Appetite Hormones in Binge Eating Disorder

肥胖症在全球范围内继续增加。相当一部分肥胖者有暴饮暴食的现象 疾病（床），并摄入大量的食物，没有清除贪食症神经。床，最常见的 饮食失调会导致很多痛苦和痛苦。还有一群被研究的瘦BED 有肥胖风险的个体。通过包括它们，BED的病理生理学可以与肥胖分开。 BED的心理学方面比生物学方面得到了更好的研究。初步 研究表明，影响食欲的激素存在差异，特别是生长激素释放肽， 食欲，在固定的早餐前胃促生长素水平较低，在肥胖的早餐后下降幅度较小。 BED科目。这一发现是违反直觉的，因为ghrelin预计会更高。有可能 生长激素释放肽在白天自然增加，在晚上睡觉的人比不睡觉的人高 大多数暴饮暴食发生的时间。在固定的晚间试餐之后， 在床上的ghrelin，这可能会导致更多的后续食物摄入。在36例卧床和36例非卧床受试者中， 将研究与食欲有关的激素，包括生长激素释放肽，以及与食欲有关的激素。 饱腹感肽、GLP-1和PYY，在早晨和晚上固定餐后2小时内。 然后受试者可自由进食直至吃饱。预计BED的摄入量会更大，尤其是在 傍晚将在另一天应用社会压力协议（特里尔），以提高这些受试者的皮质醇。 BED患者的皮质醇反应增强与更大的饥饿感和膳食摄入有关。这 BED病理生理学模型假定进餐开始（晚上较高的ghrelin， 应激后皮质醇升高）和进餐终止（GLP-1、PYY降低，尤其是在晚上）。接下来， 最有希望的几种急性干预措施：a）阻断皮质醇的产生，以及B）PYY，或c） GLP-1给药将在研究2中实施。这些研究应该有助于揭示BED 病理生理学，并通过纠正潜在的紊乱食欲激素模式，确定什么 维持这种紊乱，并为新的药物治疗提供基础。公众：这项研究的重点是食欲 可能维持暴食症（BED）的激素，肥胖个体中常见。然后我们将 试图纠正最不正常的食欲激素，以测试一种新的药物治疗方法在床上。

Obesity, continues to increase in prevalenceworldwide. A sizable subset of obese subjects has binge eating disorder (BED), and ingest large meals, without the purging of bulimia nervosa. BED, the mostcommon eating disorder, causes much suffering and distress. There is also a group of understudied lean BED individuals, at risk for obesity. By including them, the pathophysiologyof BED can be parceled from obesity. The psychological aspects of BED have been better studied than the biological aspects. In preliminary studies, there were differences in hormonesinfluencing appetite, especially ghrelin, which stimulates appetite, with lower ghrelin levels before a fixed morning meal and a smaller decline afterwardsin obese BED subjects. This finding was counterintuitive because ghrelin was expected to be higher. It is possible that ghrelin, which naturally increases over the day, is higher in BEDthan in non-BED individuals in the evening when most binge eating occurs. Following a fixed evening test meal, there should also be a smaller decline in ghrelin in BED, which may lead to more subsequent food intake. In 36 BED and 36 non-BED subjects, equally divided by weight and gender, appetite-related hormones, will be studied, including ghrelin, and the satiety peptides, GLP-1, and PYY,during 2 hours after a fixed meal in the morning and in the evening. Subjects will then have an ad libitum meal until full. The intake is expectedto be greater in BED, especially in the evening. A social stress protocol (Trier) will be applied on another day to raise cortisol in these subjects. An enhanced cortisol response asociated with greater hunger and meal intake is expected in BED. This model of BED pathophysiology posits abnormalities in both meal initiation (higher ghrelin in evening, and higher cortisol following a stressor) and in meal termination (lower GLP-1, PYY,especially in evening). Next, the most promising of several acute interventions: a) blocking cortisol production, and either b) PYY, or c) GLP-1 administration, will be implemented in Study 2. These studies should help reveal BED pathophysiology, and by correcting a potential disordered appetite-hormone pattern, determine what maintains the disorder, and provide a basis for new drug treatments. Public: This study focuses on appetite hormones that may maintain binge eating disorder (BED), commonin obese individuals. We will then attempt to correct the most abnormal appetite hormone to test a new drug treatment approach in BED.