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NMN (Nicotinamide Mononucleotide),
Type 2 diabetes is a contagious disease that threatens health. There is a certain relationship between high sugar and high-fat food.
However, scientists have shown that nicotinamide adenine dinucleotide (NAD) precursor, naturally occurring nicotinamide mononucleotide) NMN can promote NAD biosynthesis and effectively restore normal blood glucose in type 2 diabetic rats.
A metabolic pathway mediates the restriction enzyme nicotinamide phosphoribonuclease (Nampt) in nad biosynthesis. Among the many functions of energy metabolism, nad activates a protein called sirtuin1 (SIRT1). It is reported that Nampt mediated nad biosynthesis and SIRT1 can regulate glucose stimulated insulin secretion in pancreatic cells.
The survey showed that healthy mice fed high-fat foods had significant diabetes within 6 months. The nad concentration in these mouse tissues decreased significantly. Because NAD can not be injected directly into mice, its toxicity can induce NAD subcutaneous injection of NMN into mice, and promote NAD concentration and decrease blood sugar concentration in diabetic animal. The application of NMN improved glucose tolerance in male diabetic mice, and successfully conducted glucose tolerance test in female diabetic mice. In addition, NMN treatment improved the insulin sensitivity of liver tissue, reversed the changes of oxidative stress and inflammation related gene expression in liver, and improved the lipid stability of diabetic rats.
The potential metabolic pathways affected by NMN are similar in mice and humans. Therefore, these findings can reveal the relationship between NMN, NAD, obesity and type 2 diabetes in humans. Although further research is needed.
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