脳が食の欲求を制御するメカニズムを解明(‘Brain Dial’ for Food Urges Discovered)

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2025-09-10 コロンビア大学

コロンビア大学ザッカーマン研究所は、マウスの脳に「食欲のダイヤル」となる神経回路を発見した。線条体終脳床核(BNST)の特定ニューロンを刺激すると、満腹でも甘味を摂り続け、抑制すると飢餓時でも摂食欲求が減少した。BNSTは味覚入力と生理的状態(空腹、塩分不足など)を統合し、摂食行動を制御する役割を持つ。さらに、抗がん治療で食欲不振に陥ったマウスではBNST刺激により体重減少が抑えられ、肥満治療薬セマグルチドもBNSTを標的として作用することが示唆された。この発見は、がん患者の食欲不振や肥満の新たな治療法につながる可能性がある。

脳が食の欲求を制御するメカニズムを解明(‘Brain Dial’ for Food Urges Discovered)
The image shows neurons in the bed nucleus of the stria terminalis that selectively respond to sweet (red) or to sodium (purple) to drive sweet or salt consumption, respectively (Li Wang and José Cánovas / Zuker lab / Columbia’s Zuckerman Institute).

<関連情報>

消費反応を制御する脳中枢 A brain center that controls consummatory responses

Jose A. Canovas ∙ Li Wang ∙ Ahmed A.M. Mohamed ∙ Larry F. Abbott ∙ Charles S. Zuker
Cell  Published:September 10, 2025
DOI:https://doi.org/10.1016/j.cell.2025.08.021

Highlights

  • The attraction to sweet stimuli is encoded by specific amygdala neurons
  • Sweet signals are translated into consummatory responses in the BNST brain region
  • The BNST is a key hub linking sensory and internal-state signals to control consumption
  • The BNST is a potential target for bidirectionally controlling body weight

Summary

The innate attraction to sweet mediates appetitive and consummatory responses. Here, we dissected the circuit driving responses to sweet and showed that amygdala neurons tuned to sweet connect to the bed nucleus of the stria-terminalis (BNST) to promote sweet-evoked consumption. Next, we demonstrate that the BNST functions as a central hub, transforming appetitive signals into consumption and linking sensory inputs to the internal state, not only for sweet but also for other stimuli such as salt or food, to flexibly regulate consummatory behaviors. Using single-cell functional imaging, we show that ensemble activity in the BNST encodes stimulus identity and the animal’s internal state. Finally, we demonstrate that manipulating BNST activity can bidirectionally transform consummatory responses. Together, these findings illustrate how the internal state modulates sensory responses, characterize a general brain dial for consumption, and provide fresh insights into sites of action of GLP1R agonists and a strategy to help promote weight gain in pathological states.

医療・健康
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