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In apoptosis, -sitosterol upregulates pro-apoptotic factors such as p53 and Bax, while downregulating anti-apoptotic proteins such as Bcl-2, leading to an increase in mitochondrial outer membrane permeability and the activation of key apoptotic enzyme cascades such as caspase-9 and 3, which induces programmed cell death (83)

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The design of high-potency unimolecular GCGR/GLP-1R dual agonists has revolved around substitutions in the mid and C-terminal segments of proposed analogues 5,14,15,16

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These results reinforce the urgency of beginning treatment without hesitation