Chronic inflammation is an important factor in the islet beta cell failure in type 2 diabetes mellitus (T2DM). Exposure to pro-inflammatory cytokines such as interleukin 1β (IL1β) and Tumor necrosis factor α (TNFα) can cause islet β cell death and inhibit insulin secretion. Because the pancreas lacks iNAMPT (intracellular Nampt), islets rely on circulating eNAMPT (extracellular Nampt) to stimulate insulin secretion. Nicotinamide mononucleotide
can restore eNampt levels, reverse the impaired insulin secretion, and protect the islets from the negative effects of pro-inflammatory factors. The CAS number of NMN
Caton et al. found that NMN can improve islet dysfunction in high fructose (FRD) mice, reverse FRD and pro-inflammatory cytokine-mediated changes in islet marker gene expression, reduce pro-inflammatory factor expression, restore insulin secretion and improve cytokine Nampt-mediated islet dysfunction. Taken together, NMN improves islet function in FRD mice and is associated with beneficial changes in gene expression involved in glucose metabolism, anti-inflammatory and apoptotic processes.