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However, studies using beta-3-adrenergic receptor knockout mice revealed a more complex picture: Long-term AOD-9604 treatment failed to produce weight loss in beta-3-AR knockout mice Acute administration still increased energy expenditure and fat oxidation in knockout mice This suggests beta-3-AR expression enhancement contributes to, but does not directly mediate, lipolytic effects The peptide appears to work through an unidentified receptor mechanism that subsequently influences beta-3-adrenergic signaling pathways

The entire body composition evidence base comes from preclinical mouse studies and cell culture experiments

Knockdown of NNMT in adipocytes was associated with increased NAD+ levels and altered expression of genes involved in energy expenditure, providing the rationale for pharmacological NNMT inhibition [2]

All analyses were implemented using R version 4.0.0 [37]

Animal data is more robust