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

作者：Lo Vivien; Erickson Bruce; Thomason Hughes Michaela; Ko Kerry W S; Dolinsky Vernon W; Nelson Randy; Lehner Richard^*

来源：The Journal of Lipid Research, 2010, 51(2): 368-377.

DOI：10.1194/jlr.M000596

• lipase
• very low density lipoprotein
• endoplasmic reticulum
• beta-oxidation

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 beta-oxidation rather than for the assembly of lipoproteins.-Lo, V., B. Erickson, M. Thomason-Hughes, K. W. S. Ko, V. W. Dolinsky, R. Nelson, and R. Lehner. Arylacetamide deacetylase attenuates fatty-acid-induced triacylglycerol accumulation in rat hepatoma cells. J. Lipid Res. 2010. 51: 368-377

• 出版日期2010-2