The Safety and Antiaging Effects of Nicotinamide Mononucleotide in Human Clinical Trials: an Update

Mitochondrial GPX4 acetylation is involved in cadmium-induced renal cell ferroptosis

“…Importantly, Cd-induced oxidized lipids and AKI were exacerbated in Sirt3 −/− mouse kidneys. NMN is a precursor of NAD + synthesis [ 46 ]. Accumulating data have demonstrated that NMN could activate mitochondrial SIRT3 signaling [ 47 , 48 ].…”

Nicotinamide Mononucleotide (NMN) Works in Type 2 Diabetes through Unexpected Effects in Adipose Tissue, Not by Mitochondrial Biogenesis

“…It was previously proposed that NMN as a NAD + precursor activates NAD + -dependent Sirt1 which, in turn, through TFAM and c-Myc transcription factors, induces mitochondrial biogenesis [ 12 ]. However, this seems to have a minor if not totally absent effect as trials in humans do not report the expected results [ 18 ]. Therefore, a discovery proteomics method was required to find hints about where glucose is going following NMN treatment.…”

“…However, human trials results are disappointing [ 18 ], and the previously proposed NMN-induced mitochondrial biogenesis idea is doubtful. Previous mechanistic approaches failed to provide a significant response to the question: If NMN works in T2DM, where is glucose going?…”

Preventing the Fatty Acid-Transporter CD36 From Taking its Toll on the Heart

“…Interestingly, from a clinical perspective, NMN and more often nicotinamide riboside have already been tested in various clinical trials with patients with mild metabolic disorders or aged but still in good health, although with somewhat lower benefits than expected from preclinical research results as regards systemic parameters such as insulin resistance or body weight loss but rather positive results in the reduction of inflammatory markers. 15,16 Future trials, however, should be better designed and focus on really sick patients to address the potential of these therapeutic strategies to reduce tissue lipotoxicity in patients with obesity.…”