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Interestingly, research has shown that even in animals lacking beta-3 adrenergic receptors, acute AOD-9604 administration still increased energy expenditure and fat oxidation, suggesting additional metabolic pathways may be involved beyond the primary beta-3 receptor mechanism

in a bile duct ligation (BDL) rat model of chronic cholestasis confirmed that the concentration of GSH and ubiquinone decreases during cholestasis, whereas an increase in lipid peroxidation is observed [183]