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Originally published In Press as doi:10.1074/jbc.M108640200 on January 23, 2002

J. Biol. Chem., Vol. 277, Issue 15, 12946-12952, April 12, 2002
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Hormone-sensitive Lipase Deficiency in Mice Changes the Plasma Lipid Profile by Affecting the Tissue-specific Expression Pattern of Lipoprotein Lipase in Adipose Tissue and Muscle*

Guenter HaemmerleDagger , Robert ZimmermannDagger , Juliane G. StraussDagger , Dagmar KratkyDagger , Monika RiedererDagger , Gabriele Knipping§, and Rudolf ZechnerDagger

From the Dagger  Institute of Molecular Biology, Biochemistry, and Microbiology and the § Institute of Medical Biochemistry and Molecular Biology, University of Graz, Graz A-8010, Austria

Hormone-sensitive lipase (HSL) is believed to play an important role in the mobilization of fatty acids from triglycerides (TG), diglycerides, and cholesteryl esters in various tissues. Because HSL-mediated lipolysis of TG in adipose tissue (AT) directly feeds non-esterified fatty acids (NEFA) into the vascular system, the enzyme is expected to affect many metabolic processes including the metabolism of plasma lipids and lipoproteins. In the present study we examined these metabolic changes in induced mutant mouse lines that lack HSL expression (HSL-ko mice). During fasting, when HSL is normally strongly induced in AT, HSL-ko animals exhibited markedly decreased plasma concentrations of NEFA (-40%) and TG (-63%), whereas total cholesterol and HDL cholesterol levels were increased (+34%). Except for the increased HDL cholesterol concentrations, these differences were not observed in fed animals, in which HSL activity is generally low. Decreased plasma TG levels in fasted HSL-ko mice were mainly caused by decreased hepatic very low density lipid lipoprotein (VLDL) synthesis as a result of decreased NEFA transport from the periphery to the liver. Reduced NEFA transport was also indicated by a depletion of hepatic TG stores (-90%) and strongly decreased ketone body concentrations in plasma (-80%). Decreased plasma NEFA and TG levels in fasted HSL-ko mice were associated with increased fractional catabolic rates of VLDL-TG and an induction of the tissue-specific lipoprotein lipase (LPL) activity in cardiac muscle, skeletal muscle, and white AT. In brown AT, LPL activity was decreased. Both increased VLDL fractional catabolic rates and increased LPL activity in muscle were unable to provide the heart with sufficient NEFA, which led to decreased tissue TG levels in cardiac muscle. Our results demonstrate that HSL deficiency markedly affects the metabolism of TG-rich lipoproteins by the coordinate down-regulation of VLDL synthesis and up-regulation of LPL in muscle and white adipose tissue. These changes result in an "anti-atherogenic" lipoprotein profile.

* This work was supported by Grants SFB-F007, SFB-F701, SFB-F713, and P14309 of the "Austrian Fonds zur Förderung der Wissenschaftlichen Forschung" and by the BIOMED-2 program, PL-963324, from the European Union.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: Institute of Molecular Biology, Biochemistry and Microbiology, University of Graz, Heinrichstr. 31a, Graz A-8010, Austria. Tel.: +43-316-380-1900; Fax: +43-316-380-9016; E-mail: rudolf.zechner@kfunigraz.ac.at.

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