Mechanistically, elevated postprandial triglycerides are due to (1) sustained postprandial VLDL-triglyceride secretion secondary to hepatic steatosis and insulin resistance; (2) competition of these VLDL-triglycerides and diet-derived triglycerides within chylomicrons for clearance; and/or (3) impaired triglyceride clearance mechanisms (e.g., decreased lipoprotein lipase activity) [15]. Here, LPL is linked to fatty liver disease.