Abstract
This review describes niacin's mechanism of action, efficacy in cardiovascular prevention, and safety. A G-protein-coupled receptor [GPR109A/HM74A, mouse PUMA-G (protein upregulated in macrophages by interferon-gamma)] was found to mediate the antilipolytic effect of niacin via inhibition of adenylyl cyclase in adipocytes. The same receptor in skin Langerhans cells mediates the common flushing side effect. The endogenous ligand for the receptor may be beta-hydroxybutyrate. Among nine controlled clinical trials using niacin, mostly combined with other drugs, statistically significant positive impact on clinical or anatomic cardiovascular end-points was found in seven, which represents a remarkably consistent record of benefit. Although niacin induces insulin resistance, deterioration of glycemic control in diabetes is usually minor, and there is no evidence of increased incidence of new onset diabetes. Hepatic toxicity is common with higher doses of sustained-release niacin but rare with immediate-release and extended-release niacin at doses up to 2000 mg/day. Extended-release and immediate-release niacin do not substantially potentiate myopathic effects when given in combination with statins. Recently developed understanding of the mechanisms, efficacy, and safety of niacin, along with progress in reducing the chief side effect of flushing, should enhance the use of this valuable agent for cardiovascular prevention.
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