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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
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Although further study of these interactions is necessary, patients receiving these agents concurrently should be monitored for the desired therapeutic response to vitamin B12
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