Opioidergic consequences of dietary-induced binge eating.
Opioidergic consequences of dietary-induced binge eating.
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DOI：
10.1016/j.physbeh.2011.04.032
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发表时间：
2011-07-25
影响因子：
2.9
通讯作者：
Moran, Timothy H.
中科院分区：
文献类型：
--
作者：
Bello, Nicholas T.;Patinkin, Zachary W.;Moran, Timothy H.
内源性阿片类物质参与进食的享乐方面。阿片样物质损伤和改变与神经性贪食症和暴食症的病理生理学有关。Bartley G的具体贡献。Hoebel进一步理解了周期性的热量限制和间歇性的可选糖溶液的获得如何导致啮齿动物的阿片样前脑神经改变和依赖性。本研究旨在研究啮齿动物模型中的尾脑干和结状神经节μ阿片受体mRNA的变化，饮食诱导的暴食加糖脂肪（植物起酥油与10%蔗糖混合）。将5组（n = 7或8）成年雌性Sprague道利大鼠暴露于各种饮食条件6周。如通过原位杂交所测量的，在暴饮暴食组中，孤束核（NTS）中的μ阿片受体mRNA减少（从初始的约25%），其具有间歇性的卡路里限制和可选的有限的甜味脂肪获取。在连续进入组中证实了类似的表达减少，其具有无限的可选的甜味脂肪和肥胖表型。在结状神经节中，仅间歇性热量限制的大鼠中μ阿片受体mRNA增加（来自含糖脂肪进入组的约30%）。我们的研究结果和Hoebel实验室的工作表明，饮食诱导的暴饮暴食可以必然改变阿片类前脑和后脑喂养相关的神经通路。未来的工作需要确定类似的改变是否参与暴食和其他相关饮食病理的维持和进展。
Endogenous opioids are involved in the hedonic aspects of eating. Opioid impairments and alterations have been implicated in the pathophysiology of bulimia nervosa and binge eating disorder. Specific contributions by Bartley G. Hoebel have furthered the understanding how cyclical caloric restriction and intermittent optional access to sugar solutions results in opioid-like forebrain neural alterations and dependency in rodents. The present study sought to investigate caudal brainstem and nodose ganglion mu-opioid receptor mRNA alterations in a rodent model of dietary-induced binge eating of sweetened fat (vegetable shortening blended with 10% sucrose). Five groups (n = 7 or 8) of adult female Sprague Dawley rats were exposed to various dietary conditions for 6 weeks. As measured by in situ hybridization, there was reduced (approximately 25% from naive) mu-opioid receptor mRNA in the nucleus of the solitary tract (NTS) in the binge access group, which had intermittent calorie restriction and optional limited access to the sweetened fat. A similar reduction in expression was demonstrated in the continuous access group, which has unlimited optional sweetened fat and an obese phenotype. In the nodose ganglion, mu-opioid receptor mRNA was increased (approximately 30% from groups with sweetened fat access) in rats with intermittent caloric restriction alone. Our findings and the body of work from the Hoebel laboratory suggest that dietary-induced binge eating can consequentially alter opioidergic forebrain and hindbrain feeding-related neural pathways. Future work is needed to determine whether similar alterations are involved in the maintenance and progression of binge eating and other related eating pathologies.
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