Metabolic Alteration in Hepatocellular Carcinoma: Mechanism of Lipid Accumulation in Well-Differentiated Hepatocellular Carcinoma

Figure 2

Metabolic gene expressions in each liver disease sate in human liver samples. Quantitative RT-PCR analysis of metabolic genes related to (a) glycolysis, (b) TCA cycle, (c) FA synthesis and uptake, (d) TG synthesis, and (e) β-oxidation, by liver disease states. The gene expression levels normalized to those of normal control tissues were presented as mean ± SE. and vs. normal control tissue. NC, normal control; CH, chronic hepatitis; LC, liver cirrhosis; HCC, hepatocellular carcinoma; G6PD, glucose-6-phosphate dehydrogenase; PK, pyruvate kinase; PDH, pyruvate dehydrogenase; ACO, aconitase; FAS, fatty acid synthase; PPAR, peroxisome proliferator-activated receptor; DGAT, diacylglycerol acyltransferase; LCAD, long chain acyl-coenzyme A dehydrogenase; HADH, hydroxyacyl-coenzyme A dehydrogenase.

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