1) Induction of lipoprotein lipolysis. This is mainly TG-rich lipoproteins (TRLs) lipolysis either through alteration of the intrinsic lipoprotein lipase (LPL) activity or the increase of the accessibility of TRLs for lipolysis by LPL, which results in a reduction of TRL apoC-III content. 2) Increase of the hepatic fatty acid (FA) uptake by the specific FA transporter protein (FATP) and promotion of acyl-CoA synthetase (ACS) activity. When there is an increased ? -oxidation activity and reduced acetyl-CoA carboxylase and FA synthase activities, there is a shift in FAA metabolism from TG synthesis to catabolism.
3) Increase of the removal of LDL particles. This increase promotes LDL catabolism through the formation of LDL with a higher affinity for the LDL receptor. 4) Lowering of plasma TRL levels. This is done through the reduction of neutral lipid (TG and cholesteryl ester) exchange between VLDL and HDL. 5) Contribution to the increase of plasma HDL production, resulting in a better reverse cholesterol transport. The increase in the production of apoA-I and apoA-II in the liver effects an increase in plasma HDL production.