LPL and hyperlipidemia: The weakened action of insulin on fat cells is deemed to be the cause of the defective suppression of the TGs breakdown inside the cells and the production of non-esterified (free) fatty acids (NEFAs) into the blood where the later elevated entry into the liver stimulates TG synthesis, thus, resulting in hypertriglyceridemia and post-prandial hyperlipidemia owing to the impaired activity of the lipoprotein lipase enzyme.