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Nicotinic acid riboside maintains NAD+ homeostasis and ameliorates aging-associated NAD+ decline
Journal article   Peer reviewed

Nicotinic acid riboside maintains NAD+ homeostasis and ameliorates aging-associated NAD+ decline

Won-Suk Song, Xiyu Shen, Kang Du, Cuauhtemoc B. Ramirez, Sang Hee Park, Yang Cao, Johnny Le, Hosung Bae, Joohwan Kim, Yujin Chun, …
Cell metabolism, Vol.37(7), pp.1499-1514.e4
07/01/2025
DOI: 10.1016/j.cmet.2025.04.007
PMCID: PMC12328062
PMID: 40315855

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Abstract

Liver-derived circulating nicotinamide from nicotinamide adenine dinucleotide (NAD+) catabolism primarily feeds systemic organs for NAD+ synthesis. We surprisingly found that, despite blunted hepatic NAD+ and nicotinamide production in liver-specific nicotinamide nucleotide adenylyltransferase 1 (NMNAT1) deletion mice (liver-specific knockout [LKO]), circulating nicotinamide and extra-hepatic organs’ NAD+ are unaffected. Metabolomics reveals a massive accumulation of a novel molecule in the LKO liver, which we identify as nicotinic acid riboside (NaR). We further demonstrate cytosolic 5′-nucleotidase II (NT5C2) as the NaR-producing enzyme. The liver releases NaR to the bloodstream, and kidneys take up NaR to synthesize NAD+ through nicotinamide riboside kinase 1 (NRK1) and replenish circulating nicotinamide. Serum NaR levels decline with aging, whereas oral NaR supplementation in aged mice boosts serum nicotinamide and multi-organ NAD+, including kidneys, and reduces kidney inflammation and albuminuria. Thus, the liver-kidney axis maintains systemic NAD+ homeostasis via circulating NaR, and NaR supplement ameliorates aging-associated NAD+ decline and kidney dysfunction. [Display omitted] •Liver produces and releases NaR when NaMN is accumulated•NT5C2 mediates liver NaR production•Kidneys use circulating NaR to produce NAD+ and circulating nicotinamide•NaR supplementation improves organ NAD+ levels and kidney dysfunction in aging Song et al. identify an alternative pathway for maintaining NAD+ homeostasis through circulating NaR production and consumption by the liver-kidney axis, and boosting this pathway ameliorates aging-associated NAD+ decline and kidney dysfunction.
Aging kidney liver NAD nicotinic acid riboside

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