Oleic acid induces the novel Apolipoprotein O and reduces mitochondrial membrane potential in chicken and human hepatoma cells

Non-alcoholic fatty liver disease (NAFLD) reflects a spectrum of chronic liver diseases characterized by hepatic fat accumulation. Apolipoprotein O (ApoO) is a new member of the apolipoprotein family that may play a role in lipid metabolism and mitochondrial electron transport activity. We hypothesized that hepatic expression of ApoO is tightly linked not only to diet-induced hepatosteatosis, but also to oxidative stress and hormones. Therefore, we compared the effects of lipid loading on ApoO regulation in chicken (LMH) with those in human (HepG2) hepatoma cells. Incubation with oleic acid (OA) induced triglyceride accumulation but did not affect cell viability. RT-qPCR and Western blot analyses showed significant increase in ApoO transcript and protein levels in both cell lines. Oxidative stress applied by H 2 O 2 revealed induction of ApoO in the same or even higher extent as monitored by OA. ApoO increased upon treatment with estrogen supporting the assumption that estrogen affects lipoprotein metabolism. Furthermore, both cell lines showed a significant decrease of the mitochondrial membrane potential upon incubation with OA. We assume that our findings support a role of ApoO as an effector of compromised mitochondrial function that likely accompanies the onset of NAFLD.