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In mouse models of highfat dietinduced liver steatosis, it significantly inhibits hepatic NNMT activity, reduces NAM methylation, increases NAD+ and SAM levels, enhances mitochondrial fatty acid oxidation, reduces hepatic triglyceride and lipid accumulation, lowers lipotoxicity markers (e.g., malondialdehyde, transaminases), improves hepatocellular injury, and reverses steatosis

However, caution must be taken regarding the possible extension of specific models

Beyond stem cell activity, another proposed mechanism involves NAD+ replenishment

The elevated homocysteine creates further oxidative stress and neuroinflammation, which in turn damages the myelin sheath and worsens the cognitive dysfunction and neuropathy