Nicotinamide mononucleotide (NMN), one of the key precursors of NAD+ and products of theNAMPT reaction , is converted to NAD+ by nicotinamide mononucleotide adenylyltransferase.
β-Nicotinamide mononucleotide, a nicotinamide phosphoribosyltransferase product and vital NAD+ precursor, exhibits pharmacological benefits in cellular biochemistry, cardioprotection, diabetes, Alzheimer's, and obesity complications[1].
体内研究
β-Nicotinamide mononucleotide, at 500 mg/kg administered intraperitoneally thrice weekly for 7-10 weeks, prevents mitochondrial DNA damage and Doxorubicin-induced cardiac dysfunction[3].
Nampt knockout significantly reduces tumor growth, whereas β-Nicotinamide mononucleotide, at 300 mg/kg body weight given intraperitoneally every other day for two weeks, increases tumor growth in C57BL/6 mice with Hepa1-6 cells[2].
β-Nicotinamide mononucleotide improves glucose intolerance by restoring NAD+ levels and enhances hepatic insulin sensitivity, modulating gene expression related to oxidative stress, inflammation, and circadian rhythm, in part through SIRT1 activation in type 2 diabetic mice induced by a high-fat diet[4].
体外研究
The pharmacological effects of β-nicotinamide mononucleotide are largely due to its involvement in NAD+ synthesis, impacting cellular biochemical functions, cardioprotection, diabetes, Alzheimer's disease, and obesity complications[1].
Nampt downregulation or inhibition decreases NAD+ levels, while supplementation with NAD+ precursors like NAM or NMN increases them, with NMN treatment impeding CD8+ T cell activation and function[2].
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