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Publication : Arylacetamide deacetylase attenuates fatty-acid-induced triacylglycerol accumulation in rat hepatoma cells.

First Author  Lo V Year  2010
Journal  J Lipid Res Volume  51
Issue  2 Pages  368-77
PubMed ID  19654421 Mgi Jnum  J:157422
Mgi Id  MGI:4430797 Doi  10.1194/jlr.M000596
Citation  Lo V, et al. (2010) Arylacetamide deacetylase attenuates fatty-acid-induced triacylglycerol accumulation in rat hepatoma cells. J Lipid Res 51(2):368-77
abstractText  Mobilization of hepatic triacylglycerol stores provides substrates for mitochondrial beta-oxidation and assembly of VLDLs; however, the identity of lipolytic enzymes involved in the regulation of this process remains largely unknown. Arylacetamide deacetylase (AADA) shares homology with hormone-sensitive lipase and therefore could potentially participate in hepatic lipid metabolism, including the regulation of hepatic triacylglycerol levels. We have established McArdle-RH7777 (rat hepatoma) cell lines stably expressing mouse AADA cDNA and performed metabolic labeling as well as lipid mass analyses. Expression of AADA cDNA in McArdle-RH7777 cells significantly reduced intracellular triacylglycerol levels and apolipoprotein B secretion and increased fatty acid oxidation. These results suggest that fatty acids released by AADA-mediated hydrolysis of lipids are channeled for -oxidation rather than for the assembly of lipoproteins.
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