Why choose NMN？

NAD+ has so many functions, how should we supplement it? Why choose NMN?

The synthesis of NAD+ is divided into salvage pathway, de novo synthesis pathway and Preiss-handler pathway according to different synthetic raw materials.

a) De novo synthesis pathway: tryptophan (Trp) is converted to quinolinic acid (QA), which is then converted to NAMN by quinolinic acid-phosphoribosyltransferase (QPRT). NAMN is converted into NAAD, which is ultimately catalyzed by NAD+ synthase (NADS) to generate NAD+.

b) P-H synthesis pathway (also called NA salvage pathway): Niacin (NA) synthesizes NAD+ through NAPRT, NMNAT, and NADS (NAD synthase).

c) Salvage synthesis pathway (also known as NR rescue pathway): nicotinamide riboside (NR) or nicotinamide (NAM) synthesizes Nicotinamide Mononucleotide (NMN) via NRK (nicotinamide riboside kinase) or NAMPT, NMNAT, NMN NAD+ is synthesized by NMNAT1-3 enzyme.

In addition, nicotinic acid riboside (NAR) can also produce NAMN through NRK catalysis, and then synthesize NAD+ through the enzymatic reaction in 1.

Transforming NR into NMN requires synthetase and consumes energy

The conversion of NR to NMN requires the synthetase NRK, and NRK is rarely distributed in the heart and brain tissue. Experiments have confirmed that neither oral nor intravenous injection of NR has a significant effect on promoting brain NAD+, and cannot be completely absorbed. All NR is degraded into NAM, and then only increases brain NAD+ levels by 5-10%;

Mitochondria can only use NMN but not NR directly. Measured by in vitro culture of skeletal muscle cell mitochondria, NMN can significantly increase mitochondrial NAD+ levels, while NA and NAM can hardly increase NAD+ levels.

Based on the above, supplementing NR may not be a good strategy, and the elderly themselves are lacking in energy in all aspects. Supplementing a precursor of NAD+ precursor may not be as efficient.

After some updates our conclusion remains the same: NMN is currently the best way to supplement NAD+.

Tag: NMN

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