Gómez-Ambrosi J, Frühbeck G, Martínez J A
Departamento de Fisiología y Nutricion, Universidad de Navarra, Spain.
J Physiol Biochem. 2002 Mar;58(1):17-23. doi: 10.1007/BF03179834.
This experimental trial was devised to assess whether selective beta3-adrenergic receptor (AR) stimulation and simultaneous blockade of alpha2-AR would affect thermoregulation. With this purpose, the individual and combined administration of a beta-AR agonist, trecadrine, and an alpha2-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 alpha2-AR antagonism blocks the thermogenic effects mediated by beta3-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.
本实验旨在评估选择性β3 - 肾上腺素能受体(AR)刺激以及同时阻断α2 - AR是否会影响体温调节。为此,对β - AR激动剂曲卡君和α2 - AR拮抗剂育亨宾的单独及联合给药进行了评估。育亨宾给药(5 mg kg(-1),腹腔注射)1小时后体温显著下降(p < 0.001),且在同时给药时阻断了曲卡君(1 mg kg(-1),腹腔注射)的产热作用。曲卡君使骨骼肌中解偶联蛋白 - 2的表达下调(p < 0.05),而育亨宾无此作用。曲卡君和育亨宾给药均未改变白色脂肪组织UCP2和肌肉UCP3。育亨宾使肝脏UCP2 mRNA表达显著降低(p < 0.05)。然而,鉴于曲卡君对肝脏UCP2产生了类似的下调作用(p < 0.05),这种下调似乎无法解释育亨宾引起的体温降低。本研究表明,与我们的预期相反,α2 - AR拮抗作用阻断了β3 - AR刺激介导的产热作用,提示这两种机制之间可能存在相互作用。此外,这些作用显然无法通过UCP2和UCP3的变化来解释。