Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/44369
Title: Developmental and tissue-specific involvement of peroxisome proliferator-activated receptor-alpha in the control of mouse uncoupling protein-3 gene expression.
Author: Pedraza González, Neus
Rosell Mañé, Meritxell
Villarroya i Terrade, Joan
Iglesias Coll, María del Rosario
Gonzalez, F.J.
Solanes Garcia, Gemma
Villarroya i Gombau, Francesc
Keywords: Transcripció genètica
Genètica molecular
Cèl·lules musculars
Obesitat
Genetic transcription
Molecular genetics
Muscle cells
Obesity
Issue Date: Oct-2006
Publisher: Association for the Study of Internal Secretions
Abstract: 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-α (PPARα) 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 PPARα-null mice both in basal conditions and under the stimulus of starvation. In contrast, UCP3 mRNA is down-regulated in adult heart both in fed and fasted PPARα-null mice. This occurs despite the increased levels of free fatty acids caused by fasting in PPARα-null mice. In neonates, PPARα-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 murine UCP3 promoter is activated by fatty acids through either PPARα or PPARδ but not by PPARγ or retinoid X receptor alone. PPARδ-dependent activation could be a potential compensatory mechanism to ensure appropriate expression of UCP3 gene in adult skeletal muscle in the absence of PPARα. However, among transcripts from other PPARα and PPARδ target genes, only those acutely induced by milk intake in wild-type neonates were altered in muscle or heart from PPARα-null neonates. Thus, PPARα-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.
Note: Reproducció del document publicat a: http://dx.doi.org/10.1210/en.2006-0226
It is part of: Endocrinology, 2006, vol. 147, num. 10, p. 4695-4704
Related resource: http://dx.doi.org/10.1210/en.2006-0226
URI: http://hdl.handle.net/2445/44369
ISSN: 0013-7227
Appears in Collections:Articles publicats en revistes (Bioquímica i Biomedicina Molecular)

Files in This Item:
File Description SizeFormat 
627029.pdf408.13 kBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.