The disturbances in lipoprotein profiles most likely originate from an elevated hepatic production of large triacylglycerol-rich VLDL1 particles, which in combination with increased cholesterylester transfer protein (CETP) mediated lipid fluxes and decreased lipoprotein lipase (LPL) mediated lipolysis results in hypertriglyceridemia and low serum HDL cholesterol concentration [8], [9], [10]. Here, LPL is linked to hypertriglyceridemia.