Racotta I S, Cabanac M, Lafrance L
Departamento de Fisiologia, Escuela Nacional de Ciencias, Biologicas, IPN, Mexico, D.F., Mexico.
Physiol Behav. 1995 Jul;58(1):125-30. doi: 10.1016/0031-9384(95)00004-3.
The purpose of this study was to determine whether the anorexia following epinephrine and glucose IP injections is due to the activation of mechanisms of satiety. Epinephrine (100 micrograms.kg-1) and glucose (4 g.kg-1) were injected IP in rats. In control sessions for epinephrine test, rats received IP saline, and IM epinephrine. In control sessions for the glucose test, rats received IP NaCl, isoosmotic to the glucose solution. Food intake or taste reactivity to a sucrose solution was recorded after these treatments. Epinephrine and glucose decreased food intake by 75% (p < 0.001), and 49% (p < 0.01), compared to their controls. No change of taste reactivity responses was observed with any of these treatments. Twelve-hour fasting did not modify the general taste reactivity responses when compared to the responses evoked in rats fed ad lib. These results might be explained by the fact that anorexia could be obtained by a suppression of hunger without the activation of the mechanisms of satiety. This in turn would imply a possible dissociation between the signals and physiological pathways normally involved in hunger and satiety.
本研究的目的是确定经腹腔注射肾上腺素和葡萄糖后出现的厌食是否归因于饱腹感机制的激活。给大鼠腹腔注射肾上腺素（100微克·千克⁻¹）和葡萄糖（4克·千克⁻¹）。在肾上腺素测试的对照实验中，大鼠接受腹腔注射生理盐水和肌肉注射肾上腺素。在葡萄糖测试的对照实验中，大鼠接受腹腔注射与葡萄糖溶液等渗的氯化钠溶液。在这些处理后记录食物摄入量或对蔗糖溶液的味觉反应性。与各自的对照组相比，肾上腺素和葡萄糖使食物摄入量分别减少了75%（p < 0.001）和49%（p < 0.01）。这些处理均未观察到味觉反应性的变化。与自由进食大鼠所引发的反应相比，禁食12小时并未改变总体味觉反应性。这些结果可能是由于厌食可能是通过抑制饥饿而不激活饱腹感机制获得的。这反过来意味着在正常参与饥饿和饱腹感的信号与生理途径之间可能存在分离。
