{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,7]],"date-time":"2026-05-07T03:57:44Z","timestamp":1778126264313,"version":"3.51.4"},"reference-count":43,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2001,11]]},"abstract":"<jats:p>\n            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 (\u226440 mg\/dL) were randomized to niacin-ER or gemfibrozil in a multicenter double-blind trial. Patients were dose-escalated with once-nightly niacin-ER (1 to 2 g) or gemfibrozil (1.2 g) for 19 weeks. Niacin-ER had a greater effect in raising HDL-C and apolipoprotein A-I levels than did gemfibrozil. Niacin-ER at 1- and 2-g doses increased LP-AI levels by 8.7\u00b14.0% (\n            <jats:italic>P<\/jats:italic>\n            =0.033) and 24.0\u00b14.4% (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.001), respectively. Gemfibrozil had no consistent effect on LP-AI levels. LP-AI+AII levels increased 5% to 8% by both agents. In vitro studies showed that niacin, but not gemfibrozil, selectively decreased the uptake of\n            <jats:sup>125<\/jats:sup>\n            I-labeled LP-AI holoparticles by Hep G2 cells. The uptake of [\n            <jats:sup>3<\/jats:sup>\n            H]cholesterol ester was \u224875% greater from LP-AI versus LP-AI+AII particles, but neither niacin nor gemfibrozil affected cholesterol ester uptake. These data indicate that unlike gemfibrozil, niacin selectively increases LP-AI compared with LP-AI+AII particle concentration in patients with low HDL-C levels. The mechanism of action of increased LP-AI concentration appears to be mediated by decreased hepatic removal of LP-AI particles, which are more efficient in reverse cholesterol transport, thus suggesting an additional mechanism by which niacin mediates its antiatherogenic properties.\n          <\/jats:p>","DOI":"10.1161\/hq1001.096624","type":"journal-article","created":{"date-parts":[[2007,9,28]],"date-time":"2007-09-28T18:27:24Z","timestamp":1191004044000},"page":"1783-1789","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":96,"title":["Niacin, but Not Gemfibrozil, Selectively Increases LP-AI, a Cardioprotective Subfraction of HDL, in Patients With Low HDL Cholesterol"],"prefix":"10.1161","volume":"21","author":[{"given":"Takaaki","family":"Sakai","sequence":"first","affiliation":[{"name":"From the Cholesterol Research Center, Department of Veterans Affairs Healthcare System, Long Beach, Calif, and the Department of Medicine, 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