Literature DB >> 20401538

[(Methyl)1-(11)c]-acetate metabolism in hepatocellular carcinoma.

Nicolas Salem1, Yu Kuang, David Corn, Bernadette Erokwu, Jeffrey A Kolthammer, Haibin Tian, Chunying Wu, Fangjing Wang, Yanming Wang, Zhenghong Lee.   

Abstract

PURPOSE: Studies have established the value of [(methyl)1-(11)C]-acetate ([(11)C]Act) combined with 2-deoxy-2[(18)F]fluoro-D-glucose (FDG) for detecting hepatocellular carcinoma (HCC) using positron emission tomography (PET). In this study, the metabolic fate of [(11)C]Act in HCC was characterized.
METHODS: Experiments with acetic acid [1-(14)C] sodium salt ([(14)C]Act) were carried out on WCH-17 cells and freshly derived rat hepatocytes. PET scans with [(11)C]Act were also carried out on woodchucks with HCC before injection of [(14)C]Act. The radioactivity levels in different metabolites were quantified with thin-layer chromatography.
RESULTS: In WCH-17 cells, the predominant metabolite was phosphatidylcholine (PC). Regions of HCCs with the highest [(11)C]Act uptake had higher radioactivity accumulation in lipid-soluble compounds than surrounding hepatic tissues. In those regions, PC and triacylglycerol (TG) accumulated more radioactivity than in surrounding hepatic tissues.
CONCLUSIONS: High [(11)C]Act uptake in HCC is associated with increased de novo lipogenesis. PC and TG are the main metabolites into which the radioactive label from [(11)C]Act is incorporated in HCC.

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Year:  2011        PMID: 20401538      PMCID: PMC4851171          DOI: 10.1007/s11307-010-0308-y

Source DB:  PubMed          Journal:  Mol Imaging Biol        ISSN: 1536-1632            Impact factor:   3.488


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