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• W3136425725 abstract "Nicotinamide adenine dinucleotide (NAD+ ) homeostasis is constantly compromised due to degradation by NAD+ -dependent enzymes. NAD+ replenishment by supplementation with the NAD+ precursors nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) can alleviate this imbalance. However, NMN and NR are limited by their mild effect on the cellular NAD+ pool and the need of high doses. Here, we report a synthesis method of a reduced form of NMN (NMNH), and identify this molecule as a new NAD+ precursor for the first time. We show that NMNH increases NAD+ levels to a much higher extent and faster than NMN or NR, and that it is metabolized through a different, NRK and NAMPT-independent, pathway. We also demonstrate that NMNH reduces damage and accelerates repair in renal tubular epithelial cells upon hypoxia/reoxygenation injury. Finally, we find that NMNH administration in mice causes a rapid and sustained NAD+ surge in whole blood, which is accompanied by increased NAD+ levels in liver, kidney, muscle, brain, brown adipose tissue, and heart, but not in white adipose tissue. Together, our data highlight NMNH as a new NAD+ precursor with therapeutic potential for acute kidney injury, confirm the existence of a novel pathway for the recycling of reduced NAD+ precursors and establish NMNH as a member of the new family of reduced NAD+ precursors." @default.
• W3136425725 created "2021-03-29" @default.
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• W3136425725 date "2021-03-16" @default.
• W3136425725 modified "2023-10-16" @default.
• W3136425725 title "Reduced nicotinamide mononucleotide is a new and potent NAD ⁺ precursor in mammalian cells and mice" @default.
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• W3136425725 doi "https://doi.org/10.1096/fj.202001826r" @default.
• W3136425725 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33724555" @default.
• W3136425725 hasPublicationYear "2021" @default.
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