Figure 2: Schematic representation demonstrating lipid transport and free fatty acid (FFA) flux in insulin resistant states. Insulin resistance results in increased FFA in plasma, which leads to increased hepatocellular triglyceride (TG) concentrations. Chylomicrons, containing apoB-48, also contributes to hepatic steatosis. FFA enter the liver via fatty acid transporters (FATP), mainly FATP5. Elevated hepatic triglycerides levels leads to increased hepatocyte secretion of very low density lipoprotein (VLDL), which contains apoB-100. Insulin resistance also leads to defective hepatic mitochondrial function, resulting in decreased fatty acid oxidation in the liver.