Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice.
Level 5 - mechanism / opinion, no new human data
Preclinical animal study without human data
PubMed 28068222 · doi:10.1016/j.cmet.2016.09.013
What was done
Wild-type C57BL/6N mice fed regular chow received oral administration of nicotinamide mononucleotide (NMN) for 12 months during normal aging. The authors evaluated tissue NAD+ synthesis, body weight gain, energy metabolism, physical activity, insulin sensitivity, plasma lipid profiles, eye function, organ gene expression, and skeletal muscle mitochondrial metabolism.
What was found
The abstract reports no numerical values, effect sizes, or confidence intervals. Qualitatively, oral NMN was rapidly utilized for tissue NAD+ synthesis, suppressed age-associated weight gain, enhanced energy metabolism, increased physical activity, improved insulin sensitivity and plasma lipids, and ameliorated eye function without apparent toxicity. NMN also prevented age-associated gene expression changes in key metabolic organs and enhanced skeletal muscle mitochondrial oxidative metabolism.
Why it matters
This study provides foundational preclinical evidence that chronic oral supplementation with an NAD+ intermediate can safely attenuate broad aspects of normal age-related metabolic and physiological decline in a mammalian model.
Limits
The study was conducted entirely in mice, so findings cannot be directly extrapolated to human efficacy or safety. The abstract provides no sample sizes, dosages, or numerical data.
Cited by
- context NMN is chemically unstable and degrades rapidly.