Abstract
The aim of this study was to determine the effects of long-term Nicotinamide mononucleotide (NMN) treatment on modulating gut microbiota diversity and composition, as well as its association with intestinal barrier function. In this study, C57BL/6J mice were fed different concentrations of NMN, and their feces were collected for detection of 16S rDNA and non-targeted metabolites to explore the effects of NMN on intestinal microbiota and metabolites. The results revealed that NMN increased the abundance of butyric acid-producing bacteria (Ruminococcae_UCG-014 and Prevotellaceae_NK3B31_group) and other probiotics (Akkermansia muciniphila), while the abundance of several harmful bacteria (Bilophila and Oscillibacter) were decreased after NMN treatment. Meanwhile, the level of bile acid-related metabolites in feces from the G1 group (0.1 mg/ml) was significantly increased compared to the control group, including cholic acid, taurodeoxycholic acid, taurocholic acid, glycocholic acid, and tauro-β-muricholic acid. In addition, long-term NMN treatment affected the permeability of the intestinal mucosa. The number of goblet cells and mucus thickness increased, as well as expression of tight junction protein. These results demonstrate that NMN reduced intestinal mucosal permeability and exerts a protective effect on the intestinal tract. This study lays the foundation for exploring NMN's utility in clinical research.
Highlights
As early as 1906, nicotinamide adenine dinucleotide (NAD+) was known to increase the fermentation rate of yeast extract, which subsequently became a hot spot in biological research
The results showed that there was no significant difference in body weight or weight gain rate between the two groups of mice (Figure 1)
Principal coordinate analysis (PCoA) results showed significant differences between the G4 group and the CON group, indicating a significant difference in microbial composition (Figure 2E). These results indicated that 0.6 mg/mL of NMN had a significant effect on the microbial composition of mouse feces
Summary
As early as 1906, nicotinamide adenine dinucleotide (NAD+) was known to increase the fermentation rate of yeast extract, which subsequently became a hot spot in biological research. The two intermediates of NAD+, NMN and nicotinamide riboside (NR), have received renewed attention [1]. NMN is synthesized by niacinamide (a form of water-soluble vitamin B3) and 5′-phosphoribosyl-1-pyrophosphate (PRPP). This process is catalyzed by the NAD+ biosynthetic rate-limiting enzyme nicotinamide phosphoribosyltransferase (NAMPT) [2, 3]. Recent studies have shown that NMN increases concentrations of NAD+ in the pancreas, liver and other tissues [4]. Long-term (1-year) oral administration of NMN (up to 300 mg/kg) did not cause any obvious deleterious or toxic effects [5]. NAD+ could stimulate intestinal goblet cells to secrete mucus to maintain the integrity of intestinal mucosa, proving that NAD+ could protect intestinal homeostasis to a certain extent [9]
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