The topic of this article will revolve around NAD+ peptide and skeletal tissue studies. If this topic sparks your curiosity, keep reading. Let’s dive right in!
Nicotinamide Adenine Dinucleotide, often known as NAD+, is a nucleotide that is regarded to be an essential endogenous nucleotide since it is suggested to be responsible for controlling key activities like as metabolism, the creation of energy, and the repair of DNA. It is also thought to operate as a secondary messenger through calcium-dependent signaling mechanisms, possibly as an immunoregulatory component [i]. This theory comes from the fact that calcium is required for the mechanism.
Researchers suggest that NAD+ can be produced spontaneously through de novo synthesis, which involves the conversion of the amino acid tryptophan through a series of enzymatic processes. Researchers speculate the creation of NAD+ involves five different substances: tryptophan, nicotinamide, nicotinic acid, nicotinamide riboside, and nicotinamide mononucleotide [ii].
Research suggests that once it is generated, it may participate in over 500 different enzymatic reactions and cellular processes [vii], which may help metabolic activities. Simply put, it is thought to perform the role of a coenzyme in redox activities, being converted to NADH in the process. This conversion may then include other metabolic processes [ii].
Table of Contents
NAD+ Peptide Overview
Researchers speculate that Nicotinamide Adenine Dinucleotide (NAD+) may function as a coenzyme with three primary types of enzymes, namely:
- Deacetylase enzymes in the sirtuin class (SIRTs).
- Poly ADP ribose polymerase enzymes (PARPs).
- Cyclic ADP ribose synthetase (cADPRS).
Research suggests each family of enzymes might interact with NAD+ in the following possible ways:
- SIRTs can potentially drive mitochondrial homeostasis, stem cell regeneration, and the prevention of nerve degeneration and loss of stem cells.
- PARPs comprising seventeen separate enzymes may work with NAD+ enzymes to create poly ADP ribose polymers, resulting in genome stability.
- cADPRS contain the immune cells CD38 and CD157, which are believed to be essential. It would appear that cADPRS are responsible for hydrolyzing NAD+. As a result, they may induce stem cell regeneration and DNA repair, which may be necessary to keep healthy cells.
Researchers hypothesize that the enzymes listed above may be NAD+ dependent and that they may carry out their function in response to the presence of nicotinamide adenine dinucleotide. The findings of some researchers suggest that if all three enzymes mentioned above depend on NAD+, they may compete with one another for their bioavailability. It has been hypothesized that the potential role of SIRTs, for example, might lead to a reduction in the activity of PARPs, potentially leading to weakened systems. Therefore, it may be of the utmost importance to balance the availability of NAD+ and its utilization [iii] to have the best possible prospective impact.
NAD+ Peptide Research and Clinical Investigations
NAD+ Peptide and Aging
Nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) are important intermediates researchers suggest NAD+ may require to function properly. The findings of several studies suggest both of these intermediates may be powerful agents that promote what is known as “productive aging.” Mice allowed to age were exposed to the NMN intermediate for one year in a study [iv]. Following the completion of the research, the scientists came to the hypothesis that NMN appeared to stimulate the production of NAD+ in the mice, which resulted in a reduction in weight gain, an increase in energy metabolism, an enhancement of physical activity, an improvement in lipid profile, and other physiological properties.
NAD+ Peptide and Neurodegenerative Activity
Scientists speculate that a failure in the mitochondria could result in various functional constraints in the electron transport chain and ATP generation, possibly leading to neurodegenerative disorders. An experiment [v] was carried out in which aged mice were given NMN, an NAD+ intermediate, for a period ranging from a few months to one year. In order to analyze the potential impact of the peptide on mitochondrial respiratory processes, fluorescent NMN protein was given to the mouse models of the study. Measurements of the rates of mitochondrial oxygen consumption were taken in the nerve and brain cells of the mice. The study results suggested that the old mice’s mitochondrial activities appeared to have been recovered. This suggests that the cells may promptly employ NMN to make NAD+, which may have a potential influence.
NAD+ Peptide and Ischemic Stress
The primary objective of this research [vi] was to evaluate the neuroprotective potential of nicotinamide adenine dinucleotide in mice subjected to ischemia stress. Ischemic stress was artificially produced in the neuronal cultures of rats for this investigation by depriving the cultures of oxygen and glucose for approximately two hours; either before or after the generated ischemia stress, the amount of NAD+ present in the culture medium was restored directly. Regardless of whether Nicotinamide Adenine Dinucleotide was added before or after inducing the ischemic stress, the researchers suggested that after 72 hours of adding NAD+ to the cultures, DNA base excision repair activity (DNA BER), cell viability, and oxidative DNA damage repair appeared to be significantly improved.
NAD+ Peptide and Skeletal Tissue
When researchers gave elderly mice NMN once a day for seven days, they hypothesized that the peptide caused enhanced ATP (energy) generation, decreased inflammation, and improved mitochondrial activities.
NAD+ Peptide and Heart Function
NAD+ researchers have hypothesized that a lack of dinucleotides could result in a reduction in the activity of SIRT. It has been hypothesized that giving NMN to mice thirty minutes before inducing ischemia appeared to result in a cardioprotective effect against the ischemic injury.
More investigation is required to explore its potential in scientific research, and these studies must continue. Only academic and scientific institutions can use NAD+ for sale online. Please be aware that the compounds mentioned are not approved for human or animal consumption. Laboratory research compounds are only for in-vitro and in-lab use. Any kind of physical introduction is illegal. Only authorized professionals and working scientists may make purchases. The content of this piece is intended only for instructional purposes.
[i] Braidy N, Liu Y. NAD+ therapy in age-related degenerative disorders: A benefit/risk analysis. Exp Gerontol. 2020 Apr;132:110831. doi: 10.1016/j.exger.2020.110831. https://pubmed.ncbi.nlm.nih.gov/31917996/
[ii] Johnson, Sean, and Shin-Ichiro Imai. “NAD + biosynthesis, aging, and disease.” F1000Research vol. 7 132. 1 Feb 2018. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5795269/
[iii] Fang, E. F., Lautrup, S., Hou, Y., Demarest, T. G., Croteau, D. L., Mattson, M. P., & Bohr, V. A. (2017). NAD+ in Aging: Molecular Mechanisms and Translational Implications. Trends in molecular medicine, 23(10), 899–916. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7494058/
[iv] Mills KF, Yoshida S, Stein LR, Grozio A, Kubota S, Sasaki Y, Redpath P, Migaud ME, Apte RS, Uchida K, Yoshino J, Imai SI. Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice. Cell Metab. 2016 Dec 13;24(6):795-806. https://pubmed.ncbi.nlm.nih.gov/28068222/
[v] Long AN, Owens K, Schlappal AE, Kristian T, Fishman PS, Schuh RA. Effect of nicotinamide mononucleotide on brain mitochondrial respiratory deficits in an Alzheimer’s disease-relevant murine model. BMC Neurol. 2015 Mar 1;15:19. https://pubmed.ncbi.nlm.nih.gov/25884176/
[vi] Wang S, Xing Z, Vosler PS, Yin H, Li W, Zhang F, Signore AP, Stetler RA, Gao Y, Chen J. Cellular NAD replenishment confers marked neuroprotection against ischemic cell death: role of enhanced DNA repair. Stroke. 2008 Sep;39(9):2587-95. https://pubmed.ncbi.nlm.nih.gov/18617666/
[vii] Rajman, Luis et al. “Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence.” Cell metabolism vol. 27,3 (2018): 529-547. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6342515/