AQP9 and metabolic dysfunction-associated steatotic liver disease: It is, therefore, tempting to speculate that part of the beneficial effects of PPARγ agonists, glitazones, in NAFLD comes from the expansion of WAT trapping glycerol in TGs, increasing insulin sensitivity and deactivating liver AQP9 function [97,98], while the lack of effects of PPARα agonists, such as fibrates or elafibranor [99,100], was due to increased liver AQP9 activity, shuttling in glycerol and overloading fatty livers with lipid synthesis precursors, in the context of exacerbated de novo lipogenesis [101].