| First Author | Wei E | Year | 2007 |
| Journal | J Lipid Res | Volume | 48 |
| Issue | 12 | Pages | 2597-606 |
| PubMed ID | 17878493 | Mgi Jnum | J:130000 |
| Mgi Id | MGI:3770562 | Doi | 10.1194/jlr.M700320-JLR200 |
| Citation | Wei E, et al. (2007) Apolipoprotein B and triacylglycerol secretion in human triacylglycerol hydrolase transgenic mice. J Lipid Res 48(12):2597-606 |
| abstractText | Apolipoprotein B (apoB)-containing lipoproteins play a critical role in whole body lipid homeostasis and the pathogenesis of atherosclerosis. The assembly of hepatic apoB-containing lipoproteins, VLDL, is governed by the availability of lipids, including triacylglycerol (TG). The majority of TG associated with VLDL is derived from the hepatic cytoplasmic lipid stores by a process involving lipolysis followed by reesterification. Microsomal triacylglycerol hydrolase (TGH) has been demonstrated to play a role in the lipolysis/reesterification process. To evaluate the potential regulatory role of TGH in hepatic VLDL assembly, we developed inducible transgenic mice expressing a human TGH minigene under the control of the mouse metallothionein promoter. Induction of human TGH by zinc resulted in liver-specific expression of the enzyme associated with 3- to 4-fold increases in lipolytic activity that could be attenuated with a TGH-specific inhibitor. Augmented TGH activity led to increased secretion of newly synthesized apoB and plasma TG levels. These results suggest that increased hepatic expression of TGH leads to a more proatherogenic plasma lipid and apoB profile. |
