PPARα activation is essential for HCV core protein–induced hepatic steatosis and hepatocellular carcinoma in mice
J. Clin. Invest. Naoki Tanaka, et al. 118:683 doi:10.1172/JCI33594 [Go to this article.]

Figure 2
Analyses of factors associated with hepatic fatty acid and triglyceride metabolism. (A) Expression of genes associated with fatty acid and triglyceride metabolism in 9-month-old mouse livers. Total RNA was extracted from each mouse liver, and mRNA levels were determined by RT-PCR. mRNA levels were normalized by those of GAPDH and subsequently normalized by those in Ppara^+/+ nontransgenic mice. Results are expressed as the mean ± SD (n = 6/group). *P < 0.05 compared with Ppara^+/+ nontransgenic mice; **P < 0.05 compared with Ppara^+/–:HCVcpTg mice; ^#P < 0.05 compared with Ppara^–/–:HCVcpTg mice. (B) Uptake of fatty acids in 9-month-old mouse livers. Liver slices obtained from 3 mice in each group were incubated in medium containing 0.8 mM [1-¹⁴C]palmitic acid for 7 h. Fatty acid uptake ability was estimated by the sum of palmitic acid converted to CO₂ and ketone bodies with that incorporated into total cellular lipids after incubation. The experiment was repeated 3 times. Results were normalized by those of Ppara^+/+ nontransgenic mice and expressed as the mean ± SD. (C) Plasma concentrations of free fatty acids, glucose, and insulin. After an overnight fast, blood was obtained from each mouse and the above variables were determined. Results are expressed as the mean ± SD (n = 6/group).