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Gene. 2017 Jul 30;622:67-71. doi: 10.1016/j.gene.2017.04.024. Epub 2017 Apr 19.

The impact of exposure to environmental contaminant on hepatocellular lipid metabolism.

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Department of Endocrinology, Qilu Hospital of Shandong University, Jinan 250012, China.
Department of Anatomy and Histoembryology, Weifang Medical University, Weifang 261031, China.
Department of Endocrinology, Qilu Hospital of Shandong University, Jinan 250012, China. Electronic address:


Increasing evidences show that ubiquitous perfluorooctanoic acid (PFOA), a representative environmental pollutant, is found to be linked to lipid dysmetabolism. However, the biological mechanism behind this outcome remains uninvestigated. In the present study, we established the PFOA-injured liver in mice to explore the underlying mechanism associated with PFOA-induced lipid disturbance in the liver via a group of biochemical and molecular assays. As results, PFOA-exposed mice showed increased transaminase (ALT), reduced triglyceride and free fatty acid contents in serum, as well as elevated level of hepatic triglyceride. Morphologically, PFOA-exposed mice displayed visible vacuolation in cytoplasm and abnormal cytoarchitecture in liver. In addition, PFOA-exposed liver showed up-regulated expressions of lipid-uptake associated mRNA of hepatic lipoprotein lipase (LPL) and fatty acid translocase (CD36) and down-regulated expression of lipid-uptake associated mRNA of apolipoprotein-B100 (APOB). Moreover, validated data from immunohistochemistry and immunoblotting found that hepatocellular LPL and CD36 proteins were increased dose-dependently, and lowered expression of hepatic APOB was observed. In conclusion, our current findings reveal that PFOA-induced lipid dysmetabolism in the liver is involved to dysregulation of fatty acid trafficking.


Homeostasis; Lipid; Liver; PFOA

[Indexed for MEDLINE]

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