Leptin and other inflammatory adipokines such as IL-6 or TNF-α (Tumor nechrosis factor) promote insulin resistance, which has been extensively described in the pathophysiology of NAFLD during the last few decades [52,53,54], as it provokes the inhibition of lipid oxidation together with increased synthesis of fatty acids and triglycerides [19,36,37]. Here, LEP is linked to metabolic dysfunction-associated steatotic liver disease.