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J. Biol. Chem., Vol. 283, Issue 1, 231-236, January 4, 2008

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Protein Kinase Cβ Deficiency Increases Fatty Acid Oxidation and Reduces Fat Storage^*

Rishipal R. Bansode, Wei Huang, Sanjit K. Roy, Madhu Mehta, and Kamal D. Mehta¹

From the Departments of Molecular and Cellular Biochemistry and Medicine, The Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University College of Medicine, Columbus, Ohio 43210

Metabolic syndrome is common in the general population, but there is little information available on the underlying signaling mechanisms regulating triglyceride (TG) content in the body. In the current study, we have uncovered a role for protein kinase Cβ (PKCβ) in TG homeostasis by studying the consequences of a targeted disruption of this kinase. PKCβ^-/- mutant mice were considerably leaner and the size of white fat depots was markedly decreased compared with wild-type littermates. TG content in the liver and skeletal muscle of PKCβ^-/- mice was also significantly low. Interestingly, mutant animals were hyperphagic and exhibited higher food intake and reduced feed efficiency versus wild type. The protection from obesity involves elevated oxygen consumption/energy expenditure and increased fatty acid oxidation in adipose tissue with concurrent increased mitochondria genesis, up-regulation of PGC-1 and UCP-2, and down-regulation of perilipin. The ability of PKCβ deficiency to promote fat burning in adipocytes may suggest novel therapeutic strategies for obesity and obesity-related disorders.

Received for publication, August 29, 2007 , and in revised form, October 10, 2007.

^* This work was supported by National Institutes of Health Grant HL079091. 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.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Table S1.

¹ To whom correspondence should be addressed: Dept. of Molecular and Cellular Biochemistry, The Dorothy M. Davis Heart and Lung Research Inst., The Ohio State University College of Medicine, 464 Hamilton Hall, 1645 Neil Ave., Columbus, OH 43210. Fax: 614-292-4118; E-mail: Mehta.80{at}osu.edu.

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