Nicotinamide mononucleotide (NMN) may be a nucleotide that’s most recognized for its role as an intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis. There is variation between eukaryote and prokaryote for biosynthetic NMN Pathway which are followed for the case of eukaryotic human. The pathway uses nicotinamide which is contrast to other pathways like phosphorylation of nicotinamide riboside.

Being well tolerated, with no reported or observed side effects during long term administration in mice, and preventing age-associated physiological decline, NMN proved to be effective in treating high fat diet-induced type 2 diabetes, by reversing mitochondrial dysfunction associated with aging and rescuing the effect of age-associated decline in neural stem cells.

Diabetes may be a chronic and progressive disease with continuously increasing prevalence, rising financial pressure on the worldwide healthcare systems.


This article focuses on the biosynthesis of NMN in mammalian and prokaryotic cells and therefore the mechanism of absorption alongside the reported pharmacological activities during a murine model. Heart failure is related to mitochondrial dysfunction in order that restoring or improving mitochondrial health is of therapeutic importance.

Recently, a reduction in NAD+ levels and NAD+-mediated deacetylase activity has been recognized as negative regulators of mitochondrial function.

There is conversion of NMN and NAD+ after the unavailability of an appropriate transporter of NMN It enters inside the mammalian cell within the sort of nicotinamide riboside. There are multiple benefits of the molecule by the pharmacological activities for the preclinical studies used for therapeutic use.

The medicine involves NAD+ bio photosynthesis involving pharmacological activities like cellular biochemical functions, cardio protection, Alzheimer’s disease, and complications related to obesity. The recent ground breaking discovery of anti-aging activities of this chemical moiety has added a valuable essence in the research involving this molecule.

By using a cardiac specific KLF4 deficient mouse lines, it is found that mitochondrial protein hyper acetylation which reduces Sirt3 and NAD+ levels under heart before stress. It suggests that there is predisposition of KLF-4 deficient and NAD+-associated defects. The Nicotinamide Mononucleotide (NMN) is successful in administering and successfully protecting the mutant mice from pressure overload-induced coronary failure.

Mechanically, we can observe that NMN preserved mitochondrial ultrastructure, reduced ROS, and prevented cell death in the heart. In cultured cardio myocytes, NMN treatment significantly increased long-chain carboxylic acid oxidation despite no direct effect on pyruvate oxidation. Collectively, these results provide proof that hyper acetylation of mitochondrial proteins is critical within the pathogenesis of cardiac diseases.


The level of nicotinamide adenine dinucleotide (NAD) decreases in Parkinson’s disease (PD), and its reduction has been reported to be involved in many age-associated neurodegenerative pathologies. And hence, from all the discussions taken into due consideration, it can be concluded that NAD prevents pathological changes in PD via decreasing mitochondrial dysfunctions.

Leave a comment

Your email address will not be published. Required fields are marked *