美国冷泉港实验室Bo Li和Alessandro Furlan共同合作近期取得重要工作进展，他们研究发现扩展杏仁核中的神经紧张素神经元控制饮食选择和能量稳态。相关论文2022年10月20日在线发表于《自然—神经科学》杂志上。

研究人员发现，小鼠前连合（IPAC）后肢间质核中表达神经紧张素的神经元，编码了对不健康的能量密集型食物的偏好。IPAC^Nts神经元的光遗传学激活促进了肥胖行为，如享乐型饮食，并调节了食物偏好。相反，急性抑制IPAC^Nts神经元减少进食和享乐性进食。IPAC^Nts神经元的长期失活再现了这些效应，减少了对甜的、非热量的味觉物质的偏好，进一步增强了运动和能量消耗。

小鼠显示出长期的体重减轻和代谢健康的改善，免受肥胖症的影响。因此，单个神经元群体的活动是双向调节能量平衡的。他们的发现可能会导致新的治疗策略，以预防和治疗肥胖症。

据了解，肥胖是一种全球流行病，与许多危及生命的疾病密切相关。除了一些罕见的遗传条件外，暴饮暴食和活动减少的生物驱动因素尚不清楚。

附：英文原文

Title: Neurotensin neurons in the extended amygdala control dietary choice and energy homeostasis

Author: Furlan, Alessandro, Corona, Alberto, Boyle, Sara, Sharma, Radhashree, Rubino, Rachel, Habel, Jill, Gablenz, Eva Carlotta, Giovanniello, Jacqueline, Beyaz, Semir, Janowitz, Tobias, Shea, Stephen David, Li, Bo

Issue&Volume: 2022-10-20

Abstract: Obesity is a global pandemic that is causally linked to many life-threatening diseases. Apart from some rare genetic conditions, the biological drivers of overeating and reduced activity are unclear. Here, we show that neurotensin-expressing neurons in the mouse interstitial nucleus of the posterior limb of the anterior commissure (IPAC), a nucleus of the central extended amygdala, encode dietary preference for unhealthy energy-dense foods. Optogenetic activation of IPACNts neurons promotes obesogenic behaviors, such as hedonic eating, and modulates food preference. Conversely, acute inhibition of IPACNts neurons reduces feeding and decreases hedonic eating. Chronic inactivation of IPACNts neurons recapitulates these effects, reduces preference for sweet, non-caloric tastants and, furthermore, enhances locomotion and energy expenditure; as a result, mice display long-term weight loss and improved metabolic health and are protected from obesity. Thus, the activity of a single neuronal population bidirectionally regulates energy homeostasis. Our findings could lead to new therapeutic strategies to prevent and treat obesity.

DOI: 10.1038/s41593-022-01178-3

Source: https://www.nature.com/articles/s41593-022-01178-3