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Research suggests it may act through beta-3 adrenergic pathways or through non-receptor-mediated effects on adipocyte lipid metabolism, rather than through classical GH receptor signaling

[12] [10] Cyanocobalamin was first manufactured in the 1940s

Most information comes from animal models and involves GH signaling in the liver, but in mouse adipose tissue GHR KO downregulates beta-3 adrenergic receptor expression and inhibits lipolysis (73)

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Possible contributing factors include bacterial or parasitic infections, immune system dysregulation and food intolerances or allergies, particularly to specific proteins