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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.

Author information

1
Department of Endocrinology, Qilu Hospital of Shandong University, Jinan 250012, China.
2
Department of Anatomy and Histoembryology, Weifang Medical University, Weifang 261031, China.
3
Department of Endocrinology, Qilu Hospital of Shandong University, Jinan 250012, China. Electronic address: chenliqilu1@163.com.

Abstract

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.

KEYWORDS:

Homeostasis; Lipid; Liver; PFOA

PMID:
28431976
DOI:
10.1016/j.gene.2017.04.024
[Indexed for MEDLINE]

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