Hyperlipidaemia and cardiovascular disease: nonantilipolytic effects of nicotiraic acid in adipose tissue

摘要

The mechanisms by which nicotinic acid exerts its beneficial effects on the cardiovascular system, be it through its triglyceride and LDL-lowering effects and/or by the rise in HDL, are still unclear. However, two recent studies using vascular imaging reassure the potency of nicotinic acid as an antiatheroclerosis agent The conventional view is that part of nicotinic acid's hypolipidaemic action is conveyed by reducing the flux of nonesterified fatty acids (NEFAs) from adipose tissue to the liver, but the one study formally testing this link suggests that the triglyceride-lowering effect is not only explained by reduced NEFA flux. With a lowering in triglycerides comes a rise in HDL, but the increase uniformly seen after nicotinic acid treatment is out of proportion to what is expected from the triglyceride reduction. The significance of the rise in HDL is still unclear, but a recent study highlights the qualitative changes of HDL by nicotinic acid. HDL from diabetic patients after nicotinic acid therapy had an improved capacity to stimulate endothelial nitric oxide production, to promote endothelial repair, and to inhibit endothelial cell oxidant stress.