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
If left untreated, severe vitamin B12 deficiency can cause irreversible damage to the nervous system
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Supplementation Protocols The way vitamin B12 is given depends on the severity and the patients health