Nicotinamide mononucleotide (NMN), a product of the NAMPT reaction and a key NAD+ intermediate, ameliorates glucose intolerance by restoring NAD+ levels in HFD-induced T2D mice. NMN also enhances hepatic insulin sensitivity and restores gene expression related to oxidative stress, inflammatory response, and circadian rhythm, partly through SIRT1 activation. NMN is used for studying binding motifs within RNA aptamers and ribozyme activation processes involving β-nicotinamide mononucleotide (Beta-NMN)-activated RNA fragments.
Nicotinamide mononucleotide in human cells play an important role in energy generation, it involved in intracellular NAD (nicotinamide adenine dinucleotide, cell energy conversion important coenzyme) synthesis, used in anti-aging, fall blood sugar and other health care products.
Nicotinamide Mononucleotide widely used for cosmetics and pharmaceutical.In cosmetics has anti-aging and anti-allergic agents effects etc.
The turnover of the oxidized form of nicotinamide adenine dinucleotide (NAD+) has attracted interest in regard to longevity. Thus, compounds that can rapidly increase the cellular NAD+ concentration have been surveyed by many researchers. Of those, β-nicotinamide mononucleotide (Beta NMN) has been focused on. Studies on the biosynthesis of NAD+ from Beta NMN have been reported at the cellular level, but not at the whole animal level. In the present study, we investigated whether β-NMN is superior to nicotinamide (Nam) as a precursor of NAD+ in whole animal experiments. To this end we compared the NAD+ concentration in the blood and the urinary excretion amounts of NAD+ catabolites. Rats were intraperitoneally injected with Beta NMN or Nam. After the injection, blood samples and urine samples were collected at 3-h intervals. The concentration of blood total NAD (NAD11NADH) in each sample showed no significant differences between the two groups. The urinary excretion amounts of NAD+ catabolites in the urine samples collected at 3-6 h after the injection were lower in the β-NMN group than in the Nam group. These results suggest that Beta NMN is retained in the body for longer than Nam.
The β-nicotinamide mononucleotide (Beta NMN) is an intermediate in NAD+biosynthesis produced from nicotinamide (NAM) and phosphoribosyl pyrophosphate (PRPP) by nicotinamide phosphoribosyl transferase enzyme (Nampt)
Being well tolerated, with no reported side effects during long term administration in mice, and preventing age-associated physiological decline, NMN proved to be effective in treating high fat diet-induced type 2 diabetes, by reversing mitochondrial dysfunction associated with aging, and rescuing the effect of age-associated decline in neural stem cells.
NAM is usually converted to NMN by enzymes involved in the NAD+ salvage pathways, such as Nampt. The action of this enzyme constitutes the main NAD+anabolic activity in the cell. The regulation of mammalian or microorganisms nucleotide metabolism and biosynthesis usually proceeds by consumption of PRPP. PRPP results from ribose-5-phosphate via both oxidative and non-oxidative branches of pentose phosphate pathway.
In bacteria, NAM is most often converted to nicotinic acid (NA) by nicotinamidase, which is integrated in Preiss-Handler pathway, this being also the case of Escherichia coli. In mammals, nicotinamidase activity was not reported; NAM is converted to NMN by one of the NAM phosphoribosyl transferase enzymes instead. Although most of bacteria lack NAM phosphoribosyl transferase, the enzyme is expressed in Haemophilus ducreyi and Shewanella oneidensis.