Appetite Hormones in Binge Eating Disorder

肥胖症在全球范围内的流行程度继续上升。相当一部分肥胖受试者暴饮暴食 紊乱(卧床)，并大量进食，无需清除神经性暴食症。床，最常见的 饮食失调，会导致许多痛苦和痛苦。还有一群未被充分研究的瘦床。 易患肥胖症的个体。通过将它们包括在内，床的病理生理可以与肥胖分开。 人们对床的心理方面的研究要好于对生物方面的研究。在预赛中 研究表明，影响食欲的激素有差异，特别是刺激食欲的胃促生长素 食欲，在固定早餐前胃促生长素水平较低，肥胖患者早餐后胃促生长素水平下降较小 床上的对象。这一发现是违反直觉的，因为预计Ghrelin会更高。有可能是 BED患者的胃促生长素水平在晚上高于没有卧床的人，Ghrelin随时间自然增加 当大多数暴饮暴食发生的时候。在固定的晚间测试餐之后，应该也会有较小的下降 在床上的生长激素，这可能会导致更多的后续食物摄取。在36个床位和36个非床位受试者中， 按体重和性别平均划分，将研究与食欲有关的激素，包括生长激素，以及 GLP-1和PYY，在早晚固定餐后的2小时内。 然后，受试者将享受一顿临时晚餐，直到吃饱为止。预计在床上的摄入量会更大，特别是在 那天晚上。另一天将应用社会压力方案(Trier)来提高这些受试者的皮质醇水平。 预计在床上，皮质醇反应增强与更多的饥饿感和进食量有关。这 床上病理生理学模型假设进食开始时(晚上Ghrelin升高，以及 应激源后皮质醇升高)和停止进餐时(GLP-1、PYY降低，尤其是在晚上)。下一首, 几种急性干预措施中最有希望的：a)阻断皮质醇的产生，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，并通过纠正潜在的食欲-激素模式，确定 维持这种紊乱，并为新药治疗提供基础。公众：这项研究关注的是食欲 荷尔蒙可能会维持暴饮暴食障碍(BED)，对肥胖的人来说很常见。到时候我们会的 尝试纠正最不正常的食欲荷尔蒙，在床上测试一种新的药物治疗方法。

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.