固有の硫化水素の生成は,食事制限の利点にとって不可欠です

Christopher Hine¹, Eylul Harputlugil¹, Yue Zhang¹

¹Department of Genetics and Complex Diseases, Harvard School of Public Health, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.

Cell

|December 28, 2014

まとめ

食事制限は,トランススルフレーション経路 (TSP) 経由で硫化水素 (H2S) の生成を増加させ,ストレス抵抗性と長寿を高めます. この保存されたメカニズムは,広範な臨床的影響を及ぼします.

科学分野:

バイオケミストリーバイオケミストリー
分子生物学は分子生物学である.
ゲロントロジーはゲロントロジーの学科です.

背景:

ダイエット制限 (DR) は長寿やストレス耐性などの健康上の利点がありますが,その背後にあるメカニズムは不明です.
硫黄アミノ酸 (SAA) は,代謝調節とストレス反応に関与する重要な栄養素です.

研究の目的:

硫黄アミノ酸 (SAA) と硫化水素 (H2S) が食事制限 (DR) の恩恵を媒介する役割を調査する.
DR媒介による長寿とストレス耐性におけるトランス硫化経路 (TSP) の進化的保存を調査する.

主な方法:

変硫化経路 (TSP) とH2S生成に対するSAA制限の影響を調べるためにDRのマウスモデルを使用しました.
SAAサプリメント,mTORC1活性化,CGL抑制がDR媒介のストレス抵抗に与える影響を調査した.
ミトコンドリアのタンパク質SQRを用いた実験室内試験を行い,さまざまなモデル生物 (酵母,ワーム,果物ハエ,ネズミ) でのTSP依存のH2S生成を調べました.

主要な成果:

SAAの制限により,シスタチオニン γ-ライアゼ (CGL) が上調され,H2Sの産生が増加し,肝臓イシュケミアの再注射傷害に対する保護が与えられました.
SAA補充,mTORC1活性化,またはCGL抑制は,H2Sレベルを下げることでDR媒介のストレス抵抗を撤廃した.
TSPに依存するH2S生成は,複数の種で保存され,DR媒介の長寿に関連していました.

結論:

硫化変異経路 (TSP) 媒介による硫化水素 (H2S) 生成は,食事制限 (DR) の利益の基礎にある保存されたメカニズムです.
この経路は,ストレス耐性と長寿をもたらし,代謝および老化関連の疾患における臨床的翻訳の可能性を示唆しています.

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