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Submitted on February 12, 2007
Accepted on April 20, 2007
Dipartimento di Scienze della Vita, Seconda Università degli Studi di Napoli, Via Vivaldi 43, 81100 Caserta, Italy; Dipartimento di Scienze Biologiche ed Ambientali, Università degli Studi del Sannio, Via Port'Arsa 11, 82100 Benevento, Italy; Dipartimento delle Scienze Biologiche, Sez. Fisiologia ed Igiene, Università degli Studi di Napoli "Federico II", Via Mezzocannone 8, 80134 Napoli, Italy; Departament de Bioquímica i Biologia Molecular. Universitat de Barcelona Avda Diagonal 645. 08028 Barcelona, Spain
* To whom correspondence should be addressed. E-mail: antonia.lanni{at}unina2.it.
T3 regulates energy metabolism by stimulating metabolic rate and decreasing metabolic efficiency. The discovery of mitochondrial uncoupling protein 3 (UCP3), its homology to UCP 1 and regulation by T3 rendered it a possible molecular determinant of the action of T3 on energy metabolism, but data are controversial. This controversy may in part be due to discrepancies observed between the regulation by T3 of UCP3 expression in rats, human and mice. To clarify this issue, we studied (a) the induction kinetics of the UCP3 gene by T3 in rat skeletal muscle, (b) the influence of fatty acids, and (c) the structure and regulation of the various UCP3 promoters by T3. Within 8 h of single-dose T3-administration, hypothyroid rats showed a rise in serum fatty acid levels concomitant with a rapid increase in UCP3 expression in gastrocnemius muscle, followed by inductions of PPAR 
(within 24 h) and PPAR target gene expression (after 24 h). This T3-induced early UCP3 expression depended on fatty acid-PPAR signaling since depleting serum fatty acid levels abolished its expression, restorable by administration of the PPAR agonist L165,041. In transfected rat L6 myoblasts only the rat UCP3 promoter positively responded to T3 and L165,041 together in the presence of MyoD, TR
1, PPAR or PPAR plus the TR dimerization partner RXR
. All promoters share a response element common to TR and PPAR (TRE 1), but the observed species differences may be due to different localizations of the MyoD response element, which in the rat maps to exon 1.
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