Nicotinamide adenine dinucleotide (NAD) is a key component in many cellular processes. Aside from being an electron carrier, NAD plays a role in sirtuin acetylases and poly(ADP ribose) polymerases. It is also a substrate for enzymes that are essential for mitochondrial functions. In the heart of the matter, it seems that NMN is the missing link in a dysfunctional KLF4 / KLF4 deficient cardiac duo.
In fact, it is possible to take a NAD+ supplement daily to produce a heart with the requisite metabolic alkalinity and mitochondrial function. The trick is to provide a sufficient dose of NMN in a safe environment that can be readily replenished with the same if needed. This is a tricky task due to the relative toxicity of the substance. Thus, a pharmacological treatment was devised.
As a reward for a dietary regimen, mice were fed a daily dose of 500 mg/kg NMN in PBS. While this might seem like overkill for a single dose, the results are impressive. Compared with control subjects, NMN-deficient mice exhibited less hypertrophic cardiomyopathy, reduced levels of oxidative stress and improved heart efficiency. NMN also rescued mitochondrial homeostasis. Lastly, the NMN-treated group exhibited a reversal of the heart failure induced by KCl. The heart was restored to its former glory in short order.
Nicotinamide adenine dinucleotide is a functional chemical that is available in most foods and is a useful part of many metabolic pathways. However, it is not a panacea. To elucidate the role of NAD in human physiology, it is essential to understand its role in the context of an individual.