小组发现，享乐性进食是由一条从周边蓝核到腹侧被盖区（VTA）的神经通路控制。利用光度校准的光遗传学，研究团队发现VTA多巴胺（VTADA）神经元编码可口性，双向调节享乐性食物消耗。进食时，VTADA神经元的反应性被semaglutide抑制，semaglutide是一种胰高血糖素样肽受体1 （GLP-1R）激动剂，作为一种抗肥胖药物。在重复的西马鲁肽治疗中，小鼠恢复了美味食物的食欲和VTADA神经元的活动，这被消费触发的VTADA神经元抑制逆转。首先，享乐性食物摄入激活VTADA神经元，使其保持进一步的消耗，这是一种对抗semaglutide减少食欲的机制。
据悉，享乐性饮食被定义为在没有生理需求的情况下，由适口性驱动的食物消费。然而，人们对美味食物摄入的神经控制知之甚少。
附：英文原文
Title: Hedonic eating is controlled by dopamine neurons that oppose GLP-1R satiety
Author: Zhenggang Zhu, Rong Gong, Vicente Rodriguez, Kathleen T. Quach, Xinyu Chen, Scott M. Sternson
Issue&Volume: 2025-03-28
Abstract: Hedonic eating is defined as food consumption driven by palatability without physiological need. However, neural control of palatable food intake is poorly understood. We discovered that hedonic eating is controlled by a neural pathway from the peri–locus ceruleus to the ventral tegmental area (VTA). Using photometry-calibrated optogenetics, we found that VTA dopamine (VTADA) neurons encode palatability to bidirectionally regulate hedonic food consumption. VTADA neuron responsiveness was suppressed during food consumption by semaglutide, a glucagon-like peptide receptor 1 (GLP-1R) agonist used as an antiobesity drug. Mice recovered palatable food appetite and VTADA neuron activity during repeated semaglutide treatment, which was reversed by consumption-triggered VTADA neuron inhibition. Thus, hedonic food intake activates VTADA neurons, which sustain further consumption, a mechanism that opposes appetite reduction by semaglutide.
DOI: adt0773
Source: https://www.science.org/doi/10.1126/science.adt0773