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(Received for publication, June 11, 1996, and in revised form, August 27, 1996)
From the Brown adipose tissue (BAT) functions in
non-shivering and diet-induced thermogenesis via its capacity for
uncoupled mitochondrial respiration. BAT dysfunction in rodents is
associated with severe defects in energy homeostasis, resulting in
obesity and hyperglycemia. Here, we report that the nuclear receptor
peroxisome proliferator-activated receptor
Volume 271, Number 47,
Issue of November 22, 1996
pp. 29909-29914
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
Promotes Brown Adipocyte
Differentiation
,
,
,
,
,
,
Department of Medicine, Section of
Gastroenterology, University of Chicago, Chicago, Illinois 60637 and Departments of § Molecular Pharmacology,
¶ Pharmacology, 
Cell Biology, ** Molecular Biochemistry,
and Pathology, Glaxo Wellcome Research and
Development, Research Triangle Park, North Carolina 27709
(PPAR), a
prostaglandin-activated transcription factor recently implicated as a
central regulator of white adipose tissue differentiation, also
regulates brown adipocyte function. PPAR is abundantly expressed in
both embryonic and adult BAT. Treatment of CD-1 rats with the
PPAR-selective ligand BRL49653, an anti-diabetic drug of the
thiazolidinedione class, results in marked increases in the mass of
interscapular BAT. In vitro, BRL49653 induces the terminal
differentiation of the brown preadipocyte cell line HIB-1B as judged by
both changes in cell morphology and expression of uncoupling protein
and other adipocyte-specific mRNAs. These data demonstrate that
PPAR is a key regulatory factor in brown adipocytes and suggest that
PPAR functions not only in the storage of excess energy in white
adipose tissue but also in its dissipation in BAT.
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