Geliebter Allan, Gluck Marci E, Hashim Sami A
Department of Medicine, New York Obesity Research Center, St. Luke's Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, New York, NY, USA.
J Nutr. 2005 May;135(5):1326-30. doi: 10.1093/jn/135.5.1326.
Binge-eating disorder (BED), characterized by binge meals without purging afterward, is found in about 30% of obese individuals seeking treatment. The study objective was to ascertain abnormalities in hormones influencing appetite in BED, especially ghrelin, an appetite-stimulating peptide, which was expected to be elevated. Measurements were made of plasma insulin, leptin, glucagon, cholecystokinin, and ghrelin, as well as glucose following an overnight 12-h fast, prior to and after ingestion (from 0 to 5 min) of a nutritionally complete liquid meal (1254 kJ) at 0830 h, at -15, 0, 5, 15, 30, 60, 90, and 120 min. Appetite ratings including hunger and fullness were also obtained. An acetaminophen tracer was used to assess gastric emptying rate. Three groups of comparably obese women (BMI = 35.9 +/- 5.5; % body fat = 44.9 +/- 4.7) participated: 12 nonbinge eating normals (NB), 14 subthreshold BED, and 11 BED. The BED subjects, compared to NB subjects, had lower baseline ghrelin concentrations prior to the meal, a lower area under the curve (AUC), with lower levels at 5, 15, 30, 90, and 120 min, and a smaller decline in ghrelin postmeal (all P < 0.03). The other blood values did not differ among groups, and neither did gastric emptying rate nor ratings of fullness. The BED subjects were then randomly assigned to treatment with cognitive-behavior therapy and diet (n = 5) or to a wait-list control (n = 4). Baseline ghrelin (P = 0.01) and AUC increased (P = 0.02), across both conditions, in which most subjects (7 of 9) stopped binge eating. The lower fasting and postmeal plasma ghrelin levels in BED are consistent with lower ghrelin levels in obese compared to lean individuals and suggests downregulation by binge eating.
暴饮暴食症（BED）的特征是暴饮暴食后不进行催吐，在寻求治疗的肥胖个体中约30%存在该病症。研究目的是确定影响暴饮暴食症患者食欲的激素异常情况，尤其是胃饥饿素，这是一种刺激食欲的肽，预计其水平会升高。在禁食12小时后的空腹状态下、上午8:30摄入营养完整的流食（1254千焦）前以及摄入后（0至5分钟）的-15、0、5、15、30、60、90和120分钟时，测量血浆胰岛素、瘦素、胰高血糖素、胆囊收缩素、胃饥饿素以及葡萄糖水平。还获取了包括饥饿和饱腹感在内的食欲评分。使用对乙酰氨基酚示踪剂评估胃排空率。三组体重相当的肥胖女性（体重指数=35.9±5.5；体脂百分比=44.9±4.7）参与了研究：12名非暴饮暴食正常者（NB）、14名阈下暴饮暴食症患者和11名暴饮暴食症患者。与NB组受试者相比，暴饮暴食症患者在餐前的基础胃饥饿素浓度较低，曲线下面积（AUC）较小，在5、15、30、90和120分钟时水平较低，且餐后胃饥饿素下降幅度较小（所有P<0.03）。其他血液值在各组之间没有差异，胃排空率和饱腹感评分也没有差异。然后将暴饮暴食症患者随机分为接受认知行为疗法和饮食治疗组（n=5）或等待名单对照组（n=4）。在两种情况下，基础胃饥饿素（P=0.01）和AUC均升高（P=0.02），大多数受试者（9名中的7名）停止了暴饮暴食。暴饮暴食症患者空腹和餐后血浆胃饥饿素水平较低，这与肥胖个体相比瘦个体胃饥饿素水平较低一致，并提示暴饮暴食导致其下调。
