Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, China.
Anhui Provincial Key Laboratory of Population Health & Aristogenics, Anhui Medical University, Hefei, China.
J Appl Toxicol. 2018 Jul;38(7):1026-1035. doi: 10.1002/jat.3612. Epub 2018 Mar 24.
Cadmium (Cd) is a persistent environmental and occupational contaminant that accumulates in humans and shows adverse effects on health. Accumulating evidence reveals that environmental Cd exposure is associated with hepatic lipid accumulation and metabolic alterations in adult male mice. However, whether Cd exposure induces hepatic lipid accumulation and metabolic alterations in female mice remains poorly understood. In the present study, we aimed to investigate the effects of Cd exposure on insulin resistance, hepatic lipid accumulation and associated metabolic pathways. Female CD1 mice were administrated with CdCl (10 and 100 mg l ) by drinking water. We found that Cd exposure did not induce obesity, insulin resistance and hepatic lipid accumulation. By contrary, mice in the Cd-100 mg l group presented a significant reduction of the glucose area under the curve during the glucose tolerance test. However, there was a significant elevation in the mRNA level of Fasn and Scd-1, which were critical genes during hepatic fatty acid synthesis. Moreover, hepatic Fabp1 and Fabp4, two genes for hepatic fatty acid uptake were upregulated in Cd-treated mice. Of interest, Lpl, a key gene for hepatic lipoprotein lysis, was also upregulated in Cd-treated mice. Collectively, our results suggest that Cd exposure upregulated mRNA level of genes related to hepatic lipid metabolism although there was no insulin resistance and hepatic lipid accumulation shown in the present study.
镉(Cd)是一种持久的环境和职业污染物,在人体内积累,并对健康产生不良影响。越来越多的证据表明,环境镉暴露与成年雄性小鼠的肝脂质积累和代谢改变有关。然而,镉暴露是否会导致雌性小鼠肝脂质积累和代谢改变仍知之甚少。在本研究中,我们旨在研究镉暴露对胰岛素抵抗、肝脂质积累和相关代谢途径的影响。通过饮用水给予 CD1 雌性小鼠 CdCl2(10 和 100mg/L)。我们发现,镉暴露不会引起肥胖、胰岛素抵抗和肝脂质积累。相反,在 Cd-100mg/L 组中,葡萄糖耐量试验期间的血糖曲线下面积显著降低。然而,Fasn 和 Scd-1 的 mRNA 水平显著升高,Fasn 和 Scd-1 是肝脂肪酸合成过程中的关键基因。此外,肝脂肪酸摄取的两个关键基因 Fabp1 和 Fabp4 在 Cd 处理的小鼠中也被上调。有趣的是,肝脂蛋白分解的关键基因 Lpl 在 Cd 处理的小鼠中也被上调。总之,尽管本研究中没有观察到胰岛素抵抗和肝脂质积累,但我们的结果表明,镉暴露上调了与肝脂质代谢相关的基因的 mRNA 水平。