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Originally published In Press as doi:10.1194/jlr.M700320-JLR200 on September 18, 2007

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Journal of Lipid Research, Vol. 48, 2597-2606, December 2007
Copyright © 2007 by American Society for Biochemistry and Molecular Biology

Apolipoprotein B and triacylglycerol secretion in human triacylglycerol hydrolase transgenic mice

Enhui Wei*, Mustafa Alam*, Fengcheng Sun{dagger}, Luis B. Agellon{dagger}, Dennis E. Vance{dagger} and Richard Lehner1,*,§

* Department of Pediatrics, Canadian Institutes of Health Research Group on the Molecular and Cell Biology of Lipids, University of Alberta, Edmonton, Alberta, Canada T6G 2S2
{dagger} Department of Biochemistry, Canadian Institutes of Health Research Group on the Molecular and Cell Biology of Lipids, University of Alberta, Edmonton, Alberta, Canada T6G 2S2
§ Department of Cell Biology, Canadian Institutes of Health Research Group on the Molecular and Cell Biology of Lipids, University of Alberta, Edmonton, Alberta, Canada T6G 2S2

Published, JLR Papers in Press, September 18, 2007.

1 To whom correspondence should be addressed. e-mail: richard.lehner{at}ualberta.ca

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.

Supplementary key words very low density lipoprotein • lipolysis • metallothionein • liver

Abbreviations: apoB, apolipoprotein B; DGAT, diacylglycerol acyltransferase; ER, endoplasmic reticulum; P-407, poloxamer-407; TG, triacylglycerol; TGH, triacylglycerol hydrolase


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