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Originally published In Press as doi:10.1074/jbc.M207281200 on September 19, 2002

J. Biol. Chem., Vol. 277, Issue 48, 45874-45879, November 29, 2002
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Acylation-stimulating Protein (ASP) Deficiency Induces Obesity Resistance and Increased Energy Expenditure in ob/ob Mice*

Zhunan Xia, Allan D. Sniderman, and Katherine CianfloneDagger

From the Mike Rosenbloom Laboratory for Cardiovascular Research, McGill University Health Center, Montreal, Quebec H3A 1A1, Canada

Acylation-stimulating protein (ASP) acts as a paracrine signal to increase triglyceride synthesis in adipocytes. ASP administration results in more rapid postprandial lipid clearance. In mice, C3 (the precursor to ASP) knockout results in ASP deficiency and leads to reduced body fat and leptin levels. The protective potential of ASP deficiency against obesity and involvement of the leptin pathway were examined in ob/ob C3(-/-) double knockout mice (2KO). Compared with age-matched ob/ob mice, 2KO mice had delayed postprandial triglyceride and fatty acid clearance; associated with decreased body weight (4-17 weeks age: male: -13.7%, female: -20.6%, p < 0.0001) and HOMA (homeostasis model assessment) index (-37.7%), suggesting increased insulin sensitivity. By contrast, food intake in 2KO mice was +9.1% higher over ob/ob mice (p < 0.001, 2KO 5.1 ± 0.2 g/day, ob/ob 4.5 ± 0.2 g/day, wild type 2.6 ± 0.1 g/day). The hyperphagia/leanness was balanced by a 28.5% increase in energy expenditure (oxygen consumption: 2KO, 131 ± 8.9 ml/h; ob/ob, 102 ± 4.5 ml/h; p < 0.01; wild type, 144 ± 8.9 ml/h). These results suggest that the ASP regulation of energy storage may influence energy expenditure and dynamic metabolic balance.

* This work was supported by a grant from Natural Sciences and Engineering Research Council of Canada (NSERC) (to K. C.) and by ServierPharmaceuticals (to A. D. S.).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.

Dagger Supported by a scholarship from the Fonds de la Recherche en Santé du Québec (FRSQ). To whom correspondence should be addressed: Cardiology, H7.30, Royal Victoria Hospital, 687 Pine Ave. W., Montreal, Quebec H3A 1A1, Canada. Tel.: 514-842-1231 (ext. 35426); Fax: 514-843-2843; E-mail: katherine.cianflone@mcgill.ca.

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