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记忆抑制与能量调节。

Memory inhibition and energy regulation.

作者信息

Davidson T L, Kanoski Scott E, Walls Elwood K, Jarrard Leonard E

机构信息

Ingestive Behavior Research Center, Purdue University, United States; Department of Psychological Sciences, Purdue University, United States.

出版信息

Physiol Behav. 2005 Dec 15;86(5):731-46. doi: 10.1016/j.physbeh.2005.09.004. Epub 2005 Nov 2.

Abstract

At a simple behavioral level, food intake and body weight regulation depend on one's ability to balance the tendency to seek out and consume food with the ability to suppress or inhibit those responses. Accordingly, any factor that augments the tendency to engage in food seeking and eating or that interferes with the suppression of these behaviors could produce (a) caloric intake in excess of caloric need; (b) increases in body weight leading to obesity. This paper starts with the idea that excess body weight and obesity stem from a failure or degradation of mechanisms that normally function to inhibit eating behavior. Unlike previous approaches, we focus not on failures of traditional physiological (e.g., neural, hormonal) regulatory control mechanisms, but on disruptions of inhibitory learning and memory processes that may help to regulate energy intake. This view of energy dysregulation as a type of "learning disorder" leads us to the hippocampus, a brain structure that has long been regarded as an important substrate for learning and memory and which we think may be critically involved with a specific type of memory inhibition function that could contribute to the suppression of food intake. With this focus, the search for environmental origins of the current obesity epidemic in Western populations is directed toward factors that alter hippocampal functioning. We conclude by offering a preliminary account of how consumption of foods high in saturated fats might lead to impaired hippocampal function, reduced ability to inhibit caloric intake and, ultimately, to increased body weight.

摘要

在简单的行为层面上,食物摄入和体重调节取决于一个人平衡寻找和进食食物的倾向与抑制这些反应的能力。因此,任何增强寻求和进食食物倾向或干扰抑制这些行为的因素都可能导致:(a)热量摄入超过热量需求;(b)体重增加导致肥胖。本文开篇提出的观点是,超重和肥胖源于正常情况下抑制进食行为的机制失灵或退化。与以往的方法不同,我们关注的不是传统生理(如神经、激素)调节控制机制的失灵,而是可能有助于调节能量摄入的抑制性学习和记忆过程的破坏。这种将能量失调视为一种“学习障碍”的观点,将我们引向了海马体,这是一个长期以来被视为学习和记忆重要基础的脑结构,我们认为它可能与一种特定类型的记忆抑制功能密切相关,这种功能可能有助于抑制食物摄入。基于这一重点,对西方人群当前肥胖流行的环境起源的探寻指向了改变海马体功能的因素。我们最后初步阐述了高饱和脂肪食物的消费如何可能导致海马体功能受损、抑制热量摄入的能力下降,并最终导致体重增加。

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