Nicotinamide mononucleotide (NMN) is an essential molecule in a large number of cellular processes. It plays a vital role in maintaining the health of cells and tissues, and in maintaining cellular energy.

This molecule is synthesized from nicotinic acid through a de novo pathway. The NMN pathway is involved in the regulation of methionine metabolism. NMN inhibits the aging-related increase of acetylation in proteins that regulate fatty acid b oxidation.

Using NNMT-KO mice, we investigated the pathological significance of NMN in CKD. Several renal markers were measured. Although NMN did not show an effect on these renal markers, it decreased acetylation in proteins that are involved in transport and translation processes.

NMN suppressed the aging-related increase of acetylation on NNT and cytochrome 3a25. Nitrogenous species were reduced in the NMN cotreated cells, and L-Isoleucine, 4,8-dimethylnonanoyl carnitine and pyruvic acid were reduced. These results suggest that NMN prevents the aggregation of the Bruchpilot protein.

Increasing the availability of NAD+ is important for healthy aging and for promoting proper cellular metabolism. A diet that contains plenty of NAD+ can also promote weight control and cardiovascular health.

NMN was administered to aged mice for four weeks. The resulting metabolites were analysed. They showed a trend similar to that seen in the UUO model. No difference was detected between the KO and WT groups.

NMN and NAM administration is attracting attention as a NAD-boosting therapy for CKD. However, the exact role of NMNAT in CKD remains unclear. There are two possible mechanisms that could explain NMNAT’s effects: a direct effect of NMNAT on fatty acid oxidation and a dual effect of NMNAT on lipid metabolism.