Mechanism of Action of Niacin on Lipoprotein Subclasses
Niacin produces large, rapid decreases in TG levels by inhibiting release of fatty acids from adipose tissue as well as hepatic synthesis of fatty acids and TG (Figure 1). Reduced TG synthesis is postulated to enhance hepatic degradation of apo B, the major lipoprotein component of VLDL, thereby reducing VLDL production and hence levels of IDL and LDL. The reduction in TG availability also results in production of smaller, TG-poor VLDL particles, with subsequent inhibition of small, dense LDL production. Niacin may elevate HDL cholesterol levels primarily by suppressing the hepatic removal of apo A-I, which increases levels of apo A-I as well as large apo A-I containing HDL particles.[30,32] Niacin also appears not to inhibit hepatic removal of cholesterol esters, and so preserves the ability of retained apo A-I to augment reverse cholesterol transport. In clinical studies, niacin has been shown to raise HDL cholesterol levels 15%-35% and to lower TG levels 20%-50%, lipoprotein(a) 24%-38%, and LDL cholesterol 5%-25%.[1,33,34]
Model of niacin's mechanism of action. HDL=high-density lipoprotein; FA=fatty acid; TG=triglycerides; apo=apolipoprotein; VLDL=very low-density lipoprotein; LDL=low-density lipoprotein. Adapted with permission from Curr Atheroscler Rep. 2000;2:36-46.
© 2004 Le Jacq Communications, Inc.
Cite this: The Effects of Niacin on Lipoprotein Subclass Distribution - Medscape - Oct 01, 2004.