Adiponectin’s role in MASLD pathogenesis might be related to its receptors in the way that adiponectin receptor expressions (AdipoR1 and AdiopR2) are decreased in the liver with steatotic changes simultaneously with hypoadiponectinemia, as our results showed, and therefore the adiponectin actions are mediated via activation of adiponectin receptors for further free fatty acid (FFA) oxidation [25,26]. This evidence concerns the gene ADIPOR1 and adiponectin deficiency.