Figure 1.

The pathogenesis of hepatic steatosis. Under physiologic conditions, the hepatic fatty acid (FA) pool is the result of a balance between FA influx from the diet and adipose tissue lipolysis, de novo lipogenesis (DNL), and disposal of FAs through β-oxidation or very-low-density lipoprotein (VLDL) assembly and secretion. Increased uptake and reduced clearance of FAs lead to the accumulation of lipid droplets (LDs) and hepatic steatosis. In red are some important proteins involved in the different pathways.

ApoB, apolipoprotein B; CD36, fatty acid translocase; ChREBP, carbohydrate-responsive element—binding protein; CMs, chylomicrons; FATP, fatty acid transport protein; FFAs, free fatty acids; MTP, mitochondrial trifunctional protein; MTTP, microsomal triglyceride transfer protein; SREBP-1c, sterol regulatory element—binding protein 1c; TAG, triacylglycerol.