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. |