NMN Inhibits the Onset of Liver Fibrosis

When our livers get injured, whether from chronic alcohol use or the buildup of cellular stress in the form of damaging molecules called reactive oxygen species, it can cause scarring, known as fibrosis. This excessive scarring can lead to diseases like liver cancer and cirrhosis and, currently, no therapeutic options to prevent it exist.

Deng and colleagues published a study in Free Radical Biology and Medicine describing how injecting mice with nicotinamide mononucleotide (NMN) prevented liver fibrosis. The research team from Tsinghua University in Beijing found that NMN supplementation inhibited gene activity typically activated in cells that promote liver fibrosis. Also, NMN promoted the presence of the protein 15-PGDH, which reduced the levels of PGE2, a lipid that drives liver fibrosis. These results could translate to helping people prevent liver fibrosis someday.

Reduced NAD+ Levels in Liver Disease and Injury

Nicotinamide adenine dinucleotide (NAD+) is a vital molecule in cellular energy production as well as maintenance of DNA integrity. But its levels decline with age in animals and humans alike, which has been linked to the onset of age-related diseases from Alzheimer’s disease to metabolic dysfunction and liver disease. Not only that, but previous research indicates that regular alcohol consumption reduces NAD+ levels in the liver, tying reduced NAD+ levels to liver injury.

There are several precursors to NAD+ including NMN. Studies indicate that supplementing mice with NMN increases levels of NAD+ in cells. For these reasons, Deng and colleagues tested whether NMN can alleviate symptoms in liver fibrosis.