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J. Biol. Chem., Vol. 278, Issue 35, 33370-33376, August 29, 2003
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Acquirement of Brown Fat Cell Features by Human White Adipocytes*
From the
Unité de Recherches sur les Obésités, Institut
National de la Santé et de la Recherche Médicale (INSERM)
Unité 586, Institut Louis Bugnard, Centre Hospitalier Universitaire de
Toulouse, Université Paul Sabatier, 31403 Toulouse, France and
Unité 9078, Centre National de la
Recherche Scientifique (CNRS), Faculté de Médecine
Necker-Enfants Malades, 75730 Paris, France
Obesity, i.e. an excess of white adipose tissue (WAT), predisposes
to the development of type 2 diabetes and cardiovascular disease. Brown
adipose tissue is present in rodents but not in adult humans. It expresses
uncoupling protein 1 (UCP1) that allows dissipation of energy as heat.
Peroxisome proliferator-activated receptor 
(PPAR) and
PPAR coactivator 1
(PGC-1) activate mouse UCP1
gene transcription. We show here that human PGC-1 induced the
activation of the human UCP1 promoter by PPAR.
Adenovirus-mediated expression of human PGC-1 increased the expression
of UCP1, respiratory chain proteins, and fatty acid oxidation enzymes in human
subcutaneous white adipocytes. Changes in the expression of other genes were
also consistent with brown adipocyte mRNA expression profile. PGC-1
increased the palmitate oxidation rate by fat cells. Human white adipocytes
can therefore acquire typical features of brown fat cells. The PPAR
agonist rosiglitazone potentiated the effect of PGC-1 on UCP1
expression and fatty acid oxidation. Hence, PGC-1 is able to direct
human WAT PPAR toward a transcriptional program linked to energy
dissipation. However, the response of typical white adipocyte targets to
rosiglitazone treatment was not altered by PGC-1. UCP1 mRNA
induction was shown in vivo by injection of the PGC-1
adenovirus in mouse white fat. Alteration of energy balance through an
increased utilization of fat in WAT may be a conceivable strategy for the
treatment of obesity.
Received for publication, May 19, 2003 , and in revised form, June 12, 2003.
* This work was supported by INSERM PROGRES Grant 4P007E. The costs of publication of this article were defrayed in part by the payment of page charges. This 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. Tel.: 33-562172950; Fax:
33-561331721; E-mail:
langin{at}toulouse.inserm.fr.
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