Background and aims: Increased glycolysis in the presence of oxygen (Warburg effect) is commonly observed in rapidgrowing human cancer cells. Glucose transport across the plasma membrane, the first rate-limiting step for glucose metabolism, is mediated by glucose transporter (GLUT) proteins. However, the expression of class 1 GLUT family in hepatocellular carcinoma (HCC), typical glycolytic tumor, is not fully elucidated yet. In this study, alteration to expression of GLUT and uptake value of [18F]fluorodeoxyglucose positron emission tomography (FDG?PET) were evaluated in patients with HCC. Methods: Nineteen HCC tissues and matched non-tumorous liver tissues were obtained from surgical specimens of chronic hepatitis B patients. Levels of expressions of GLUT-1, GLUT-2 and GLUT-4 were quantified by qPCR and normalized to GAPDH. HBV pregenomic RNA of matched tissue samples were measured by real-time RT-PCR. Results: Expressions of GLUT-1 and GLUT-4 were up-regulated in 47% and 32%, respectively in HCC tissues compared to surrounding non-neoplastic tissue, whereas, GLUT-2, livertype glucose transporter, was suppressed in 47% of HCC. The concordance of enhancement or suppression between GLUT-1 and GLUT-4 was 16%. At least one glucose transporter was over-expressed in 14 patients (74%). There was no significant correlation between level of GLUT expression and FDG uptake value in FDG-PET imaging. Conclusions: About two-thirds of HBV-related HCC over-express class I GLUT. The GLUT over-expression may have an implication for specific regulation of metabolic phenotype in HCC.