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Originally published In Press as doi:10.1074/jbc.M107914200 on December 19, 2001

J. Biol. Chem., Vol. 277, Issue 9, 7405-7411, March 1, 2002
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Inactive Lipoprotein Lipase (LPL) Alone Increases Selective Cholesterol Ester Uptake in Vivo, Whereas in the Presence of Active LPL It Also Increases Triglyceride Hydrolysis and Whole Particle Lipoprotein Uptake*

Martin MerkelDagger §, Jörg HeerenDagger , Wiebke DudeckDagger , Franz RinningerDagger , Herbert Radner, Jan L. Breslow||, Ira J. Goldberg**, Rudolf ZechnerDagger Dagger , and Heiner GretenDagger

From the Dagger  Department of Medicine, University Hospital Eppendorf, 20246 Hamburg, Germany, the  Department of Neuropathology, University of Bonn, Medical Center, 53105 Bonn, Germany, the Dagger Dagger  Institute of Molecular Biology, Biochemistry and Microbiology, Karl-Franzens University, 8010 Graz, Austria, the || Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York, New York 10021, and the ** Department of Medicine, Columbia University College of Physicians & Surgeons, New York, New York 10032

We have previously shown that transgenic expression of catalytically inactive lipoprotein lipase (LPL) in muscle (Mck-N-LPL) enhances triglyceride hydrolysis as well as whole particle lipoprotein and selective cholesterol ester uptake. In the current study, we have examined whether these functions can be performed by inactive LPL alone or require the presence of active LPL expressed in the same tissue. To study inactive LPL in the presence of active LPL in the same tissue, the Mck-N-LPL transgene was bred onto the heterozygous LPL-deficient (LPL1) background. At 18 h of age, Mck-N-LPL reduced triglycerides by 35% and markedly increased muscle lipid droplets. In adult mice, it reduced triglycerides by 40% and increased lipoprotein particle uptake into muscle by 60% and cholesterol ester uptake by 110%. To study inactive LPL alone, the Mck-N-LPL transgene was bred onto the LPL-deficient (LPL0) background. These mice die at ~24 h of age. At 18 h of age, in the absence of active LPL, inactive LPL expression did not diminish triglycerides nor did it result in the accumulation of muscle lipid droplets. To study inactive LPL in the absence of active LPL in the same tissue in adult animals, the Mck-N-LPL transgene was bred onto mice that only expressed active LPL in the heart (LPL0/He-LPL). In this case, Mck-N-LPL did not reduce triglycerides or increase the uptake of lipoprotein particles but did increase muscle uptake of chylomicron and very low density lipoprotein cholesterol ester by 40%. Thus, in the presence of active LPL in the same tissue, inactive LPL augments triglyceride hydrolysis and increases whole particle triglyceride-rich lipoprotein and selective cholesterol ester uptake. In the absence of active LPL in the same tissue, inactive LPL only mediates selective cholesterol ester uptake.

* This work was supported by the German Research Foundation (Deutsche Forschungsgemeinschaft) Grant Me-1507/2-1 (to M. M.). Histological preparations were supported by the Förderprogramm an den Medizinischen Einrichtungen Bonn (BONFOR 154/41) (to H. R.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ To whom correspondence should be addressed: Dept. of Internal Medicine, University Hospital Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany. Tel.: 49-40-42803-5542; Fax: 49-40-42803-8903; E-mail: merkel@uke.uni-hamburg.de.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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