NMN supplementation restored hepatic NAD+ levels in alcohol-fed mice, which attenuated liver steatosis, inflammation, and oxidative stress through restoration of the Hamp iron-regulation pathway. The mechanism involves C/EBPα-mediated transcriptional control of Hamp expression, linking NAD+ metabolism to iron homeostasis and lipid metabolism. This identifies NMN as a targeted dietary therapeutic for alcohol-associated liver disease (ALD) with a well-characterized molecular pathway, offering practitioners a science-backed rationale for recommending NMN to patients with metabolic liver dysfunction.
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NMN restored NAD+ and improved hepatic steatosis in alcohol-fed mice via iron-regulatory Hamp pathway, supporting its consideration in metabolic liver support.