**5.2. LRP**

LRP share 63% homology with the catalytic region of HIV-1 protease. LRP binds to LPL on the capillary endothelium, and the formation of this LRP-LPL complex promotes cleavage of fatty acids from TG, thereby promoting FFA accumulation in peripheral adipocytes. A possible hypothesis is that the binding of PIs to LRP may inhibit the complex normal function of LRP-LPL and interfere with fatty acid storage, leading to hyperlipidemia. Hyperlipidemia is characterized by elevations in cholesterol levels, principally in the LDL and VLDL cholesterol fractions, because fatty acids released into the bloodstream subsequently reach the liver and promote a secondary hepatic synthesis of TG and VLDL [48, 59, 61].
