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When hepatic lipid export is impaired, triglycerides accumulate in liver cells (hepatic steatosis), which disrupts insulin signaling and shifts metabolism toward fat storage rather than fat oxidation

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Previous studies showed that several PAMs of GLP-1R, such as the most characterized electrophilic chemotypes-compound BETP 23,24 and the substituted quinoxalines compound 2 (6,7-dichloro-3-methanesulfonyl-2-tert-butylamino-quinoxaline) 25,26 , were able to initiate or promote receptor activation 9,27