Feedback inhibition of DHCR24 by lipid accumulation such as cholesterol and fatty acids is possible in HPI cell, although further study will be needed. Collectively, we strongly suggest that desmosterol could be a new biomarker for liver steatosis. Enrichment of fatty acid pool was demonstrated in HPI cells. We speculate that was because of increase in the synthesis by the up-regulation of ACACA and/or because of decrease in the release by the down-regulation of DGAT1 and MTTP, both of which facilitate VLDL release. It is Verteporfin considered that downregulation of LIPC and up-regulation of PNPLA3 might be a negative feedback reaction against the excess amount of fatty acid pool, triacylglycerol and LD. Increase of desaturated fatty acids, which have more than 2 double bonds of carbons, were observed in the HPI cell. This could be elucidated mainly by the upregulation of SCD, an enzyme to catalyze desaturations. Since HCV core alone up-regulates SCD and accumulates NADH resulting in reductive status and enhancement of fatty acid desaturation, core protein might be most responsible also in HPI cell. Clomifene citrate Moreover, ethanol enhances HCV replication through lipid metabolism and elevated NADH/NAD+. Although NADH level was not elevated in the HPI cell, NADPH was more increased, indicating that NADPH might play a predominant role in the desaturation of fatty acids. Intriguingly, we observed that these cells were rich in 20-carbon fatty acids such as arachidonic acid, which is a precursor of inflammatory mediators, the so-called eicosanoids, and can cause chronic inflammation, inducing inflammatory signals around the cell. The Warburg effect is the well-established theory that cancer cells preferentially utilize glycolysis. However, in spite that HPI cells are originated form hepatocellular carcinoma, the TCA cycle was more activated than the glycolysis. Thus we speculate that, contrary to common cancers, hepatic cancer infected with HCV might preferentially utilize the TCA cycle in aerobic condition as previously reported. In fact, hepatic cancers are vascular-rich and prone to demand more oxygen.