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fMRI and Ghrelin in Obesity and Binge Eating Disorder

fMRI and Ghrelin in Obesity and Binge Eating Disorder
fMRI 和 Ghrelin 在肥胖和暴食症中的作用
批准号:
7106137
负责人:
ALLAN GELIEBTER
金额:
$16.14万
依托单位国家:
美国
项目类别:
财政年份:
2006
资助国家:
美国
项目状态:
已结题
起止时间:
2006-09-30 至 2008-08-31

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项目成果

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中文摘要
翻译
描述(由申请人提供):在美国和全球范围内,肥胖症的患病率持续上升。肥胖导致发病率和死亡率增加,尤其是糖尿病和心脏病。大约30%寻求治疗的肥胖者患有暴食症(BED)。他们会像神经性贪食症患者一样,吃下大量的食物后不进行清理。BED是最常见的饮食失调症状,它会造成很多痛苦,并导致肥胖。虽然对BED的心理因素进行了研究,但对BED的生物学因素了解甚少。这项临床研究将重点关注饭后的脑成像和肠道激素,以检查BED和非BED受试者之间的差异。将有24名肥胖BED (12 m, 12 f)和24名体重匹配的肥胖非BED (12 m, 12 f)受试者。一天,进食固定的液体餐(750 ml),并抽血测量各种食欲激素,包括胃饥饿素,PYY和GLP-1,分别在进食前和进食后2小时内测量。与非BED受试者相比,BED患者空腹胃饥饿素水平较低,餐后下降幅度较小。与非BED受试者相比,BED患者空腹水平较低,餐后PYY和GLP-1升高较小。在另一天,只摄入水(750毫升)作为这些激素的昼夜变化的控制。在固定餐或水后135分钟,将使用功能成像(fMRI)检查大脑激活区域对暴饮暴食、非暴饮暴食和非食物的视觉和听觉刺激的反应。与非BED组相比,BED组在暴食反应中前额叶皮层等区域的激活程度更高。由于暴饮暴食通常发生在没有饥饿感的情况下,因此即使在进食状态下,暴食刺激的激活也会增加。第三天,将使用各种心理量表来评估饮食行为和情绪。将测量身体成分以获得体脂百分比,以验证两组的身体成分相似。这项关于脑成像和饮食相关的食欲激素的研究应该提高我们对暴饮暴食症(BED)潜在生物学因素的认识。这可能会改善诊断和治疗,帮助BED患者恢复正常的食欲、激素水平和大脑活动。BED是一种与肥胖一起日益流行的疾病。
英文摘要
DESCRIPTION (provided by applicant): The prevalence of obesity continues to increase in the US and globally. Obesity results in increased morbidity and mortality, especially from diabetes and heart disease. Approximately 30% of obese individuals seeking treatment have binge eating disorder (BED). They ingest very large meals without purging afterwards as in bulimia nervosa. BED, the most common characterized eating disorder, causes much distress and contributes to the development of obesity. Although psychological factors have been studied, little is known about the biological factors of BED. This clinical research study will focus on brain imaging and gut hormones following a meal to examine differences between BED and non-BED subjects. There will be 24 obese BED (12 m, 12 f) and 24 weight-matched obese non-BED (12 m, 12 f) subjects. On one day, a fixed liquid meal (750 ml) will be ingested and blood drawn to measure various appetite hormones including ghrelin, PYY, and GLP-1, measured before and during a 2-hour period afterwards. The prediction is a lower fasting level of ghrelin and a smaller postprandial fall in BED compared to non-BED subjects. Also predicted are lower fasting levels and smaller postprandial increases of PYY and GLP-1 in BED compared to non-BED subjects. On another day, only water (750 ml) will be ingested as a control for diurnal variation in these hormones. At 135 min after the fixed meal or water, functional imaging (fMRI) will be employed to examine brain activation areas in response to visual and auditory stimuli of binge foods, nonbinge foods, and nonfoods. Greater activation is expected in such areas as the prefrontal cortex in response to binge foods relative to the other stimuli groups in BED than in nonBED subjects. Increased activation is also expected to binge food stimuli in the BED subjects even in the fed state as binge eating often occurs in the absence of hunger. On a third day, various psychological scales to assess eating behavior and mood will be administered. Body composition will be measured to obtain percentage body fat to verify similar body composition in the two groups. This study on brain imaging and meal-related appetite hormones should improve our knowledge of the underlying biological factors in Binge Eating Disorder (BED). This may lead to improved diagnosis and treatments to help restore normal appetite hormone levels and brain activity in BED, a disorder which is increasing in prevalence alongside obesity.
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