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Once active, AKT is thought to phosphorylate numerous proteins including phosphodiesterase 3 B (PDE3B), which leads to the hydrolysis of cAMP, and dampening of catabolic signals that promote adipocyte lipolysis (118, 119)

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By blocking NNMT, it prevents the enzymatic diversion of nicotinamide away from the NAD+ salvage pathway, preserving intracellular NAD+ levels and SAM availability