Metabolic syndrome is increasing worldwide and is becoming a global health concern because it is a critical risk for various life-threatening diseases, including cardiovascular diseases, stroke, and cancer. Its pathophysiology is based on obesity, which consequently causes diabetes, dyslipidemia, and hypertension.
The development of metabolic syndrome is closely associated with nutrient status and lifestyle. Excess energy intake and sedentary lifestyle cause obesity and subsequent metabolic disorders. In mammalian cells, energy-sensing pathways are important for maintaining an adequate balance between energy production and expenditure.
Disturbance of these pathways results in various metabolic disorders, such as insulin resistance and fatty liver. Endogenous metabolites reflect the nutrient status in cells, and their levels regulate the activity of energy-sensing molecules. For instance, adenosine monophosphate (AMP) and adenosine triphosphate (ATP) levels regulate AMP-activated protein kinase (AMPK) activity and control glucose and lipid metabolism.
A DIVE INTO THE STRUCTURE AND BEHAVIOUR OF β- NICOTINAMIDE MONONUCLEOTIDE (NMN):
Nicotinamide adenine dinucleotide (NAD) is an essential coenzyme that engages in different energy metabolism pathways, including glycolysis, β-oxidation, and oxidative phosphorylation. Besides, it is a required cofactor for post-translational modifications such as ADP-ribosylation and deacetylation by poly (ADP-ribose) polymerases (PARPs) and sirtuins, respectively.
Thus, NAD coordinates energy metabolism, DNA damage repair, gene expression, and stress reply by these enzymes. Various researches have confirmed that NAD levels decline with aging and under disordered nutrient circumstances, such as obesity. Additionally, a deterioration in NAD levels is strictly correlated to the growth of several metabolic ailments, including diabetes and fatty liver disease.
Besides, countless investigations have exposed that the management of NAD precursors, such as β-Nicotinamide Mononucleotide (NMN) and nicotinamide riboside (NR), efficiently boost NAD levels in multiple networks and block such metabolic diseases. Certain NAD precursors are restrained in typical foods, such as cow milk, vegetables, and meats.
Consequently, remodeled NAD metabolism can be a possible spot for nutritional interference. Latterly, numerous individual clinical trials using NAD precursors have been administered to examine the safety, pharmacokinetics, and efficacy versus metabolic disorders such as glucose intolerance. In this piece, we have compiled the contemporary information on the entanglements of NAD metabolism in metabolic diseases and explain the upshots of modern human clinical trials.
SIDE EFFECTS WHICH HAS BEEN RAISED BY THE CONSUMPTION OF β- NICOTINAMIDE MONONUCLEOTIDE:
Nicotinamide riboside is possible safe with some — if any — side results. In human studies, taking 1,000–2,000 mg per day had no harmful effects. However, most human studies are short and have very few participants. For a more specific approach of its protection, more robust human knowledges are required. Some people have recorded mild to modest side outcomes, such as vomiting, weakness, neuralgias, diarrhea, abdomen discomfort, and indigestion.
RESULT AND CONCLUSION:
The department of nicotinamide mononucleotide (NMN) has been designated to alleviate aging-related dysfunctions like Resveratrol at https://www.cofttek.com/product/501-36-0/ . However, the safety of NMN in humans has remained unclear.
