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In white adipose tissue of obese, insulin-resistant and aged mammals, NNMT is dramatically upregulated and because it consumes both the universal methyl donor (SAM) and the NAD precursor (nicotinamide), its hyperactivity simultaneously depletes the cellular methylation reserve and the NAD-salvage pool [1,2]

Reduced Formation of 1-Methylnicotinamide Researchers use reduced 1-methylnicotinamide as a pharmacodynamic marker that NNMT activity has been inhibited