腸内微生物群は,長い非コーディングRNA Snhg9 を介して腸内脂質代謝を再プログラムします

Yuhao Wang^1,2,3,4, Meng Wang¹, Jiaxin Chen⁵

¹Zhejiang Provincial Key Laboratory of Pancreatic Disease of The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310029, China.

Science (New York, N.Y.)

|August 24, 2023

まとめ

腸内微生物群は,腸内の特定のRNA分子,小核RNA宿主遺伝子9 (Snhg9) の発現を減少させることで,脂肪の吸収を制御する. このメカニズムは宿主の代謝と肥満に影響します

科学分野:

微生物学
分子生物学
代謝の調節

背景:

腸内微生物群は,吸収,代謝,貯蔵を含む宿主の脂質代謝を調節する上で重要な役割を果たします.
長いノンコーディングRNA (lncRNA) は,様々な生物学的プロセスにおける規制機能としてますます認識されています.

研究の目的:

ホストの脂質代謝の再プログラムにおける腸内微生物の役割を調査する.
腸内脂質代謝の微生物の調節に関与する lncRNA を含む特定の分子機構を特定する.

主な方法:

マウスの小腸上皮細胞における遺伝子発現の分析.
lncRNA Snhg9,PPARγ,sirtuin 1,およびCCAR2の相互作用を調査する
ネズミの脂質代謝に対するSnhg9強制発現の影響を研究.
微生物媒介によるSnhg9抑制に関与する免疫経路を調べる.

主要な成果:

腸内微生物群は,腸内上皮細胞における lncRNA Snhg9 の発現を抑制する.
Snhg9は,シルトゥイン1およびCCAR2との相互作用に影響することによって,ペロキシソーム増殖器活性化受容体 γ (PPARγ) の活性を否定的に調節する.
ネズミのSnhg9の発現は脂質吸収を阻害し,体脂肪を減少させ,食事による肥満から保護します.
微生物群によるSnhg9抑制には,骨髄性細胞と3群の先天性リンパ性細胞を含む免疫リレーが含まれます.

結論:

lncRNA Snhg9は腸内脂質代謝に対する微生物のコントロールの重要な媒介である.
微生物群は,Snhg9の発現を免疫感知経路を通じて調節することによって宿主脂質代謝を再プログラムします.
これらの発見は腸内微生物群が宿主のエネルギーバランスと肥満に影響を与える新しいメカニズムを明らかにしています

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