Fig. 5.

Lack of MGL prevents hepatic steatosis by favoring lipid storage in AT and intestinal malabsorption. MGL deficiency determines intestinal malabsorption, which delivers less FAs to the peripheral tissues. In adipocytes, a large portion of FA is hydrolyzed and reesterified to TGs in a futile cycle with upregulation of lipogenic genes such as Pparγ2 and Dgat1. This translates into increased adiponectin production, resulting in diminished de novo lipogenesis (DNL) in the liver as indicated by downregulation of Srebp1c and increased hepatic FA oxidation (Pparα and its target Cpt1α) and less hepatic inflammation. WAT, white AT.