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This version published online on December 23, 2004
Molecular Endocrinology, doi:10.1210/me.2004-0343
A more recent version of this article appeared on April 1, 2005
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Submitted on September 1, 2004
Accepted on December 13, 2004

Deletion of the RII{beta} subunit of Protein Kinase A decreases body weight and increases energy expenditure in the obese, leptin-deficient ob/ob mouse

Kathryn J. Newhall, David E. Cummings, Michael A. Nolan, and G. Stanley McKnight*

Department of Pharmacology, University of Washington, Seattle, WA; Division of Metabolism, Endocrinology and Nutrition, University of Washington, Veterans Affairs Puget Sound Health Care System, Seattle, WA; Wyeth Research, Collegeville, PA

* To whom correspondence should be addressed. E-mail: mcknight{at}u.washington.edu.

Disruption of the RII{beta} regulatory subunit of Protein Kinase A (PKA) results in mice with a lean phenotype, nocturnal hyperactivity, and increased resting metabolic rate. In this report we have examined whether deletion of RII{beta} would lead to increased metabolism and rescue the obese phenotype of the leptin-deficient ob/ob (ob) mouse. Body-weight gain and food consumption were decreased, whereas basal oxygen consumption and nocturnal locomotor activity were increased in the double mutant animals compared with ob mice. The ob mice are unable to maintain body temperature when placed in a cold environment due to a loss of brown adipose tissue activation and this cold sensitivity was partially rescued by concomitant disruption of RII{beta}. These findings indicate that PKA modifies the phenotype of the leptin-deficient mouse leading to increases in both thermogenesis and energy expenditure.
Key words: PKA • obesity • ob/ob • energy expenditure • thermogenesis • uncoupling protein • BAT




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