カロリー制限による酵母寿命の延長は,NADの変動から独立しています

Rozalyn M Anderson¹, Magda Latorre-Esteves¹, Ana Rute Neves²

¹Department of Pathology, Harvard Medical School, 200 Longwood Avenue, Boston MA 02115, USA.

Science (New York, N.Y.)

|November 8, 2003

まとめ

カロリー制限 (CR) は,核のNAD+レベルを下げることで老化を遅らせます. しかし,鍵となる酵素Sir2は,

科学分野:

老化に関する研究.
分子生物学は分子生物学である.
遺伝学遺伝学とは

背景:

カロリー制限 (CR) は,様々な種で寿命を延ばすことが知られている食事介入です.
酵母 (Saccharomyces cerevisiae) のタンパク質Sir2 (Sirtuin 2) は,CRの老化を遅らせる効果を媒介するために重要である.
Sir2は保存されたNAD+依存型脱酸化酵素であり,老化におけるNAD+代謝の役割を示唆しています.

研究の目的:

核NAD+レベルに対するCRの効果を in vivoで調査する.
NAD+:NADH比がSir2とヒトの同型SIRT1.1の活性に影響するかどうかを判断する.
CRがSir2活動を規制する代替メカニズムを特定する.

主な方法:

酵母における核NAD+レベルをCR条件下で測定する.
Sir2およびSIRT1.1の活性を評価するためのインビトロアッセイ.
NAD+:NADH比を操作して,酵素活性への影響を観察する.

主要な成果:

カロリー制限は,核のNAD+レベルを in vivoで低下させることが判明しました.
酵母Sir2とヒトSIRT1の両方の酵素活性は,NAD+:NADH比の生理学的変化によって有意に変化しませんでした.
これらの発見は,NAD+レベル低下がCRによるSir2/SIRT1活動調節の主な要因ではないことを示唆しています.

結論:

酵母におけるCR媒介による寿命延長は,Sir2/SIRT1の活性に影響するNAD+:NADH比の変化によって制御されるようには見えない.
CRによるSir2/SIRT1の代替的調節経路は,老化プロセスに関与している可能性が高い.
このCRによるSir2調節の代替メカニズムを明らかにするために,さらなる研究が必要である.

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