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The reduced enzymatic activity increases cellular concentrations of both substrates that NNMT would otherwise consume: S-adenosyl-L-methionine (the universal cellular methyl donor) and nicotinamide (the NAD + salvage precursor)

Tontonoz, P., Kim, J

When a neuron is damaged due to B12, B1, or B6 vitamin deficiencies, the neuron no longer fires a signal

Yes, and in fact, some research designs do exactly that to separate endocrine-mediated effects from direct fat cell effects in the same experimental system
