Figure 5.

Impact of adipose tissues on liver steatosis and dyslipidemia. MAFLD is associated with hypertrophic WAT, which is characterized by increased flux of FFA to the liver. In hepatocytes, several transporter and enzymes (FATP5, CD36, THEM2, GPAT4, DGAT1) were found to be involved in the preferential incorporation of circulation-derived fatty acids into triglycerides. On the other hand, little evidence exists that these triglycerides are selectively used for VLDL, as plasma FFA-derived triglycerides are also efficiently incorporated into lipid droplet triglycerides. Interventions reverting WAT hypertrophy generally improve MAFLD by reducing the lipid flux to the liver. The mass and function of brown adipose tissue (BAT) is generally decreased in metabolically unhealthy states such as obesity and probably also in MAFLD, a process called BAT involution. As BAT can take up substantial amounts of lipid from the circulation and combust it, reactivation of BAT has the potential to divert lipid from the liver and thus ameliorate MAFLD.