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When activated in the context of ER stress these factors can lead to cell apoptosis in T2DM thus contributing to the disease pathogenesis (Valds et al., 2014

Mechanism: AOD 9604 stimulates lipolysis and inhibits lipogenesis in fat cells via beta-3 adrenergic receptors

Methotrexate exacerbates NAFLD by inhibiting antioxidant activity, boosting lipid buildup, and generating mitochondrial dysfunction, which leads to increased hepatocyte apoptosis and inflammation

In rodent knockout models where beta-3 adrenergic receptors were removed, the lipolytic response to AOD 9604 was eliminated, confirming the receptor-specific mechanism

Gynecol Endocrinol 37(10):914919 Nie Z, Zhang L, Chen W, Zhang Y, Hua R, Wang W, Zhang T, Wu H (2020) The protective effects of pretreatment with resveratrol in cyclophosphamide-induced rat ovarian granulosa cell injury: In vitro study