Neuroscience Institute & Department of Psychology, Georgia State University, Box 5030, Atlanta, GA 30303-5030, United States.
School of Psychology, University of Birmingham, Edgbaston, Birmingham, BI5 2TT, United Kingdom.
Neurosci Biobehav Rev. 2022 Jan;132:110-129. doi: 10.1016/j.neubiorev.2021.10.051. Epub 2021 Nov 20.
This paper reviews evidence demonstrating a bidirectional relationship between memory and eating in humans and rodents. In humans, amnesia is associated with impaired processing of hunger and satiety cues, disrupted memory of recent meals, and overconsumption. In healthy participants, meal-related memory limits subsequent ingestive behavior and obesity is associated with impaired memory and disturbances in the hippocampus. Evidence from rodents suggests that dorsal hippocampal neural activity contributes to the ability of meal-related memory to control future intake, that endocrine and neuropeptide systems act in the ventral hippocampus to provide cues regarding energy status and regulate learned aspects of eating, and that consumption of hypercaloric diets and obesity disrupt these processes. Collectively, this evidence indicates that diet-induced obesity may be caused and/or maintained, at least in part, by a vicious cycle wherein excess intake disrupts hippocampal functioning, which further increases intake. This perspective may advance our understanding of how the brain controls eating, the neural mechanisms that contribute to eating-related disorders, and identify how to treat diet-induced obesity.
本文综述了人类和啮齿动物中记忆与进食之间存在双向关系的证据。在人类中,健忘症与饥饿和饱腹感线索的处理受损、近期进食记忆中断以及过度进食有关。在健康参与者中,与进餐相关的记忆会限制随后的摄食行为,而肥胖与记忆受损和海马体紊乱有关。来自啮齿动物的证据表明,背侧海马体的神经活动有助于与进餐相关的记忆控制未来的摄食量,内分沁和神经肽系统在腹侧海马体中发挥作用,提供有关能量状态的线索,并调节与进食相关的学习方面,而高热量饮食的消耗和肥胖会破坏这些过程。总的来说,这些证据表明,饮食引起的肥胖可能至少部分是由一个恶性循环引起的,其中过量摄入会破坏海马体的功能,从而进一步增加摄入量。这种观点可能有助于我们理解大脑如何控制进食、导致与进食相关的障碍的神经机制,并确定如何治疗饮食引起的肥胖。