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Originally published In Press as doi:10.1074/jbc.C200362200 on July 31, 2002

J. Biol. Chem., Vol. 277, Issue 38, 34658-34661, September 20, 2002
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ACCELERATED PUBLICATION
Increased beta -Oxidation but No Insulin Resistance or Glucose Intolerance in Mice Lacking Adiponectin*

Ke Ma, Agatha Cabrero, Pradip K. Saha, Hideto Kojima, Lan Li, Benny Hung-Junn Chang, Antoni Paul, and Lawrence ChanDagger

From the Section of Endocrinology & Metabolism, Departments of Medicine and Molecular & Cellular Biology, Baylor College of Medicine and the St. Luke's Episcopal Hospital, Texas Medical Center, Houston, Texas 77030

Previous reports showed that recombinant fragments of adiponectin (adipo) displayed pharmacological effects when injected into rodents, but the relevance of these observations to the physiological function of adipo is unclear. We generated Adipo-/- mice by gene targeting. Adipo-/- mice are fertile with normal body and fat pad weights. Plasma glucose and insulin levels of Adipo-/- and Adipo+/+ mice are similar under fasting conditions and during an intraperitoneal glucose tolerance test (GTT). Insulin tolerance test (ITT) also produces similar plasma glucose and insulin levels in the two groups of mice. Hyperinsulinemic-euglycemic clamp analysis showed that Adipo-/- and Adipo+/+ mice have similar glucose infusion rates to maintain a similar serum glucose. High-fat diet feeding for 7 months led to similar weight gain and similar GTT and ITT responses. We next measured beta -oxidation and found it to be significantly increased in muscle and liver of Adipo-/- mice. In conclusion, our study indicates that absence of adipo causes increased beta -oxidation but does not cause glucose intolerance or insulin resistance in mice.


* This work was supported by National Institutes of Health Grants HL-51568 and HL-16512 and by a Betty Rutherford Chair for Diabetes Research (to L. C.).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.

Dagger To whom correspondence should be addressed: Division of Endocrinology & Metabolism, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030. Tel.: 713-798-4478; Fax: 713-798-8764; E-mail: lchan@bcm.tmc.edu.


Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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