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Expression levels were normalized to beta-actin (Actb) and further quantified [1]

These effects are largely indirect, stemming from the compounds ability to inhibit nicotinamide N-methyltransferase (NNMT) , a regulatory enzyme that consumes nicotinamide and depletes methyl donor pools (Kraus D, 2014)

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[DOI] [PubMed] [Google Scholar] 5.Vinson J.A

Aging Pathobiology and Therapeutics (2022) 4

To further explore whether AOD 9604s lipolytic interactions depend solely on enhanced receptor expression, investigations were also conducted using mice with genetically ablated lipolytic receptors in laboratory settings