 患者的尿液和血浆中双酚 A 水平均显著升高（P < 0.0001），且在 30 例非酒精性脂肪性肝炎患者中高于 30 例单纯性脂肪变性患者（P < 0.05），与 T2DM 无关。在接受 1 个月无双酚 A 饮食后，NAFLD 患者的循环双酚 A 水平显著降低（P < 0.05），但尿液水平无显著降低。与对照组相比，用 0.05 μM 双酚 A 处理的 H-HepG2 细胞在 48 小时时增殖增加（P < 0.0001）。双酚 A 在 48 小时时使 TBARS 水平较对照组升高。
我们的研究揭示了双酚 A 作为一种环境因素，可能在促进 NAFLD 方面发挥作用，特别是在 T2DM 患者中。
