Hagan Mary M, Chandler Paula C, Wauford Pamela K, Rybak Rachel J, Oswald Kimberly D
Department of Psychology, Behavioral Neuroscience Division, University of Alabama at Birmingham, 35294-1170, USA.
Int J Eat Disord. 2003 Sep;34(2):183-97. doi: 10.1002/eat.10168.
Dieting and stress are etiological factors in eating disorders, and dieting strongly predicts stress-induced overeating in the nonclinical population. We developed an animal model of binge eating in sated rats that is evoked by stress, but only in rats with a history of caloric restriction and only if highly palatable food (HPF) is available after stress. This study investigated the effect of known binge triggers, a taste of HPF and of hunger, on this type of binge eating.
Female rats were cycled through the R/S protocol but this time were given just a taste of HPF with ad lib regular chow. After another R/S cycle, rats were stressed during restriction (while hungry) and were given HPF and chow.
Although binge eating did not occur if only chow was available after stress, just a taste of HPF sufficed to increase chow intake to more than 160% (p < 0.001) of rats with a history of restriction only, stress-only, or neither. Hunger increased the proportion of chow consumed by both restricted groups, but stress magnified this hunger-induced overeating by increasing HPF intake to 137% of restriction-only rats (p < 0.001).
These effects suggest that binge eating in this model is motivated by reward, not metabolic need, and parallels observations of binge triggers described in clinical binge-eating disorders. This strengthens the validity of using this animal model to target the physiology and treatment of eating disorders preceded by dieting and stress.
节食和压力是饮食失调的病因,节食能有力预测非临床人群中压力诱发的暴饮暴食。我们开发了一种饱足大鼠暴饮暴食的动物模型,该模型由压力诱发,但仅在有热量限制史的大鼠中出现,且只有在压力后提供高适口性食物(HPF)时才会发生。本研究调查了已知的暴饮暴食触发因素,即品尝HPF和饥饿,对这种类型暴饮暴食的影响。
对雌性大鼠采用禁食/再喂养(R/S)方案循环处理,但这次只给它们品尝HPF并随意提供常规食物。在另一个R/S循环后,在禁食期间(饥饿时)对大鼠施加压力,并给予HPF和常规食物。
尽管压力后仅提供常规食物时不会发生暴饮暴食,但仅品尝HPF就足以使仅有限制史、仅受压力或两者皆无的大鼠的常规食物摄入量增加到160%以上(p<0.001)。饥饿增加了两个限制组消耗的常规食物比例,但压力通过将HPF摄入量增加到仅有限制组大鼠的137%,放大了这种饥饿诱发的暴饮暴食(p<0.001)。
这些效应表明,该模型中的暴饮暴食是由奖励驱动的,而非代谢需求,这与临床暴饮暴食障碍中描述的暴饮暴食触发因素的观察结果相似。这增强了使用这种动物模型来针对节食和压力导致的饮食失调的生理机制及治疗方法进行研究的有效性。