Importantly, Zheng et al. [37] et al. found that SAL could abrogate nonalcoholic fatty liver disease through the AMPK-dependent TXNIP / NLRP3 pathway, again consistent with the results in vivo validation experiments in our study, where AMPK was activated in the mouse IR model group, and after SAL treatment AMPK was further activated. Here, NLRP3 is linked to metabolic dysfunction-associated steatotic liver disease.