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The effects of kappa opioid receptor antagonism on binge eating behavior in a biobehavioral animal model of obese binge eating.

机译:在肥胖暴饮暴食的生物行为动物模型中,κ阿片受体拮抗作用对暴饮暴食行为的影响。

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Obesity, a spreading epidemic in the U.S., is often associated with negative health consequences. Approximately, 20–30% of those who seek treatment for obesity are binge eaters. As a distinct obesity subgroup, these individuals may have unique treatment needs. Obese binge eating (OBE) is characterized by the consumption of large quantities of food over a short period of time, loss of control over eating, and a failure to perceive satiation. Current evidence supports a theoretical model that operationalizes OBE as a primary biological satiation defect associated with alterations in several neurochemicals (corticosterone, insulin and opioids) thought to influence satiation.; The obese Zucker rat (OZR) exhibits a hyperphagic eating pattern similar to the OBE and this model was used to examine the relationship among these altered neurochemicals and satiation (meal size). Using an experimental design, a kappa opioid receptor antagonist, nor-binaltorphamine (N-BNI), known to influence food intake, corticosterone (CORT), and insulin levels, was injected into the lateral ventricle of the brain of OZR (n = 11), while a control group (n = 2) received a saline injection. Over 2 weeks, meal size and frequency was assessed continually with computerized real-time monitoring equipment, while total intake and body weight were measured daily; plasma for CORT and insulin levels was obtained at intervals. Cumulative food intake over the largest meal of the day was examined with curve estimation for a food intake pattern of satiation.; Two distinctive responses emerged. Some subjects responded to central injection of N-NBI with a reduction in body weight and food intake (responders); others exhibited a lesser response (poor responders). Repeated measures ANOVA showed a significant decrease in body weight (p = .001) and food intake (p = .03) in responders, when compared to poor responders and controls. Satiation was influenced to a greater extent in responders who showed a reduction in meal size and a rate of intake slowing over the largest meal of the day indicating building satiation. There were no significant reductions in CORT and insulin levels.; Greater understanding of the biological mechanisms that regulate ingestive behavior and weight maintenance are critical to finding effective biobehavioral nursing interventions for binge eating and weight loss.
机译:肥胖是在美国流行的一种流行病,通常会给健康带来负面影响。寻求肥胖治疗的人中大约有20%至30%是暴食者。作为独特的肥胖亚组,这些个体可能有独特的治疗需求。肥胖暴饮暴食(OBE)的特点是在短时间内食用大量食物,失去对饮食的控制能力以及无法感知饱腹感。当前的证据支持一种理论模型,该模型可将OBE视为与几种可能影响饱足感的神经化学物质(皮质酮,胰岛素和阿片类药物)发生变化相关的主要生物学饱足性缺陷。肥胖的Zucker大鼠(OZR)表现出与OBE相似的食欲亢进模式,该模型用于检查这些神经化学物质变化与饱食感(餐量)之间的关系。通过实验设计,将已知会影响食物摄入,皮质酮(CORT)和胰岛素水平的κ阿片受体拮抗剂去甲双甲酚胺(N-BNI)注入OZR的大脑侧脑室(n = 11 ),而对照组(n = 2)则接受盐水注射。在2周内,使用计算机实时监控设备连续评估进餐量和进餐频率,同时每​​天测量总摄入量和体重。间隔获取血浆的CORT和胰岛素水平。用曲线估计法检查一天中最大的一餐的累积食物摄入量,以确定食物的饱食程度。出现了两个独特的反应。一些受试者对集中注射N-NBI有所反应,体重和食物摄入减少(响应者)。其他人的反应较小(反应不佳)。重复测量ANOVA显示,与较差的反应者和对照组相比,反应者的体重(p = .001)和食物摄入(p = .03)显着降低。在当天最大的一餐中,进餐量减少和摄入速度减慢的反应者对饱腹感的影响更大,表明建筑物感到饱食。 CORT和胰岛素水平没有明显降低。深入了解调节摄入行为和体重维持的生物学机制,对于寻找有效的饮食和减肥生物行为护理干预至关重要。

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