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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]

Significantly raises levels of NAD+, a molecule cells need for energy, by blocking an enzyme called NNMT

The goal is to isolate which variables drive which outcomes
