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Originally published In Press as doi:10.1074/jbc.M910177199 on March 22, 2000

J. Biol. Chem., Vol. 275, Issue 21, 16251-16257, May 26, 2000
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Lack of Obesity and Normal Response to Fasting and Thyroid Hormone in Mice Lacking Uncoupling Protein-3*

Da-Wei GongDagger §, Shadi Monemdjou§||, Oksana GavrilovaDagger , Lisa R. LeonDagger , Bernice Marcus-SamuelsDagger , Chieh J. ChouDagger , Carrie EverettDagger , Leslie P. Kozak**, Cuiling LiDagger Dagger , Chuxia DengDagger Dagger , Mary-Ellen Harper||§§, and Marc L. ReitmanDagger §§

From the Dagger  Diabetes Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, || Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada, ** Pennington Biomedical Research Center, Baton Rouge, Louisiana 70808, and Dagger Dagger  Mammalian Genetics Section, Genetics of Development and Disease Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892

Uncoupling protein-3 (UCP3) is a mitochondrial protein that can diminish the mitochondrial membrane potential. Levels of muscle Ucp3 mRNA are increased by thyroid hormone and fasting. Ucp3 has been proposed to influence metabolic efficiency and is a candidate obesity gene. We have produced a Ucp3 knockout mouse to test these hypotheses. The Ucp3 (-/-) mice had no detectable immunoreactive UCP3 by Western blotting. In mitochondria from the knockout mice, proton leak was greatly reduced in muscle, minimally reduced in brown fat, and not reduced at all in liver. These data suggest that UCP3 accounts for much of the proton leak in skeletal muscle. Despite the lack of UCP3, no consistent phenotypic abnormality was observed. The knockout mice were not obese and had normal serum insulin, triglyceride, and leptin levels, with a tendency toward reduced free fatty acids and glucose. Knockout mice showed a normal circadian rhythm in body temperature and motor activity and had normal body temperature responses to fasting, stress, thyroid hormone, and cold exposure. The base-line metabolic rate and respiratory exchange ratio were the same in knockout and control mice, as were the effects of fasting, a beta 3-adrenergic agonist (CL316243), and thyroid hormone on these parameters. The phenotype of Ucp1/Ucp3 double knockout mice was indistinguishable from Ucp1 single knockout mice. These data suggest that Ucp3 is not a major determinant of metabolic rate but, rather, has other functions.

* 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.

§ These authors contributed equally to this work.

Current address: Division of Endocrinology, Diabetes and Nutrition, University of Maryland School of Medicine, Baltimore, MD 21201.

§§ To whom correspondence should be addressed: Bldg. 10, Rm. 8N-250, Diabetes Branch, NIDDK, NIH, Bethesda, MD 20892-1770. Tel.: 301-496-6090; Fax: 301-402-0573; E-mail: mlr@helix.nih.gov (to M. Reitman); Dept. of Biochemistry, Microbiology and Immunology, University of Ottawa, 451 Smyth Road, Ottawa, Ontario K1H 8M5, Canada. Tel.: 613-562-5800 (ext. 8235); Fax: 613-562-5440; E mail: mharper{at}uottawa.ca (to M. E. Harper).

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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