Appetite Hormones in Binge Eating Disorder

暴食症中的食欲激素

基本信息

批准号：
7212478
负责人：
ALLAN GELIEBTER
金额：
$ 33.33万
依托单位：
ST. LUKE'S-ROOSEVELT INST FOR HLTH SCIS
依托单位国家：
美国
项目类别：
财政年份：
2007
资助国家：
美国
起止时间：
2007-09-01 至 2012-12-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7212478
关键词：
Acute Air Appetite Disorder Appetite Regulation Area BES Behavior Behavioral Binge Eating Binge eating disorder Biological Biological Factors Body Composition Body Weight Body fat Bulimia Categories Cholecystokinin Clinical Research Comparative Study Condition Consumption Cross-Over Studies Desire for food Diagnostic Disease Disinhibition Distress Double-Blind Method Eating Eating Behavior Eating Disorders Emotional Endocrinology Energy Intake Exhibits Fasting Fatty acid glycerol esters Food Functional disorder Gastric Emptying Gender Glucose Height Hormones Hour Human Hunger Hydrocortisone Individual Infusion procedures Insulin Intake Intervention Laboratories Lead Leptin Magnetic Resonance Imaging Maintenance Measurement Measures Mediator of activation protein Mental Depression Methods Metyrapone Modeling National Institute of Diabetes and Digestive and Kidney Diseases Obesity Pattern Peptides Peripheral Pharmaceutical Preparations Pharmacological Treatment Placebo Control Placebos Plasma Prevalence Principal Investigator Production Protocols documentation Psychological Factors Psychology Questionnaires Rate Reporting Research Personnel Residual state Satiation Science Score Stress Testing United States National Institutes of Health Visceral Week Weight anorexigenic peptide base biological adaptation to stress blind day desire falls ghrelin glucagon-like peptide 1 improved increased appetite interest men obesity risk placebo controlled study prevent programs psychologic purge response restraint size social social stress stressor subcutaneous

项目摘要

DESCRIPTION (provided by applicant): Obesity continues to increase in prevalence worldwide. A sizable subset of obese subjects has binge eating disorder (BED), and ingest large meals, without the purging of bulimia nervosa. BED, the most common 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 pathophysiology of 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 hormones influencing appetite, especially ghrelin, which stimulates appetite, with lower ghrelin levels before a fixed morning meal and a smaller decline afterwards in 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 BED than 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 expected to 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 associated 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), common in obese individuals. We will then attempt to correct the most abnormal appetite hormone to test a new drug treatment approach in BED.

描述（由申请人提供）：全世界肥胖的患病率持续增加。相当多的肥胖受试者患有暴食症（BED），他们吃大餐，但神经性贪食症却没有得到根除。暴食症是最常见的饮食失调症，会造成很多痛苦和困扰。还有一群尚未得到充分研究的偏瘦的暴饮暴食者，也面临着肥胖的风险。通过将它们纳入其中，暴饮暴食的病理生理学可以与肥胖区分开来。 BED 的心理方面比生物学方面得到了更好的研究。在初步研究中，影响食欲的激素存在差异，尤其是刺激食欲的生长素释放肽，肥胖的暴饮暴食者在固定早餐前的生长素释放肽水平较低，而随后的下降幅度较小。这一发现是违反直觉的，因为生长素释放肽预计会更高。白天自然增加的生长素释放肽可能在暴饮暴食发生的晚上，在暴饮暴食者中比非暴饮暴食者更高。在固定的晚上测试膳食之后，BED 中的生长素释放肽也应该有较小的下降，这可能会导致随后摄入更多的食物。将在 36 名暴食症受试者和 36 名非暴食症受试者中，按体重和性别等分，在固定膳食后 2 小时内研究与食欲相关的激素，包括生长素释放肽、饱腹感肽、GLP-1 和 PYY。早上和晚上。然后受试者将随意进食直至吃饱。预计睡前摄入量会更高，尤其是在晚上。另一天将应用社会压力方案（特里尔）来提高这些受试者的皮质醇。 BED 患者的皮质醇反应增强，与饥饿感和进餐量增加相关。这种 BED 病理生理学模型假定进餐开始（晚上生长素释放肽升高，应激源后皮质醇升高）和进餐终止（GLP-1、PYY 降低，尤其是晚上）出现异常。接下来，研究 2 将实施几种急性干预措施中最有希望的一种：a) 阻断皮质醇产生，以及 b) PYY 或 c) GLP-1 给药。这些研究应有助于揭示 BED 病理生理学，并通过纠正潜在的 BED 病理生理学。紊乱的食欲激素模式，确定维持这种紊乱的原因，并为新的药物治疗提供基础。公众：这项研究的重点是可能维持暴食症（BED）的食欲激素，暴食症在肥胖者中很常见。然后，我们将尝试纠正最异常的食欲激素，以测试新的 BED 药物治疗方法。