AT-specific DPP4 knocked-out rodents displayed better glucose tolerance, higher insulin sensitivity, and lower hepatic fat content than wild types when fed with a high-fat diet; these mice had lower circulating sDPP4, confirming the major contribution of the AT as a source of serum sDPP4, along with the impact of AT DPP4 in NAFLD development in obesogenic conditions [74]. Here, DPP4 is linked to metabolic dysfunction-associated steatotic liver disease.