期刊
NATURE COMMUNICATIONS
卷 12, 期 1, 页码 -出版社
NATURE PORTFOLIO
DOI: 10.1038/s41467-021-27080-3
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资金
- JSPS KAKENHI [20K20655, 18K17921, 21K11593]
- Kobayashi Foundation
- Takeda Science Foundation
- Tamura Science & Technology Foundation
- Takeda Medical Research Foundation
- Takahashi Industrial and Economic Research Foundation
- LOTTE Foundation
- Moonshot RD [JPMJMS2021]
- Honjo International Scholarship Foundation [1190817]
- Otsuka Toshimi Scholarship Foundation
- Rotary Yoneyama Memorial Foundation
- Grants-in-Aid for Scientific Research [21K11593, 20K20655, 18K17921] Funding Source: KAKEN
Nicotinamide riboside increases NAD(+) levels through two pathways, directly generating NAD(+) via the NR salvage pathway and contributing to NAD(+) production through the Preiss-Handler pathway after being hydrolyzed by BST1.
Nicotinamide riboside (NR) is one of the orally bioavailable NAD(+) precursors and has been demonstrated to exhibit beneficial effects against aging and aging-associated diseases. However, the metabolic pathway of NR in vivo is not yet fully understood. Here, we demonstrate that orally administered NR increases NAD(+) level via two different pathways. In the early phase, NR was directly absorbed and contributed to NAD(+) generation through the NR salvage pathway, while in the late phase, NR was hydrolyzed to nicotinamide (NAM) by bone marrow stromal cell antigen 1 (BST1), and was further metabolized by the gut microbiota to nicotinic acid, contributing to generate NAD(+) through the Preiss-Handler pathway. Furthermore, we report BST1 has a base-exchange activity against both NR and nicotinic acid riboside (NAR) to generate NAR and NR, respectively, connecting amidated and deamidated pathways. Thus, we conclude that BST1 plays a dual role as glycohydrolase and base-exchange enzyme during oral NR supplementation.
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