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Please use this identifier to cite or link to this item: http://hdl.handle.net/10171/17784

Title: Interactions between an alpha2-adrenergic antagonist and a beta3-adrenergic agonist on the expression of UCP2 and UCP3 in rats.
Other Titles: Interacciones entre un antagonista adrenérgico α2 y un agonista adrenérgico β3 en la expresión de UCP2 y UCP3 en ratas
Author(s) : Gomez-Ambrosi, J. (Javier)
Frühbeck, G. (Gema)
Martinez, J.A. (José Alfredo)
Issue Date: 2002
Publisher: Springer. The original publication is available at www.springerlink.com
Citation: Gomez-Ambrosi J, Fruhbeck G, Martinez JA. Interactions between an alpha2-adrenergic antagonist and a beta3-adrenergic agonist on the expression of UCP2 and UCP3 in rats. J Physiol Biochem 2002 Mar;58(1):17-23.
Keywords: Trecadrine
Yohimbine
β3-adrenoceptor
α2-adrenoceptor
Lipolysis
Thermogenesis
Abstract: This experimental trial was devised to assess whether selective β3-adrenergic receptor (AR) stimulation and simultaneous blockade of α2-AR would affect thermoregulation. With this purpose, the individual and combined administration of a β3-AR agonist, trecadrine, and an α2-AR antagonist, yohimbine, were evaluated. Yohimbine produced a marked decrease (p < 0.001) in body temperature one hour after administration (5 mg kg−1, i.p.) and blocked the thermogenic effect of trecadrine (1 mg kg−1, i.p.) when simultaneously administered. Uncoupling protein-2 expression in skeletal muscle was downregulated (p < 0.05) by trecadrine, while yohimbine had no effect. White adipose tissue UCP2 and muscle UCP3 were not modified by either trecadrine or yohimbine administration. Liver UCP2 mRNA expression was significantly decreased by yohimbine (p < 0.05). However, this downregulation does not seem to explain the reduction in temperature produced by yohimbine given the fact that trecadrine produced a similar downregulation of hepatic UCP2 (p < 0.05). The present work indicates that α2-AR antagonism blocks the thermogenic effects mediated by β3-AR stimulation, contrary to our expectations, suggesting a possible interplay between both mechanisms. Moreover, these effects are not apparently explained by changes in UCP2 and UCP3.
URI: http://hdl.handle.net/10171/17784
Publisher version (URL): http://www.springerlink.com/content/v43337361g286147/
Appears in Collections:DA - Medicina - Endocrinología - Artículos de revista
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DA - CIFA - Laboratorio de investigación metabólica - Artículos de Revista
DA - Farmacia - CAFT - Artículos de revista

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