| First Author | Ko KW | Year | 2009 |
| Journal | Biochim Biophys Acta | Volume | 1791 |
| Issue | 12 | Pages | 1133-43 |
| PubMed ID | 19651238 | Mgi Jnum | J:164855 |
| Mgi Id | MGI:4835398 | Doi | 10.1016/j.bbalip.2009.07.006 |
| Citation | Ko KW, et al. (2009) Es-x/Ces1 prevents triacylglycerol accumulation in McArdle-RH7777 hepatocytes. Biochim Biophys Acta 1791(12):1133-43 |
| abstractText | Mouse esterase-x/carboxylesterase 1 (Es-x/Ces1) is a close homolog of triacylglycerol hydrolase/carboxylesterase 3 (TGH/Ces3). Es-x possesses a conserved esterase/lipase active site motif, suggesting that like TGH it could play a role in hepatic triacylglycerol (TG) metabolism. McArdle-RH7777 cells stably transfected with Es-x cDNA accumulated significantly less TG and had increased production of acid-soluble metabolites (an indicator of beta-oxidation) during incubations with 0.4mM oleic acid when compared to empty vector or TGH cDNA transfected cells. Reduction of cellular TG persisted in the presence of esterase/lipase inhibitor E600 indicating that Es-x-mediated TG lowering can be largely explained by reduced partitioning of exogenous fatty acids to TG and increased redirection to beta-oxidation, rather than by increased TG turnover. Glycerol supplementation increased TG synthesis in both control and Es-x expressing cells to similar extent suggesting that Es-x expression did not reduce flux of metabolic intermediates through the glycerol-3-phosphate pathway. While Es-x expression reduced cellular TG levels, secretion of TG and apolipoprotein B remained unchanged when compared to control cells. Overall, these results suggest that Es-x limits hepatic TG accumulation by promoting beta-oxidation. |
