| First Author | Yaku K | Year | 2021 |
| Journal | Nat Commun | Volume | 12 |
| Issue | 1 | Pages | 6767 |
| PubMed ID | 34799586 | Mgi Jnum | J:334708 |
| Mgi Id | MGI:6833612 | Doi | 10.1038/s41467-021-27080-3 |
| Citation | Yaku K, et al. (2021) BST1 regulates nicotinamide riboside metabolism via its glycohydrolase and base-exchange activities. Nat Commun 12(1):6767 |
| abstractText | 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. |
