Appetite Hormones in Binge Eating Disorder

暴食症中的食欲激素

基本信息

批准号：
7483499
负责人：
ALLAN GELIEBTER
金额：
$ 6.43万
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 2012-08-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7483499
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 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

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.

肥胖症在全球范围内的患病率持续增加。相当一部分肥胖受试者有暴饮暴食的情况暴食症（BED），吃大餐，但没有消除神经性贪食症。 BED，最常见的饮食失调会造成很多痛苦和困扰。还有一组正在研究的精益BED 有肥胖风险的人。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。在初步研究表明，影响食欲的激素存在差异，尤其是生长素释放肽，它会刺激食欲食欲，固定早餐前胃饥饿素水平较低，肥胖者饭后胃饥饿素水平下降较小 BED 科目。这一发现是违反直觉的，因为生长素释放肽预计会更高。有可能的是生长素释放肽在白天自然增加，在晚上，睡前的人比非睡前的人要高大多数暴饮暴食发生的时候。晚上固定测试餐后，下降幅度应该会更小 BED 中含有胃饥饿素，这可能会导致随后摄入更多食物。在 36 名 BED 受试者和 36 名非 BED 受试者中，将按体重和性别平分，研究与食欲相关的激素，包括生长素释放肽（ghrelin）和饱腹感肽、GLP-1和PYY，在早上和晚上固定膳食后2小时内。然后受试者将随意进食直至吃饱。 BED 的摄入量预计会更高，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 BED 病理生理学模型假定进餐开始时存在异常（晚上胃饥饿素较高，压力源后皮质醇升高）和进餐终止时（GLP-1、PYY 降低，尤其是晚上）。下一个，几种急性干预措施中最有希望的：a）阻止皮质醇的产生，b）PYY，或c） GLP-1 给药，将在研究 2 中实施。这些研究应有助于揭示 BED 病理生理学，并通过纠正潜在的食欲激素紊乱模式，确定什么维持疾病，并为新药物治疗提供基础。公众：这项研究的重点是食欲可能维持暴食症（BED）的激素，常见于肥胖者。我们随后将试图纠正最不正常的食欲激素，以测试BED的新药物治疗方法。