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The goal of ongoing research is to expand the therapeutic uses of this particular peptide and further clarify its mechanisms

Because nicotinamide would otherwise re-enter the NAD+ salvage pathway through NAMPT and NMN, NNMT activity sits at a junction between cellular methylation capacity and NAD+ regeneration, which is why the enzyme became a target after Kraus and colleagues (Nature, 2014) reported the consequences of antisense Nnmt knockdown in white adipose tissue and liver

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Research suggests this may be due to higher concentrations of beta-3 adrenergic receptors in these fat depots

By midlife, NAD+ can drop by 50%, exacerbated by inflammation and lifestyle.[14] Factors like poor diet, sedentary behavior, or chronic stress further deplete NAD+ by activating consuming enzymes, creating a vicious cycle