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乳腺節のジップは,ダイエットによる肥満を予防します

Feng Zhang¹, Georgia Zarkada¹, Jinah Han¹

¹Cardiovascular Research Center, Yale University School of Medicine, New Haven, CT 06510-3221, USA.

Science (New York, N.Y.)

|August 11, 2018

まとめ

Neuropilin1 (Nrp1) と血管内皮成長因子受容体1 (Vegfr1) を削除することによって乳児のキロミクロン吸収を防ぐことは,食事による肥満から保護します. これは,乳腺の結節が食事中の脂肪の吸収を管理するための重要なターゲットであることを示唆しています.

科学分野:

血管生物学
代謝疾患
胃腸内科

背景:

肥満は過剰な脂肪摂取によるものです
食中の脂質は腸細胞によって吸収され,キロミクロンに詰め込まれ,乳細胞を通して血流に運ばれます.

研究の目的:

乳児のキロミクロン吸収におけるニューロピリン1 (Nrp1) と血管内皮成長因子受容体1 (Vegfr1) の役割を調査する.
腸内脂質吸収を調節することで,ダイエットによる肥満を予防するための潜在的な治療目標を探求する.

主な方法:

ネズミのNrp1とVegfr1の誘導性内皮の遺伝子消去
クイロミクロン輸送と乳腺結合の整合性の分析
VEGFR2とVE-カデリンを含むVEGF-Aシグナル伝達経路の役割を調査する.

主要な成果:

Nrp1とVegfr1の遺伝子削除は,マウスの食事による肥満を予防しました.
Nrp1とVegfr1の欠如は乳腺結節のジッパー化とキロミクロンの吸収不良を引き起こした.
VEGFR2とVE-カデリンシグナル伝達阻害による乳腺結合の浸透性を回復させ,キロミクロン輸送を救出する.
VE- カデリン分解によって誘発された乳腺結節ジップは,野生型のマウスのキロミクロン吸収を防止しました.

結論:

乳腺の結合はキロミクロンの吸収に不可欠です.
NRP1とFLT1のシグナル伝達経路は乳腺結合の透過性を調節する.
乳腺の結節をターゲットにすることで食中の脂肪の吸収と肥満を防ぐ新しい戦略が生まれます

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