The study found that nicotinamide mononucleotide
can significantly improve age-related physiological decline in mice, such as inhibiting age-related weight gain, enhancing energy metabolism, improving insulin sensitivity and plasma lipid distribution, and improving ocular function. The CAS number of the NMN
is 1094-61-7. NMN prevents age-related changes in gene expression through tissue-specific means and enhances oxidative metabolism of mitochondria in skeletal muscle, at least in part, mediating its anti-aging effects. In rats, NMN as an anti-aging candidate compound has a longer retention time than Nam. Because Nampt is inhibited by NAD+, Nam is not converted to NAD+ by the Nam→NMN→NAD+ pathway, but prepare NAD+ by Nam→nicotinic acid (NiA)→nicotinic acid mononucleotide (NaMN)→nicotinic acid adenine dinucleotide (NaAD). )→NAD+ pathway. On the other hand, NAD+ synthesis from NMN is not regulated by cellular NAD+ levels, so an increase in NAD+ is easier. According to metabolic control mechanisms and many reports on NMN, NMN may be more effective as a NAD+ precursor than Nam. Since Sirt1 is an NAD+-dependent enzyme, supplementation with NMN accelerates the turnover of remedial biosynthesis of NAD+, thereby activating the Sirt1 response. Sirt1 can induce DNA silencing, helping to fight aging and prolong life. Studies have also shown that in addition to mammals, enhanced NAD+ biosynthesis can extend the lifespan of yeast, worms and flies.