Hunsinger R N, Wilson M C
Int J Obes. 1986;10(3):205-10.
Considerable interest has been recently expressed in the theory that there is a set point which is responsible for regulating body weight. Supporters of this theory propose that anorectics reduce such a set point, and that food consumption is then secondarily affected to achieve a new body weight. We report in this study data obtained in rats which favor the set point theory. The major support for this conclusion is derived from an experiment in which the 'appetite suppressor,' fenfluramine, was administered in a paradigm which dissociated its ability to reduce food intake from its capacity to decrease body weight. Under these conditions, the body weight of a control group increased by 17 g; whereas that of the fenfluramine group was reduced by 11 g. In general, the fenfluramine-treated subjects ate as much as the controls. However, the controls increased body weight; whereas, the treated subjects demonstrated a decrease rather than an increase in this parameter. This result suggests that the fenfluramine group did not gain weight because the drug-altered 'set point' was lower in this group than in the controls.
最近，关于存在一个负责调节体重的设定点的理论引起了人们极大的兴趣。该理论的支持者提出，厌食症患者会降低这样一个设定点，然后食物摄入量会受到次生影响，以达到新的体重。我们在本研究中报告了在大鼠身上获得的数据，这些数据支持设定点理论。这一结论的主要依据来自一项实验，在该实验中，“食欲抑制剂”芬氟拉明以一种将其减少食物摄入量的能力与其减轻体重的能力分离的模式给药。在这些条件下，对照组的体重增加了17克；而芬氟拉明组的体重减少了11克。一般来说，接受芬氟拉明治疗的受试者与对照组吃得一样多。然而，对照组体重增加；而接受治疗的受试者在这个参数上表现出下降而非增加。这一结果表明，芬氟拉明组没有增重是因为该组药物改变后的“设定点”低于对照组。
