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J. Biol. Chem., Vol. 280, Issue 11, 10034-10039, March 18, 2005

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Induction of Leptin Receptor Expression in the Liver by Leptin and Food Deprivation^*

Paul Cohen, Guoqing Yang¶||, Xinxin Yu¶||, Alexander A. Soukas, Cara S. Wolfish, Jeffrey M. Friedman**, and Cai Li¶||

From the Laboratory of Molecular Genetics, ^**Howard Hughes Medical Institute, The Rockefeller University, New York, New York 10021, ^¶Touchstone Center for Diabetes Research, ^||Department of Physiology, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas 75390-8854

Leptin resistance is a common feature of obesity and the metabolic syndrome. However, the regulated expression of the leptin receptor (Ob-R) has not been studied in detail. Expression profiling of liver mRNA in leptin-treated wild-type mice revealed a marked increase in leptin receptor mRNA levels, which had not previously been described. This was confirmed by isoform-specific real-time PCR, which showed a >25-fold increase in the mRNAs encoding the short forms (Ob-Ra, Ob-Rc) and a >10-fold increase in the mRNA encoding the long (Ob-Rb) form of the leptin receptor in liver. In parallel, we also observed induction of plasma-soluble leptin receptor (SLR) protein by leptin administration, pair feeding, and short term food restriction. However, induction of SLR by leptin is abolished in mice with selective deletion of Ob-R from liver using Cre-LoxP technology. These data suggest that the liver is a major source of Ob-R mRNA expression under conditions of negative energy balance. Membrane-bound Ob-R is then shed into the circulation as SLR. Our study thus reveals an unexpected role of the liver in modulating total circulating leptin levels and possibly its biological activity.

Received for publication, December 6, 2004 , and in revised form, January 10, 2005.

^* This work was supported by National Institutes of Health Grant DK60137 (to C. L.) and Medical Scientist Training Program Grant GM07739 (to P. C. and A. A. S.). 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.

These authors contributed equally to this work.

^¶¶ An investigator of the Howard Hughes Medical Institute. To whom correspondence may be addressed. Tel.: 212-327-8800; Fax: 212-327-7420; E-mail: friedj{at}mail.rockefeller.edu. ¶¶ To whom correspondence may be addressed. Tel.: 214-648-3340; Fax: 214-648-9191; E-mail: Cai.Li{at}UTSouthwestern.edu.

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