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J. Biol. Chem., Vol. 275, Issue 42, 33059-33067, October 20, 2000
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From the Departments of § Medicine and
The three known subtypes of
Central Leptin Regulates the UCP1 and ob
Genes in Brown and White Adipose Tissue via Different
-Adrenoceptor
Subtypes*
,§
Biochemistry and Molecular Biology, Division of
Gastroenterology and Hepatology, Medical University of South Carolina,
Charleston, South Carolina 29425 and ¶ Amgen Inc.,
Thousand Oaks, California 91320
-adrenoreceptors
(1-AR, 2-AR, and
3-AR) are differentially expressed in brown and white
adipose tissue and mediate peripheral responses to central modulation of sympathetic outflow by leptin. To assess the relative roles of the
-AR subtypes in mediating leptin's effects on adipocyte gene
expression, mice with a targeted disruption of the
3-adrenoreceptor gene (3-AR KO) were
treated with vehicle or the 1/2-AR
selective antagonist, propranolol (20 µg/g body weight/day) prior to
intracerebroventricular (ICV) injections of leptin (0.1 µg/g body
weight/day). Leptin produced a 3-fold increase in UCP1 mRNA in
brown adipose tissue of wild type (FVB/NJ) and 3-AR KO
mice. The response was unaltered by propranolol in wild type mice, but
was completely blocked by this antagonist in 3-AR KO
mice. In contrast, ICV leptin had no effect on leptin mRNA in
either epididymal or retroperitoneal white adipose tissue (WAT) from
3-AR KOs. Moreover, propranolol did not block the
ability of exogenous leptin to reduce leptin mRNA in either WAT
depot site of wild type mice. These results demonstrate that the
3-AR is required for leptin-mediated regulation of
ob mRNA expression in WAT, but is interchangeable with
the 1/2-ARs in mediating leptin's effect
on UCP1 mRNA expression in brown adipose tissue.
*
This work was supported by United States Public Health
Service Grants DK 53981 (to T. W. G.) and GM08716 (to S. P. C.) and by United States Department of Agriculture Research
Grant NRICGP/USDA 9800699 (to T. W. G.).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.
To whom correspondence should be addressed: 916-G Clinical
Science Bldg., Medical University of South Carolina, 96 Jonathan Lucas
St., Charleston, SC 29425. Tel.: 843-792-0206; Fax: 843-792-0200; E-mail: gettystw@musc.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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