beta-Nicotinamide mononucleotide

beta-Nicotinamide mononucleotide (β-NMN) is an intermediate in the biosynthesis of nicotinamide adenine dinucleotide[1].

In a Nampt^+/- mouse model of metabolic disease, β-NMN (50-100 µM) has been used to enhance NAD biosynthesis and glucose-stimulated insulin secretion, demonstrating a role for Nampt in β cell function[2].

Furthermore, at 500 mg/kg/day, β-NMN has been shown to ameliorate glucose intolerance in high-fat diet-induced type 2 diabetes mice by restoring NAD⁺ levels[3].

References:

[1]. Gallí M, Van Gool F, Rongvaux A, et al. The nicotinamide phosphoribosyltransferase: A molecular link between metabolism, inflammation, and cancer. Cancer Research, 2010, 70: 8-11.

[2]. Revollo J R, Körner A, Mills K F, et al. Nampt/PBEF/visfatin regulates insulin secretion in Β cells as a systemic NAD biosynthetic enzyme. Cell Metabolism, 2007,  6(5): 363-375.

[3]. Yoshino J, Mills K F, Yoon M J, et al. Nicotinamide mononucleotide, a key NAD+ intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell Metabolism, 2011, 14(4): 528-536.