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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

The mechanism of GLP-1-induced nausea involves central GLP-1R activation in the brainstem, specifically in the area postrema, which is the chemoreceptor trigger zone for vomiting

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