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NRK1 controls nicotinamide mononucleotide and nicotinamide riboside metabolism in mammalian cells
Journal article   Open access   Peer reviewed

NRK1 controls nicotinamide mononucleotide and nicotinamide riboside metabolism in mammalian cells

Joanna Ratajczak, Magali Joffraud, Samuel A J Trammell, Rosa Ras, Núria Canela, Marie Boutant, Sameer S Kulkarni, Marcelo Rodrigues, Philip Redpath, Marie E Migaud, …
Nature communications, Vol.7(1), 13103
10/11/2016
DOI: 10.1038/ncomms13103
PMCID: PMC5476803
PMID: 27725675
url
https://doi.org/10.1038/ncomms13103View
Published (Version of record) Open Access

Abstract

NAD is a vital redox cofactor and a substrate required for activity of various enzyme families, including sirtuins and poly(ADP-ribose) polymerases. Supplementation with NAD precursors, such as nicotinamide mononucleotide (NMN) or nicotinamide riboside (NR), protects against metabolic disease, neurodegenerative disorders and age-related physiological decline in mammals. Here we show that nicotinamide riboside kinase 1 (NRK1) is necessary and rate-limiting for the use of exogenous NR and NMN for NAD synthesis. Using genetic gain- and loss-of-function models, we further demonstrate that the role of NRK1 in driving NAD synthesis from other NAD precursors, such as nicotinamide or nicotinic acid, is dispensable. Using stable isotope-labelled compounds, we confirm NMN is metabolized extracellularly to NR that is then taken up by the cell and converted into NAD . Our results indicate that mammalian cells require conversion of extracellular NMN to NR for cellular uptake and NAD synthesis, explaining the overlapping metabolic effects observed with the two compounds.
Niacinamide - analogs & derivatives Mammals - metabolism Animals Niacinamide - metabolism Humans Injections, Intraperitoneal NAD - biosynthesis Nicotinamide Mononucleotide - metabolism Hepatocytes - metabolism Hep G2 Cells Mice, Knockout Phosphotransferases (Alcohol Group Acceptor) - metabolism

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