Nutritional Sciences Dept., College of Health and Human Development, The Pennsylvania State University, University Park, PA 16802, United States.
Physiol Behav. 2011 Jul 25;104(1):87-97. doi: 10.1016/j.physbeh.2011.04.041. Epub 2011 May 1.
Research has focused on understanding how overeating can affect brain reward mechanisms and subsequent behaviors, both preclinically and in clinical research settings. This work is partly driven by the need to uncover the etiology and possible treatments for the ongoing obesity epidemic. However, overeating, or non-homeostatic feeding behavior, can occur independent of obesity. Isolating the variable of overeating from the consequence of increased body weight is of great utility, as it is well known that increased body weight or obesity can impart its own deleterious effects on physiology, neural processes, and behavior. In this review, we present data from three selected animal models of normal-weight non-homeostatic feeding behavior that have been significantly influenced by Bart Hoebel's 40+-yr career studying motivation, feeding, reinforcement, and the neural mechanisms that participate in the regulation of these processes. First, a model of sugar bingeing is described (Avena/Hoebel), in which animals with repeated, intermittent access to a sugar solution develop behaviors and brain changes that are similar to the effects of some drugs of abuse, serving as the first animal model of food addiction. Second, another model is described (Boggiano) in which a history of dieting and stress can perpetuate further binge eating of palatable and non-palatable food. In addition, a model (Boggiano) is described that allows animals to be classified as having a binge-prone vs. binge-resistant behavioral profile. Lastly, a limited access model is described (Corwin) in which non-food deprived rats with sporadic limited access to a high-fat food develop binge-type behaviors. These models are considered within the context of their effects on brain reward systems, including dopamine, the opioids, cholinergic systems, serotonin, and GABA. Collectively, the data derived from the use of these models clearly show that behavioral and neuronal consequences of bingeing on a palatable food, even when at a normal body weight, are different from those that result from simply consuming the palatable food in a non-binge manner. These findings may be important in understanding how overeating can influence behavior and brain chemistry.
研究重点在于理解暴饮暴食如何影响大脑奖励机制以及随后的行为，包括临床前和临床研究环境。这项工作的部分驱动力来自于揭示当前肥胖症流行的病因和可能的治疗方法的需求。然而，暴饮暴食或非稳态进食行为可能独立于肥胖发生。将暴饮暴食的变量与体重增加的后果分离具有很大的作用，因为众所周知，体重增加或肥胖会对生理、神经过程和行为产生自身的有害影响。在这篇综述中，我们介绍了三个经过精心挑选的正常体重非稳态进食行为动物模型的数据，这些模型受到了 Bart Hoebel 40 多年来研究动机、进食、强化以及参与这些过程调节的神经机制的显著影响。首先，描述了一种糖暴食模型（Avena/Hoebel），其中反复间歇性地接触糖水的动物会发展出类似某些滥用药物的行为和大脑变化，这是第一个食物成瘾的动物模型。其次，描述了另一个模型（Boggiano），其中节食和压力的历史可以使进一步暴食美味和非美味食物的行为永久化。此外，还描述了一个允许将动物分类为具有暴食倾向与暴食抵抗行为特征的模型（Boggiano）。最后，描述了一个有限摄入模型（Corwin），其中非食物剥夺的大鼠间歇性地、有限地接触高脂肪食物会发展出暴食样行为。这些模型是在它们对大脑奖励系统的影响的背景下考虑的，包括多巴胺、阿片类物质、胆碱能系统、血清素和 GABA。总的来说，从使用这些模型中获得的数据清楚地表明，即使在正常体重的情况下，暴食美味食物对大脑的行为和神经元的影响与简单地以非暴食方式食用美味食物的影响不同。这些发现对于理解暴饮暴食如何影响行为和大脑化学物质可能很重要。
