Two types of antioxidants, NAD+ and NMN, have been shown to improve cell health. NMN has shown superior effects in multiple tissues, such as the liver and kidneys. Its ability to increase protein synthesis in the mitochondria is a key factor in the beneficial effects of NMN. The next study aims to further investigate the benefits of NMN. The results will be reported in a journal soon.
NMN can be rapidly synthesized into NAD+ in the tissues of aged mice. It also improves insulin sensitivity, skeletal muscle and mitochondrial metabolism, and inhibits age-related gene expression. In addition, it reduces reactive oxygen species and delays cognitive decline in Alzheimer’s disease mouse models. NMN and NAD+ also improve antioxidant activity and may help maintain the blood-brain barrier integrity.
There are two main pathways in the body for producing NAD+. One is the de novo pathway, which starts from the first precursor of NAD+, tryptophan. The other is the salvage pathway, which creates NAD+ from degradation products of proteins. In order to make these enzymes, all proteins must be regularly degraded. Similarly, the two types of antioxidants are derived from different sources, so the body can recycle them as needed.
In a study at the Keio University School of Medicine, in Japan, NMN was measured in skeletal muscle, white adipose tissue, and liver. NMN was found to be stable in the absence of FBS, and the levels were elevated at 11 months of age. In contrast, NAD+ was measured in the brain and skeletal muscle, which were significantly higher after NMN administration.
NMN is larger than NR, and needs to be broken down in order to enter cells. NR, on the other hand, is more effective at converting degradation products into NAD+. The de novo pathway starts with tryptophan as the earliest precursor of NAD+. The salvage pathway begins with the amino acid niacin, which is used to regenerate proteins.
The biochemical role of NAD+ in the body is important. However, it is also known to be a potential energy transfer molecule. The mononucleotide form of NMN is stable in the absence of cells, but degrades rapidly in the presence of cells. In the absence of cells, NMN degrades rapidly into Nam and NR. When taken by humans, the mononucleotide forms were more stable than NR.
In addition to its role in the biochemical functions of NAD, NMN also has many potential therapeutic benefits. Besides improving energy metabolism, NMN also protects the heart from ischemia and preserves the skeletal muscle of elderly mice. It has also shown positive effects on inflammatory and aging, including reduced risk for Alzheimer’s disease. It has also been found to reduce the number of reactive oxygen species in the blood and lowers the incidence of hypertension, a major cause of ischemic stroke.
The biochemical reactions between NMN and NAD+ are crucial for the health of the body. In mice, the levels of NMN were decreased significantly in the liver and the amount of NAD+ in the brain was reduced to a minimum of 40%. In contrast, NMN and NR were not detected in the presence of cells. These studies show that NMN and NAD+ are beneficial in a variety of ways. They increase the production of the antioxidant enzyme, which is responsible for a reduction in the production of NAD+.
NMN has many potential therapeutic uses in the body. It helps the brain produce more NAD+. NMN is also beneficial in the prevention of aging. It enhances physical activity and prevents the expression of age-related genes. Its biochemical role in energy metabolism is unknown. Although NMN and NAD+ have many benefits, it remains a controversial substance for the development of diseases.
The conversion of NAD+ to NAMN takes the same steps as that of NA. Moreover, NR is more potent than NR and is more beneficial in preventing dysregulation of the epigenome. The metabolite quinolinic acid (QAPRT) is a precursor of NAMN. When converted to NAD+, NAMN increases the body’s fat-free mass.