SEROTONIN FUNCTION IN PATIENTS WITH EATING DISORDERS

描述(改编自申请者摘要)：饮食失调 神经性暴食症和神经性厌食症是严重的精神症状。 影响2%至3%的年轻女性，虽然规模较小，但意义重大 年轻人的数量。患有神经性暴食症或神经性厌食症的女性 中枢神经系统5-羟色胺调节明显异常 (中枢神经系统)神经递质参与食物摄入量、情绪和 冲动/强迫症行为。当前项目的目标是 评估5-羟色胺调节反射异常是否反映 与特征相关的特征表现在饮食不良的个体身上 无序。 反复节食是神经性暴食症和厌食症的常见先兆 神经质。在健康对照组中，节食会降低血液中的色氨酸水平， 导致中枢神经系统5-羟色胺合成明显减少。通常， 5-羟色胺能通路通过增强而对节食作出反应 突触后受体反应性。据推测，在女性中 具有进食障碍的神经生物学易感性，中枢神经系统受体 没有足够的反应来补偿与饮食相关的减少 在5-羟色胺的合成中。这一缺陷可能导致 进食障碍症状。 研究小组将包括从神经性贪食症中恢复过来的女性， 已从神经性厌食症中恢复的女性，以及健康的女性对照组。 基于随机、受控、交叉设计，受试者将 参加为期八天的低色氨酸和正常色氨酸研究饮食。 与对照组的结果相比，长期缓解的患者组 预计对低色氨酸饮食的反应显著 饮食受损导致右芬氟拉明刺激的催乳素增加 回应。间接测量对饮食的生理/代谢反应 包括血瘦素浓度在内的变化将在研究中进行比较 组。这些研究将提供重要的新信息 节食和5-羟色胺在进食发展中的潜在作用 精神错乱。

DESCRIPTION (Adapted from the Applicant's Abstract): The eating disorders bulimia nervosa and anorexia nervosa are serious psychiatric syndromes affecting 2 to 3 percent of young women, and significant although smaller number of young men. Women with bulimia nervosa or anorexia nervosa manifest abnormalities in regulation of serotonin, a central nervous system (CNS) neurotransmitter involved in regulation of food intake, mood and impulsive/obsessional behaviors. The goal of the current project is to evaluate whether abnormalities in serotonin regulation reflection reflect trait-related characteristics present in individuals who develop an eating disorder. Recurrent dieting is a frequent precursor to bulimia nervosa and anorexia nervosa. In healthy controls, dieting decreases blood tryptophan levels, resulting in an apparent decrease in CNS serotonin synthesis. Normally, serotonergic pathways are though to respond to dieting through augmentation of post-synaptic receptor responsiveness. It is hypothesized that in women with a neurobiological predisposition to eating disorders, CNS receptors are not able to respond adequately to compensate for diet-associated decreases in serotonin synthesis. This deficiency could contribute to the onset of eating disorder symptoms. Study groups will include women who have recovered from bulimia nervosa, women who have recovered from anorexia nervosa, and healthy female controls. Based on a randomized, controlled, crossover design, subjects will participate in low-tryptophan and normal tryptophan eight-day study diets. In comparison to results in controls, the long-term remitted patient groups are anticipated to respond to a low-tryptophan diet with significantly impaired diet-induced augmentation of dexfenfluramine-stimulated prolactin response. Indirect measures of physiological/metabolic response to dietary changes, including blood leptin concentration, will be compared across study groups. These studies will provide important new information on the potential roles of dieting and serotonin in the development of eating disorders.