Perfluorooctanoic acid (PFOA), a kind of manufactured material, is widely accumulated around environmental system and into wildlife, including human beings. Toxicologically, PFOA induces hepatomegaly (liver enlargement) in the dose- and time-dependent manners. However, biological mechanism of hepatotoxicity warrants to be further investigated. In the present study, mature male mice were exposed to dosed PFOA for 21 days before conducting biochemical tests and immunoassays. As results, decreased fast blood glucose and elevated insulin contents were observed in PFOA-dosed mice. In addition, PFOA-dosed mice resulted in increased liver functional enzymes (GPT, GOT) in serum. And lipid contents (TG, lipoproteins) in serum and liver were changed abnormally. As shown in immunohistochemistry, increased insulin- and poly (ADP-ribose) polymerase (PARP)-positive cells were showed in PFOA-exposed pancreatic tissues. Moreover, CD36-positive cells were increased in PFOA-exposed livers, while ApoB-labeled cells were reduced. Further, immunoblot data showed that hepatocellular fibroblast growth factor 21 (FGF21) in PFOA-exposed liver was down-regulated dose-dependently. Taken together, our preliminary findings demonstrated that PFOA-induced hepatocellular lipotoxicity may be linked to impairing lipid-regulated proteins, as well as inducing insulin expression from pancreatic tissue.
Keywords: Lipids; Liver; Metabolism; PFOA; Pancreas.