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Originally published In Press as doi:10.1074/jbc.C100189200 on May 23, 2001

J. Biol. Chem., Vol. 276, Issue 28, 25651-25653, July 13, 2001
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ACCELERATED PUBLICATION
Adipose Tissue Resistin Expression Is Severely Suppressed in Obesity and Stimulated by Peroxisome Proliferator-activated Receptor gamma  Agonists*

James M. WayDagger §, Cem Z. Görgün§, Qiang Tong, K. Teoman Uysal, Kathleen K. BrownDagger , W. Wallace HarringtonDagger , William R. Oliver Jr.Dagger , Timothy M. WillsonDagger , Steven A. KliewerDagger , and Gökhan S. Hotamisligil||

From Dagger  GlaxoSmithKline Research and Development, Research Triangle Park, North Carolina 27709 and  Division of Biological Sciences and Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts 02115

Elevated levels of the hormone resistin, which is secreted by fat cells, are proposed to cause insulin resistance and to serve as a link between obesity and type 2 diabetes. In this report we show that resistin expression is significantly decreased in the white adipose tissue of several different models of obesity including the ob/ob, db/db, tub/tub, and KKAy mice compared with their lean counterparts. Furthermore, in response to several different classes of antidiabetic peroxisome proliferator-activated receptor gamma  agonists, adipose tissue resistin expression is increased in both ob/ob mice and Zucker diabetic fatty rats. These data demonstrate that experimental obesity in rodents is associated with severely defective resistin expression, and decreases in resistin expression are not required for the antidiabetic actions of peroxisome proliferator-activated receptor gamma  agonists.


* This work was supported in part by Grant DK52539 from the National Institutes of Health (to G. S. H.).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.

§ Contributed equally.

|| To whom correspondence should be addressed: Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115. Tel.: 617-432-1950; Fax: 617-432-1941; E-mail: ghotamis@hsph.harvard.edu.


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


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