| dc.contributor.author |
Pedraza González, Neus |
| dc.contributor.author |
Rosell, Meritxell |
| dc.contributor.author |
Villarroya, Joan |
| dc.contributor.author |
Iglesias, Roser |
| dc.contributor.author |
Gonzalez, Frank J. |
| dc.contributor.author |
Solanes, Gemma |
| dc.contributor.author |
Villarroya, Francesc |
| dc.date |
2017-01-18T11:15:58Z |
| dc.date |
2006 |
| dc.date |
10000-01-01 |
| dc.identifier |
0013-7227 |
| dc.identifier |
http://hdl.handle.net/10459.1/59021 |
| dc.identifier |
https://doi.org/10.1210/en.2006-0226 |
| dc.identifier.uri |
http://hdl.handle.net/10459.1/59021 |
| dc.description |
Uncoupling protein-3 (UCP3) is a member of the mitochondrial
carrier family expressed preferentially in skeletal muscle
and heart. It appears to be involved in metabolic handling
of fatty acids in a way that minimizes excessive production of
reactive oxygen species. Fatty acids are powerful regulators
of UCP3 gene transcription. We have found that the role of
peroxisome proliferator-activated receptor- (PPAR ) on the
control of UCP3 gene expression depends on the tissue and
developmental stage. In adults, UCP3 mRNA expression is
unaltered in skeletal muscle from PPAR -null mice both in
basal conditions and under the stimulus of starvation. In contrast,
UCP3mRNAis down-regulated in adult heart both in fed
and fasted PPAR -null mice. This occurs despite the increased
levels of free fatty acids caused by fasting in PPAR -
null mice. In neonates, PPAR -null mice show impaired UCP3
mRNA expression in skeletal muscle in response to milk intake,
and this is not a result of reduced free fatty acid levels.
The murineUCP3promoter is activated by fatty acids through
either PPAR or PPAR but not by PPAR or retinoid X receptor
alone. PPAR -dependent activation could be a potential
compensatory mechanism to ensure appropriate expression
of UCP3 gene in adult skeletal muscle in the absence of
PPAR . However, among transcripts from other PPAR and
PPAR target genes, only those acutely induced by milk intake
in wild-type neonates were altered in muscle or heart
from PPAR -null neonates. Thus, PPAR -dependent regulation
is required for appropriate gene regulation of UCP3 as
part of the subset of fatty-acid-responsive genes in neonatal
muscle and heart. |
| dc.description |
We thank Drs. S. Green, P. Grimaldi, R. Evans, and L. Fajas for kindly supplying expression vectors and Dr. Chandraratna for AGN 194204. Address all correspondence and requests for reprints to: Dr. G. Solanes, Departament de Bioquı´mica i Biologia Molecular, Universitat de Barcelona, Avda Diagonal 645, E-08028 Barcelona, Spain. E mail: gsolanes@ub.edu. This work was supported by Grants SAF2002-03648 and SAF2005- 01722 from Ministerio de Educacio´n y Ciencia and Grant C03/08 from Instituto de Salud Carlos III, Ministerio de Sanidad y Consumo, Spain. Disclosure of potential conflicts of interest: N.P., M.R., J.V., R.I., F.J.G., G.S., and F.V. have nothing to declare |
| dc.language |
eng |
| dc.publisher |
Endocrine Society |
| dc.relation |
MICYT/PN2000-2003/SAF2002-03648 |
| dc.relation |
MIECI/PN2004-2007/SAF2005-01722 |
| dc.relation |
Reproducció del document publicat a https://doi.org/10.1210/en.2006-0226 |
| dc.relation |
Endocrinology, 2006, vol. 147, núm. 10, p. 4695-4704 |
| dc.rights |
(c) The Endocrine Society, 2006 |
| dc.rights |
info:eu-repo/semantics/restrictedAccess |
| dc.title |
Developmental and Tissue-Specific Involvement of Peroxisome Proliferator-Activated Receptor-α in the Control of Mouse Uncoupling Protein-3 Gene Expression |
| dc.type |
article |
| dc.type |
publishedVersion |
