Enhancement effect of oral NMN on NAD+

Multiple experiments have shown that oral administration of NMN can effectively enhance NAD+ levels in humans and animal models. As a regulatory factor closely related to energy metabolism, NAD+ exists in many tissues, but its expression varies greatly in different tissues. In rodent studies, oral administration or injection of NMN can effectively enhance NAD+ biosynthesis in various tissues, including pancreas, liver, adipose tissue, heart, skeletal muscle, and kidney, and NAD+ levels in the hippocampus and hypothalamic brain regions also increase rapidly .

The above results show that NMN can cross the blood-brain barrier and serve as a substrate for NAD+ biosynthesis in brain regions, providing evidence that NAD+ can improve neurodegenerative diseases.

The transporter of NMN, SLC12A8, is most highly expressed in the small intestine, so after NMN administration, the most significant increase in NAD+ was detected in the small intestine. Alessia et al. fed mice with the double-labeled isotope NMN (O18-D-NMN) and clearly detected 018-D-NMN in the jejunum and ileum after 10 min. NMN in the small intestine is absorbed into the blood through SLC12A8 on the small intestinal villi.

Furthermore, in experiments by Alessia et al., who fed mice NMN at 500 mg/kg body weight, plasma NMN levels significantly increased 5 minutes after feeding. There appear to be differences in the efficiency of intestinal absorption of different doses of NMN fed.

In a study by Kathryn et al., feeding mice at 300 mg/kg resulted in a rapid increase in plasma NAD+ levels within 2.5 minutes and a sustained increase within 5-10 minutes.

In experiments in humans, oral administration of NMN resulted in increased plasma NMN and NAD+ concentrations similar to those observed in rodents.

In a clinical trial of oral NMN in Japan in 2020, it was found that adult males who took 100, 250 or 500 mg NMN capsules orally had significant changes in plasma NMN metabolites, with the most significant changes at a dose of 500 mg/kg.

The liver contains most of the enzymes required for the NAD+ biosynthetic pathway.

Using isotope-tracing techniques and quantitative flux analysis, Liu et al. showed that the liver accounts for more than 95% of circulating nicotinamide in mice, suggesting that the major site of conversion of NMN to NAD+ via the biosynthetic pathway is in the liver.

In a study by Kathryn et al., mice were fed the double-labeled isotope NMN (C13-D-NMN) at a dose of 300 mg/kg body weight and mass spectrometry was used to track these markers NAD+ in the liver, and it was found that although the liver The increase in NMN was not as pronounced and rapid as in blood, but double-labeled NAD+ (C10-D-NAD+ ) was clearly detected at 13 minutes, with a further increase in C30-D-NAD+ levels at 13 minutes.

Oral or injected NMN also increases NAD+ water in the muscles. Furthermore, in experiments by Kathryn et al., C30-D-NAD+ was detected in mouse muscles 13 min after feeding.

In experiments by Golam et al., they injected mice with a dose of 500 mg/kg body weight intraperitoneally and found increased NAD+ levels in the muscles of mice.

In a 2021 study of NMN improving CICI-induced cognitive impairment, it was found that feeding C57 mice at a dose of 250 mg/kg body weight increased NAD+ levels in the hippocampus.

Similarly, in this experiment, they injected C57BL/6N mice with a dose of 250 mg/kg body weight and found that injecting NMN into the body effectively increased NAD+ levels in the brain.

A higher dose of NMN was tested in a trial by Chidambaram et al. They administered a dose of 400 mg/kg body weight orally to C57/B6J mice and examined the brain tissue of the mice 45 minutes after the feeding and found a significant increase in NAD+ levels in the brain.

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