Mechanism of action of niacin on lipoprotein metabolism.

摘要: It is generally accepted that the increased concentrations of apolipoprotein (apo) B containing very low-density lipoproteins (VLDL) and (LDL), decreased levels apo AI high-density (HDL) are correlated to atherosclerotic cardiovascular disease. Current evidence indicates post-translational apo-B degradative processes regulate hepatic assembly secretion VLDL subsequent generation LDL particles. The availability triglycerides (TG) for addition during intracellular processing appears play a central role in targeting either degradation or as Based on TG, liver secretes dense TG-poor VLDL2 large TG-rich VLDL1 particles, these particles serve precursors formation more buoyant small, by lipid transfer protein- lipase-mediated processes. HDLs heterogenous class lipoproteins, (the major protein HDL) participates reverse cholesterol transport, process which excess eliminated. Recent studies indicate HDL only A-I (LPA-I) effective transport anti-atherogenic than both A-II (LPA-I+A-II).