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肠道-大脑营养感应与食物奖赏

Gut-brain nutrient sensing in food reward.

机构信息

Department of Medicine, Columbia University, New York, NY 10032, United States.

Departments of Medicine & Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, United States.

出版信息

Appetite. 2018 Mar 1;122:32-35. doi: 10.1016/j.appet.2016.12.009. Epub 2016 Dec 20.

Abstract

For the past several decades, vagal and hormonal gut-brain negative feedback signaling mechanisms that promote satiety and subsequent suppression of food intake have been explored. In addition, a separate positive feedback process termed "appetition," involving postoral signaling from the gut to the brain, has been shown to promote food intake and produce flavor-nutrient preference conditioning. Afferent fibers emerging from the vagus nerve form the main pathway by which information is relayed from the abdominal viscera to the hindbrain and eventually other higher brain regions involved in food intake. Using a specialized subdiaphragmatic vagal deafferentation technique, it was observed that gut vagal and splanchnic afferents play a role in the negative feedback control of satiety after nutrient intake; however, these afferents are not required for nutrient reinforcement or flavor-nutrient preference conditioning, thereby highlighting the distinction between the processes of satiation and appetition. By linking these physiological and behavioral processes to a neurochemical mechanism, it was found that striatal dopamine release induced by intragastric glucose infusion is involved in sweet appetite conditioning. The mechanisms underlying appetition are still being investigated but may involve other nondopaminergic neurochemical systems and/or presently undiscovered hormonal mediators. Future work to delineate the biological mechanisms whereby appetition drives increased intake and conditioned food preference in response to ingestion should take a multifaceted approach by integrating hormonal, neurophysiological, and behavioral techniques.

摘要

在过去的几十年中,人们一直在探索促进饱腹感并随后抑制食物摄入的迷走神经和激素肠道-大脑负反馈信号机制。此外,还发现了一种称为“食欲”的独立正反馈过程,涉及肠道向大脑的口后信号,它可以促进食物摄入并产生风味-营养偏好条件作用。从迷走神经发出的传入纤维构成了主要途径,通过该途径将信息从腹部内脏传递到后脑,最终传递到参与食物摄入的其他更高脑区。使用专门的膈下迷走神经去传入技术,观察到肠道迷走神经和内脏传入纤维在营养摄入后的饱腹感负反馈控制中发挥作用;然而,这些传入纤维对于营养强化或风味-营养偏好条件作用并不必需,从而突出了饱腹感和食欲之间的区别。通过将这些生理和行为过程与神经化学机制联系起来,发现胃内葡萄糖输注诱导的纹状体多巴胺释放参与了甜食食欲条件作用。食欲的机制仍在研究中,但可能涉及其他非多巴胺能神经化学系统和/或目前尚未发现的激素介质。未来的工作应该采用多方面的方法,整合激素、神经生理学和行为技术,以阐明食欲驱动摄入增加和条件性食物偏好的生物学机制。

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