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Neurobiology of Binge-type Behavior

暴饮暴食行为的神经生物学

基本信息

批准号：
8444527
负责人：
REBECCA L CORWIN
金额：
$ 9.14万
依托单位：
PENNSYLVANIA STATE UNIVERSITY, THE
依托单位国家：
美国
项目类别：
财政年份：
2004
资助国家：
美国
起止时间：
2004-05-12 至 2013-08-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8444527
关键词：
Accounting Address Affect Amygdaloid structure Animal Model Anterior Anxiety Behavior Binge Eating Binge eating disorder Biological Neural Networks Body Weight decreased Bypass Comorbidity Consumption Cues Data Development Disease Dopamine Dopamine D1 Receptor Dopamine D2 Receptor Eating Fatty acid glycerol esters Feeding behaviors Female Food Goals Home environment Hypothalamic structure Impairment Intake Lateral Learning Lesion Ligands Macronutrients Nutrition Maintenance Maps Medial Midbrain structure Modeling Moods Neurobiology Nucleus Accumbens Obesity Obsessive compulsive behavior Operative Surgical Procedures Outcome Prefrontal Cortex Prevalence Process Prosencephalon Rattus Relapse Reporting Research Review Literature Signal Transduction Site Societies Substance Use Disorder Sucrose Surveys Testing United States Universities Weight Workplace bariatric surgery base binge type behavior cingulate cortex clinically relevant cost dopaminergic neuron effective therapy experience food consumption human subject male meetings preference programs public health relevance receptor response social sugar treatment strategy

项目摘要

DESCRIPTION (provided by applicant): Binge eating is a form of compulsive food intake in which short-term homeostatic control of meal size is periodically and dramatically compromised. About 14 million people in the United States engage in binge eating. Binge relapse rates are high, treatment options are limited and the high co-morbidity with other disorders makes treatment a particular challenge. Understanding the factors that contribute to the transition from casual to compulsive binge-type consumption of food is critical for the development of new and effective treatment strategies. What accounts for the loss of control that occurs during these brief, but extremely large meals? Bingeing is characterized by the intermittent, excessive consumption of forbidden foods that are typically high in fat and sugar. Data from an animal model we have developed indicate that intermittent consumption, in-and-of itself, contributes to bingeing. While the effect of intermittency on palatable food intake has been well characterized in our model, the reason why intermittency enhances intake has not. Such information would have clinical relevance, since most people binge intermittently. We hypothesize that rats with intermittent access to optional palatable foods "learn to binge", and that this process involves an integrated neural network composed of forebrain targets of midbrain dopamine projections, as well as functional alterations in D1 and D2 receptor actions. Data collected over the past project period using our model support this scenario, and suggest that the behavior of our bingeing rats is more compulsive than that of control rats, and that the response to dopamine ligands, as well as the involvement of dopamine projection sites, differ between these groups. The results we have obtained map nicely onto findings reported in human subjects; therefore, we believe that our model provides a reasonable way to begin to clarify some of the factors that contribute to the development and maintenance of binge-type eating. The Aims of the proposed research are to: 1) determine specific components of intermittent access that promote binge eating (cue predictability, binge experience, macronutrient composition of the food), 2) identify forebrain regions that are critical to the development of binge eating, and 3) determine the contributions of dopamine D1- and D2-like receptors to the binge intake. Binge eating is a form of compulsive food intake in which short-term homeostatic control of meal size is periodically and dramatically compromised. About 14 million people in the United States engage in binge eating. Binge relapse rates are high, treatment options are limited and the high co-morbidity with other disorders makes treatment a particular challenge. Understanding the factors that contribute to the transition from casual to compulsive binge-type consumption of food is critical for the development of new and effective treatment strategies.

描述（由申请人提供）：暴饮暴食是一种强迫性食物摄入的形式，在这种情况下，对食物量的短期内平衡控制会周期性地、戏剧性地受到损害。在美国，大约有1400万人暴饮暴食。暴饮暴食的复发率很高，治疗选择有限，与其他疾病的高合并症使治疗成为一项特别的挑战。了解导致从随意到强迫性暴饮暴食的转变的因素对于开发新的有效治疗策略至关重要。是什么导致了在这些短暂而又极其丰盛的一餐中发生的失控呢？暴饮暴食的特点是间歇性地、过量地食用通常高脂肪和高糖的违禁食物。我们开发的动物模型数据表明，间歇性消费本身就会导致暴饮暴食。虽然我们的模型已经很好地描述了间歇性对美味食物摄入的影响，但间歇性增加摄入的原因还没有。这些信息具有临床意义，因为大多数人都是间歇性暴食。我们假设，间歇性获得可选美味食物的大鼠“学会暴食”，这一过程涉及一个由前脑目标组成的综合神经网络，中脑多巴胺投射，以及D1和D2受体作用的功能改变。在过去的项目期间使用我们的模型收集的数据支持这一设想，并表明我们的大鼠的行为比对照组的大鼠更具强迫性，并且对多巴胺配体的反应，以及多巴胺投射位点的参与，在这些组之间是不同的。我们获得的结果与在人类受试者中报道的结果很好地吻合；因此，我们相信我们的模型提供了一种合理的方式来开始澄清导致暴饮暴食的发展和维持的一些因素。拟议研究的目的是：1)确定促进暴饮暴食的间歇性获取的特定成分（提示可预测性，暴饮暴食体验，食物的宏量营养素组成），2)确定对暴饮暴食发展至关重要的前脑区域，3)确定多巴胺D1和d2样受体对暴饮暴食的贡献。暴饮暴食是一种强迫性食物摄入的形式，在这种情况下，对食物量的短期内平衡控制会周期性地、戏剧性地受到损害。在美国，大约有1400万人暴饮暴食。暴饮暴食的复发率很高，治疗选择有限，与其他疾病的高合并症使治疗成为一项特别的挑战。了解导致从随意到强迫性暴饮暴食的转变的因素对于开发新的有效治疗策略至关重要。