J. Lipid Res.
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A more recent version of this article appeared on October 1, 2006

Papers In Press, published online ahead of print July 30, 2006
J. Lipid Res., doi:10.1194/jlr.M600213-JLR200
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Submitted on May 15, 2006
Revised on July 24, 2006
Accepted on July 30, 2006

Short-term hepatic overexpression of DGAT1 or DGAT2 in female mice increases hepatic triglyceride synthesis without changing VLDL triglyceride or ApoB production

John S. Millar, Scot J. Stone, Uwe J. F. Tietge, Brian Tow, Jeffrey T. Billheimer, Jinny S. Wong, Robert L. Hamilton, Robert V. Farese . Jr, and Daniel J. Rader

Pharmacology, University of Pennsylvania, Philadelphia, PA 19104

Corresponding Author: jsmillar{at}mail.med.upenn.edu

Increased triglyceride synthesis resulting from enhanced flux of fatty acids into liver is frequently associated with VLDL overproduction. This has led to the common belief that hepatic triglyceride synthesis can directly modulate VLDL production. We used adenoviral vectors containing either murine DGAT1 or DGAT2 cDNA to determine the effect of a short-term increase in hepatic triglyceride synthesis on VLDL triglyceride and apoB production in female wild-type mice. Hepatic DGAT1 and DGAT2 overexpression in resulted in a 2.0-fold and 2.4-fold increase in the triglyceride content of liver, respectively. However, the increase in hepatic triglyceride content had no effect on the production rate of VLDL triglyceride or apoB in either case. Liver subfractionation showed that DGAT1 and DGAT2 overexpression significantly increased the content of cytoplasmic TG within the cytoplasmic lipid fraction with no change in the triglyceride content of the microsomal membrane or microsomal VLDL. The increased cytoplasmic triglyceride content was observed in electron micrographs of liver sections from mice overexpressing DGAT1 or DGAT2. Overexpression of DGAT1 or DGAT2 resulted in enhanced [3H]-glycerol tracer incorporation into triglyceride within cytoplasmic lipids. These results suggest that increasing the cytoplasmic triglyceride pool in hepatocytes does not directly influence VLDL TG or apoB production. In the presence of adequate cytoplasmic lipid stores, factors other than triglyceride synthesis are rate limiting for VLDL production.


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