Niacin, but not gemfibrozil, selectively increases LP-AI, a cardioprotective subfraction of HDL, in patients with low HDL cholesterol.

T Sakai, V S Kamanna, M L Kashyap

Journal: Arteriosclerosis, thrombosis, and vascular biology 2001;21(11):1783-9

PMID: 11701466

Abstract

Evidence indicates that the high density lipoprotein (HDL) subfraction containing apolipoprotein A-I without apolipoprotein AII (LP-AI) is more antiatherogenic than HDL particles containing apolipoprotein A-I and apolipoprotein A-II (LP-AI+AII). This study examined the effect of extended-release niacin (niacin-ER) and gemfibrozil on LP-AI and LP-AI+AII particles in patients with low levels of HDL cholesterol (HDL-C). Mechanisms by which these agents modulate HDL particles were investigated by in vitro studies using human hepatoblastoma (Hep G2) cells. A total of 139 patients with low HDL-C (

Address: Cholesterol Research Center, Department of Veterans Affairs Healthcare System, Long Beach, California, USA.

DOI: 10.1161/hq1001.096624

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MeSH Terms: Apolipoprotein A-I, Apolipoprotein A-II, Arteriosclerosis, Cholesterol, HDL, Dose-Response Relationship, Drug, Double-Blind Method, Gemfibrozil, Hepatocytes, Humans, Hypolipidemic Agents, Lipids, Lipoproteins, HDL, Niacin, Tumor Cells, Cultured