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[46] It achieves glycemic control primarily through a glucose-dependent mechanism: by binding to GLP-1 receptors on beta cells, it elevates intracellular levels of cyclic AMP (cAMP) and activates protein kinase A (PKA) and related signaling pathways

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GLP-1RAs also downregulate the expression of MMPs and tissue inhibitors of MPs (TIMPs) for anti-inflammation [110]

These results prove that GLP-1-based therapy may reduce inflammation and improve fatty liver disease in animal and human models