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Nicotinamide mononucleotide (NMN) is one of the important precursors of NAD+ in mammals. The production reaction in the body depends on the catalysis of nicotinamide ribose phosphate (Nampt) (Hosseini et al., 2019). NMN in the human body is mainly derived from external food intake and the body's synthesis. Some fruits and vegetables that we know contain NMN, such as tomatoes, avocados, edamame, broccoli, cabbage, beef, and shrimp.
Nicotinamide adenine dinucleotide (NAD+) is an important hydrogen carrier of oxidoreductase in cells (Park et al., 2016). Its level fluctuations will affect mitochondrial function and metabolism, circadian rhythm, immune response and inflammation, DNA Repair, cell division, protein-protein signaling, epigenetics (Yoshino et al., 2011, Oresic et al., 2011, Canto et al., 2015).
NMN VS NAD:
The physiological function of NMN depends on being converted into NAD+ in the body to play a role, for example, to maintain a state of redox balance, regulate various metabolic activities of cells, etc. (Kiss et al., 2019, Xie et al., 2020, Alano et al., 2007, Revollo et al., 2007). In recent years, studies have found that NAD+ is also involved in multiple biological processes related to the nervous system, including regulating nerve cell mitochondrial energy metabolism and apoptosis (Wang et al., 2016). However, with age, the level of NAD+ in mammals gradually decreases, and this decrease hurts cellular respiration and ATP. On the one hand, in recent years, the use of NAD+ precursors to restore NAD+ levels has received widespread attention as a promising treatment method (Xie et al., 2020). On the other hand, the increase in the level of NMN in the mitochondria confirms that the synthesis of NAD+ in the mitochondria is dependent on NMN to a certain extent. Studies have shown that in animal models, NMN can reduce neuronal death and ROS generation, and improve cognitive impairment (Kiss et al., 2019).
As a signal molecule, NAD+ can control hundreds of physiological processes such as energy metabolism and cell survival by regulating NAD+ sensing enzymes. Due to changes in food intake, exercise, and age, NAD+ rises and falls accordingly (Yoshino et al., 2018, Jun Li, 2017, Tineke van de Weijer, 2015). NAD+ levels steadily decrease with age, leading to metabolic changes and increased disease susceptibility. Restoring NAD+ levels in old or sick animals can promote health and prolong the lifespan, prompting people to find safe and effective NAD+ promoting molecules, which have therapeutic effects on one disease or even many diseases, enhance the body's elasticity, and prolong the health Human life span (Rajman L 2018).
Nicotinamide mononucleotide reduces oxidative stress in cells by increasing the expression of NAD+, thereby enhancing cell antioxidant levels and SOD enzyme activity, restoring mitochondrial function. Then, SIRT3, which locates mitochondria as an NAD+-dependent protein, combined with its inhibitor 3-TYP to reversely prove the experiment found that nicotinamide mononucleotide does upregulate SIRT3 through the NAD+ metabolic pathway to achieve D-galactose-induced The anti-aging effect of HT22 cells.
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