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Originally published In Press as doi:10.1074/jbc.M009795200 on December 1, 2000

J. Biol. Chem., Vol. 276, Issue 9, 6343-6349, March 2, 2001
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Modulation of Circulating Leptin Levels by Its Soluble Receptor*

Lu HuangDagger §, Zhuowei WangDagger , and Cai LiDagger §||

From the Dagger  Touchstone Center for Diabetes Research, Departments of § Physiology and  Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas 75390-8854

Leptin is an adipocyte-derived hormone with potent weight reducing effects. Genetically obese rodents with mutations of leptin or the leptin receptor are defective in leptin signaling and develop morbid obesity and diabetes. Interestingly, the levels of both leptin mRNA and protein are increased by up to 20-fold in these animals, suggesting the existence of a feedback mechanism controlling the amount of leptin in circulation. In this report, we attempted to determine whether the up-regulation of circulating leptin in Zucker Diabetic Fatty rats, which are nonresponsive to leptin due to a receptor point mutation, is entirely due to increased expression of leptin. We demonstrate that the high level of circulating leptin in these rats is attributable to at least two factors: increased leptin expression by the adipose tissue and delayed clearance of leptin from circulation due to binding to its soluble receptor. The latter conclusion was supported by three lines of evidence: 1) The soluble leptin receptor is up-regulated by about 20-fold in Zucker Diabetic Fatty rats; 2) Adenovirus-mediated overexpression of the soluble leptin receptor results in a similar -fold increase of circulating leptin; 3) In ob/ob mice, which have no endogenous leptin, exogenously administered leptin reaches a higher level when the soluble leptin receptor is overexpressed. The weight-reducing effect of leptin is enhanced in C57Bl/6 ob/ob mice with overexpression of the soluble leptin receptor. Soluble leptin receptor may be a significant factor determining the amount of total leptin in circulation.

* This work was supported in part by a grant from Novo Nordisc A/S and Welch Foundation Grant I-1470.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.

|| Recipient of a career development award from the American Diabetes Association. To whom correspondence should be addressed: Touchstone Center for Diabetes Research, The University of Texas Southwestern Medical Center, 5323 H. Hines Blvd., Dallas, TX 75390-8854. Tel.: 214-648-3340; Fax: 214-648-9191; E-mail: Cai.Li@UTSouthwestern.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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