GCs impact multiple aspects of lipid metabolism, including (i) promotion of insulin resistance, (ii) increase in VLDL from hepatic synthesis, (iii) reduction in LPL, (iv) increase in the conversion of VLDL to LDL, (v) downregulation of the LDL, and (vi) increase in the activity of 3-hydroxy-3-methylglutaryl coenzyme A. These effects on GCs develop hypertriglyceridemia (48). This evidence concerns the gene LPL and hypertriglyceridemia.