NAD+ (100mg & 750mg)

NAD+ Peptide Overview

NAD+, or Nicotinamide Adenine Dinucleotide, stands as a vital endogenous nucleotide crucial for regulating fundamental processes including metabolism, energy generation, and DNA repair. It is recognized as a secondary messenger, potentially participating in calcium-dependent signaling pathways and contributing to immunoregulation. The synthesis of NAD+ is believed to occur through a de novo mechanism, involving the conversion of the amino acid tryptophan through a series of enzymatic steps. Researchers identify five key components in NAD+ synthesis, encompassing tryptophan, nicotinamide, nicotinic acid, nicotinamide riboside, and nicotinamide mononucleotide. Once produced, NAD+ is implicated in over 500 enzymatic reactions and cellular processes, acting as a crucial coenzyme in redox functions and undergoing conversion to NADH to engage in various metabolic pathways.

Overview

Researchers propose that Nicotinamide Adenine Dinucleotide (NAD+) serves as a coenzyme, engaging with three primary classes of enzymes, namely: (A) deacetylase enzymes within the sirtuin class (SIRTs), (B) enzymes of poly ADP ribose polymerase (PARPs), and (C) cyclic ADP ribose synthetase (cADPRS). Investigations indicate that each enzyme class potentially interacts with NAD+ in distinct ways, influencing various cellular processes. This intricate interplay showcases the versatility of NAD+ as a coenzyme, participating in the modulation of deacetylation processes, poly ADP ribose polymerization, and the synthesis of cyclic ADP ribose, each contributing to vital cellular functions.
. (A) SIRTs, part of the sirtuin class of deacetylase enzymes, are thought to play a role in maintaining the balance of mitochondria, supporting the regeneration of stem cells, and possibly influencing the loss of stem cells and nerve degeneration.

. (B) PARPs, consisting of 17 diverse enzymes, collaborate with NAD+ enzymes to generate poly ADP ribose polymers. This synthesis is believed to contribute to genome stability, suggesting a crucial function in cellular genetic integrity.

. (C) cADPRS, encompassing CD38 and CD157, serve as essential components in immunological cells. These cADPRS enzymes seem to hydrolyze NAD+, potentially triggering stem cell regeneration and DNA repair processes. This activity is deemed significant for sustaining overall cellular health.

The NAD+-dependent enzymes mentioned above are theorized by researchers to engage in actions influenced by the presence of Nicotinamide Adenine Dinucleotide. It is postulated that these three enzymes, reliant on NAD+, might contend for bioavailability within the cellular environment. The suggested interplay between these enzymes implies that the potential functions of one, like SIRTs, could impact the activity of others, such as reducing PARPs activity. This intricate relationship underscores the importance of maintaining a delicate balance in the availability and utilization of NAD+ for achieving optimal impact on cellular processes. Striking this balance is considered crucial for preventing potential disruptions in cellular systems.

Scientific Investigations and Clinical Trials

NAD+ Peptide and Enhanced Aging Outcomes

Studies highlight the crucial role of nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) as vital intermediates in the promotion of favorable aging outcomes. In an investigation spanning 12 months,(7) aging mice were administered NMN, resulting in augmented NAD+ synthesis. The findings of the study suggested that NMN intervention contributed to mitigated weight gain, heightened energy metabolism, increased physical activity, and improved lipid profile in the aging mice.

NAD+ Peptide and Mitochondrial Revitalization

Researchers delve into the relationship between mitochondrial dysfunction and the onset of neurodegenerative diseases, emphasizing the impact on electron transport chain and ATP synthesis. In a comprehensive study,(8) aging mice were administered NMN, a key NAD+ intermediate, over a period of 3 to 12 months. The primary objective was to assess the potential influence of the peptide on mitochondrial respiratory processes, employing fluorescent NMN protein in the mouse models. Post-peptide administration, mitochondrial oxygen consumption rates in nerve and brain cells were scrutinized. The results hinted at a restoration of mitochondrial functions in the aged mice, suggesting that NMN could be promptly assimilated by cells to generate NAD+, potentially fostering positive outcomes.

NAD+ Peptide and Neuronal Protection Post-Ischemic Stress

In this research endeavor,(11) the central focus was on unraveling the neuroprotective potential inherent in Nicotinamide Adenine Dinucleotide against ischemic stress-induced damage in mice. To simulate ischemic stress, neuronal cultures in rats were subjected to a 2-hour deprivation of oxygen and glucose. NAD+ was introduced directly into the culture medium, either preceding or following the induced ischemic stress. The subsequent analysis, conducted 72 hours after NAD+ introduction, revealed a noteworthy enhancement in DNA base excision repair activity (DNA BER), cell viability, and repair of oxidative DNA damage. Remarkably, these improvements were observed regardless of whether Nicotinamide Adenine Dinucleotide was administered prior to or after the initiation of ischemic stress.

NAD+ Peptide and Metabolic Health

In studies involving mice, the administration of the NAD+ peptide to boost Nicotinamide Adenine Dinucleotide levels to normal concentrations showed promising effects in preventing obesity and alcoholic hepatitis. Additionally, it was suggested that the peptide might enhance glucose homeostasis and overall liver health. In another facet of research focusing on aged mice kidney cells, the supplementation of NAD+ appeared to stimulate SIRTs activity. This activation, in turn, demonstrated potential neuroprotective effects against glucose-induced kidney cell hypertrophy. Moreover, the introduction of NMN, an NAD+ intermediate, showed indications of promoting neuroprotective responses in the context of cisplatin-induced kidney injury.

NAD+ Peptide and Musculoskeletal Health

In experiments involving aged mice, daily administration of NMN for seven days exhibited potential benefits for musculoskeletal health. It was proposed by researchers that the peptide may contribute to heightened ATP (energy) production, diminished inflammation, and improved mitochondrial functions in skeletal tissues.

Cardiometabolic Impact of NAD+ Peptide

Researchers propose that an insufficiency of Nicotinamide Adenine Dinucleotide might result in diminished SIRT activity, leading to compromised energy production and aortic constriction. In a study involving mice, the administration of NMN 30 minutes prior to induced ischemia demonstrated a potential cardioprotective effect against ischemic injury. It is important to note that the NAD+ peptide is exclusively available for research and laboratory purposes. Prospective users are advised to thoroughly review and adhere to our Terms and Conditions before placing an order.