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In a 2001 study published in Endocrinology , Heffernan and colleagues reported that chronic AOD-9604 administration reduced body weight gain, decreased adipose tissue mass, and increased fat oxidation in obese mice without altering IGF-1 levels or glucose metabolism effects that were abolished in beta3 adrenergic receptor (3-AR) knockout mice, implicating 3-AR signaling as the mechanism of action [1]

In a recent investigation undertaken by our group, adult mice with partial IGF-1 showed a decrease in the expression of genes involved in glucose metabolism (phosphoenolpyruvate carboxylase-1, glucose-6-phosphatase, pyruvate dehydrogenase kinase isoenzyme-4, and ATP-citrate lyase), resulting serious hyperglycaemia [164]

Journal of periodontology, 10.1002/JPER.24-0688

Its value in a clinical setting comes from what it is not: it does not disrupt appetite, hormones, insulin, or IGF-1