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J. Lipid Res.
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A more recent version of this article appeared on October 1, 2007

Papers In Press, published online ahead of print July 30, 2007
J. Lipid Res., doi:10.1194/jlr.M700279-JLR200
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Submitted on June 14, 2007
Revised on July 23, 2007
Accepted on July 30, 2007

CGI-58 facilitates mobilization of cytoplasmic triglyceride for lipoprotein secretion in hepatoma cells

J. Mark Brown, Soonkyu Chung, Akash Das, Gregory Shelness, Lawrence L. Rudel, and Liqing Yu

Pathology Section on Lipid Research, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1040

Corresponding Author: lyu{at}wfubmc.edu

Comparative Gene Identification-58 (CGI-58) is a member of alpha/beta-hydrolase family of proteins. Mutations in the human CGI-58 gene are associated with Chanarin-Dorfman syndrome, a rare autosomal recessive genetic disease in which excessive TG accumulation occurs in multiple tissues. In this study, we investigated the role of CGI-58 in cellular lipid metabolism in several cell models, and discovered a role for CGI-58 in promoting the packaging of cytoplasmic TG into secreted lipoprotein particles in hepatoma cells. Using both gain-of-function and loss-of-function approaches we have demonstrated that CGI-58 facilitates the depletion of cellular TG stores without altering cellular cholesterol or phospholipid accumulation. This depletion of cellular TG is due solely to augmented hydrolysis, while TG synthesis was not affected by CGI-58. Furthermore, CGI-58-mediated TG hydrolysis can be completely inhibited by known lipase inhibitors DEUP and E-600, but not by PCMB. Intriguingly, CGI-58-driven TG hydrolysis was coupled to increases in both fatty acid oxidation and secretion of TG. Collectively, this study reveals a role for CGI-58 in coupling lipolytic degradation of cytoplasmic TG to oxidation and packaging into TG-rich lipoproteins for secretion in hepatoma cells.


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