腸-脳軸におけるセロトニンシグナル伝達に対する高脂肪食の影響を調べる

Taylor Gray¹, Yewande O Fasina², Scott H Harrison¹

¹Department of Biology, College of Science and Technology, North Carolina Agricultural and Technical State University, Greensboro, NC, USA.

Nutritional neuroscience

|August 25, 2025

まとめ

脂肪が多い食事は腸と脳のセロトニン信号伝達を妨げますこのダイエットはセロトニンのレベルを変化させ気分や食欲腸の機能に影響し腸内微生物が重要な役割を果たします

科学分野:

神経科学
胃腸内科
代謝に関する研究

背景:

セロトニンは生理学的,神経学的,行動的機能を調節する重要な神経伝達物質です.
周辺と中央のセロトニン系は腸の運動,血管の調節,食物の摂取,気分,認知に重要な役割を果たします
腸-脳軸は双方向のコミュニケーションを容易にしホメオスタシスの維持に不可欠です

研究の目的:

慢性的な高脂肪食 (HFD) の摂取が腸と脳のセロトニンシグナル伝達にどのように影響するか調べる
腸-脳セロトナージック軸のHFD誘発障害の背後にあるメカニズムを解明する.
HFDに関連したセロトニン機能障害の潜在的治療標的を特定する.

主な方法:

セロトニンシグナル伝達に対するHFD効果に関する既存の文献のレビュー.
セロトニンレベルと受容体の活性における経路特有の変化の分析
短鎖脂肪酸などの微生物代謝物の作用を調査する.

主要な成果:

HFDは腸内セロトニンのレベルを上げると同時に脳の特定の領域に変化をもたらします
HFDはセロトニンの生合成を増加させますが,5-HT1A自己受容体の活動を高め,セロトニンの放出を減少させます.
セロトニンのレベルが低下したのは,降解が増加し,放出が抑制されたため,海馬と下垂体で観察された.
微生物代謝産物,特に短鎖脂肪酸は,HFD誘発のセロトニン機能障害に大きく寄与する.

結論:

HFDは複雑な経路特有のメカニズムで腸-脳セロトニン基軸を深刻に破壊します
腸内微生物群とその代謝物は,HFD誘発のセロトニン調節障害の中心的媒介物である.
これらのメカニズムを理解することで肥満や気分障害や胃腸疾患の新規の治療戦略の可能性が生まれます

キーワード:

脳について HFD 中央部腸に腸-脳軸周辺機器セロトニン短鎖脂肪酸

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