Multiple functions of β-NMN

Nicotinamide Mononucleotide (NMN) is a natural bioactive nucleotide that exists in two isomers, α and β, where the β isomer is the active form of NMN. β-NMN is one of the key precursors for the production of nicotinamide adenine dinucleotide (NAD+). NAD+ is a redox coenzyme that is widely involved in various biological effects such as intracellular energy metabolism, DNA repair, and signal transduction. Plays an important role in the generation of cellular energy in living organisms.

β-NMN increases NAD+ levels in animals and exerts its functions through NAD+. Studies have found that β-NMN can enter the blood within 2 to 3 minutes after supplementation, increase the content of β-NMN in tissues within 15 minutes, and rapidly increase the level of NAD+ in the body to exert its functions, such as activating lysine with NAD+ as the only substrate Acid deacetylase, regulate cell survival and death process, maintain intracellular redox state, etc.

Recent studies have shown that regulating the level of β-NMN in organisms can have a better effect on intestinal health, cardiovascular and cerebrovascular diseases, neurodegenerative diseases, and anti-aging.

Skin aging can be regarded as the accumulation of cell and tissue changes due to the disorder of biological regulation mechanism, which can be divided into endogenous aging and exogenous aging. Intrinsic aging is genetically determined and manifests as an inevitable physiological process developing fine lines on dry and thin skin. Exogenous aging is affected by external factors, such as light, air pollution, smoking, etc., which can lead to rough skin texture, deep and thick wrinkles. These all contribute to the skin's appearance of aging, fatigue, loss of vitality and attractiveness.

With the intensification of global aging, anti-aging has become one of the most important demands of consumers in recent years.

NMN achieves anti-aging effects by affecting the NAD+ level in the body. In nematode and Drosophila models of Werner syndrome, sufficient expression of NAD+ can significantly prolong the lifespan of nematodes and Drosophila in the model, delay the aging rate and improve stem cell dysfunction.

In an ATM mouse model, feeding NMN increased intracellular NAD+ levels, reduced the severity of A-T neuropathology, normalized neuromuscular function, delayed memory loss, and extended lifespan. The binding of NAD+ to the NHD (Nudix homology domains) domain of DBC1 (deleted in breast cancer 1) prevents it from inhibiting PARP1 (Poly (ADP-Ribose Polymerase) 1, poly (adenosine diphosphate-ribose) polymerase), PARP1 is A key DNA repair protein.

LIJ et al found that as mice age and NAD+ concentrations decrease, DBC1 increasingly binds to PARP1, leading to DNA damage accumulation. This process rapidly reverses NDA damage by replenishing NAD+. Thus, NAD+ directly regulates protein-protein interactions, the regulation of which can protect against cancer, radiation and aging.

MILLSKF et al. found that NMN can effectively alleviate the age-related physiological decline of mice after feeding mice with NMN for a long time. In the absence of any overt toxic or deleterious effects, NMN suppressed age-related weight gain, enhanced energy metabolism, promoted physical activity, improved insulin sensitivity and plasma lipid profile, and improved ocular function and other Pathophysiology. NMN prevented age-related gene expression changes in key metabolic organs and enhanced mitochondrial oxidative metabolism and mitochondrial nucleoprotein imbalance in skeletal muscle.

In addition, studies have shown that NMN can improve the intestinal structure of aging mice, the mitochondrial function of vascular endothelial cells, and rejuvenate aging blood vessels.

Tag: NMN

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