NMN’s Liver Protection Validated: Targeting Hamp to Improve Alcohol-Induced Hepatic Steatosis

Recently, a research team from Zhejiang Chinese Medical University published a new study in Communications Biology, uncovering a novel mechanism by which nicotinamide mononucleotide (NMN) alleviates chronic alcohol-triggered liver injury. The research verifies that restoring hepatic Hamp (hepcidin) expression serves as the core target for NMN to relieve alcoholic fatty liver disease.

Excessive long-term alcohol intake reduces hepatic NAD⁺ levels and suppresses Hamp expression, disrupting iron homeostasis, triggering oxidative stress and lipid buildup, and ultimately leading to fatty liver and liver damage. Based on mouse models and cellular experiments, supplementation with NMN replenishes hepatic NAD⁺, activates the C/EBPα transcriptional pathway and upregulates Hamp, thereby mitigating iron overload, lipid accumulation and hepatic inflammation.

Experimental data proves NMN treatment markedly lowers hepatic lipid deposition and optimizes indicators including transaminase and triglyceride levels. For the first time, this study clarifies the regulatory role of the NAD⁺–C/EBPα–Hamp axis in alcoholic liver disease. It provides solid academic evidence for developing NMN-based liver-protective and hangover-relief functional foods and fuels NMN’s industrial expansion from anti-aging into liver health sectors.

FOR DETAIL: https://doi.org/10.1038/s42003-026-10398-3

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