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J. Biol. Chem., Vol. 281, Issue 52, 40236-40241, December 29, 2006

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Adipose Triglyceride Lipase and Hormone-sensitive Lipase Are the Major Enzymes in Adipose Tissue Triacylglycerol Catabolism^*

Martina Schweiger¹, Renate Schreiber¹, Guenter Haemmerle, Achim Lass, Christian Fledelius, Poul Jacobsen, Hans Tornqvist^¶, Rudolf Zechner, and Robert Zimmermann²

From the Institute of Molecular Biosciences, University of Graz, A-8010 Graz, Austria, the Diabetes Research Unit, Novo Nordisk A/S, Novo Nordisk Park, DK-2706 Måløv, Denmark, and the ^¶Department of Clinical Sciences, Diabetes, and Endocrinology, Malmö University Hospital, Lund University, S-22100 Lund, Sweden

The mobilization of free fatty acids from adipose triacylglycerol (TG) stores requires the activities of triacylglycerol lipases. In this study, we demonstrate that adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) are the major enzymes contributing to TG breakdown in in vitro assays and in organ cultures of murine white adipose tissue (WAT). To differentiate between ATGL- and HSL-specific activities in cytosolic preparations of WAT and to determine the relative contribution of these TG hydrolases to the lipolytic catabolism of fat, mutant mouse models lacking ATGL or HSL and a mono-specific, small molecule inhibitor for HSL (76-0079) were used. We show that 76-0079 had no effect on TG catabolism in HSL-deficient WAT but, in contrast, essentially abolished free fatty acid mobilization in ATGL-deficient fat. CGI-58, a recently identified coactivator of ATGL, stimulates TG hydrolase activity in wild-type and HSL-deficient WAT but not in ATGL-deficient WAT, suggesting that ATGL is the sole target for CGI-58-mediated activation of adipose lipolysis. Together, ATGL and HSL are responsible for more than 95% of the TG hydrolase activity present in murine WAT. Additional known or unknown lipases appear to play only a quantitatively minor role in fat cell lipolysis.

Received for publication, August 22, 2006 , and in revised form, October 10, 2006.

^* This research was supported by Grant P18434 [GenBank] -B05 from the Austrian Fonds zur Förderung der wissenschaftlichen Forschung (FWF) and by a GOLD-Genomics of Lipid-associated Disorders (part of the Austrian Genome Project, "GEN-AU Genome Research in Austria") Grant from the Austrian Ministry for Education, Research, and Culture. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ These authors contributed equally to this work.

² To whom correspondence should be addressed: Inst. of Molecular Biosciences, University of Graz, Heinrichstrasse 31A, A-8010 Graz, Austria. Tel.: 43-316-3801900; E-mail: robert.zimmermann{at}uni-graz.at.

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