on June 19, 2008
Published online before print June 19, 2008, doi: 10.1161/ATVBAHA.108.164541
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Submitted on February 7, 2008
Accepted on June 5, 2008
Extended-Release Niacin Alters the Metabolism of Plasma Apolipoprotein (Apo) A-I–and ApoB-Containing Lipoproteins
Stefania Lamon-Fava *;
From the Lipid Metabolism Laboratory (S.L.-F., M.R.D., A.B., M.N., K.V.H., B.F.A., S.O., M.A., E.J.S.), the Cardiovascular Nutrition Laboratory (N.R.M., A.H.L.), and the Mass Spectrometry Laboratory (G.G.D.), Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, and the Friedman School of Nutrition Science and Policy at Tufts University and Tufts University School of Medicine, Boston, Mass; and the School of Medicine and Pharmacology (P.H.R.B.), University of Western Australia, Perth, Australia.
* To whom correspondence should be addressed. E-mail: stefania.lamon-fava{at}tufts.edu.
Objectives—Extended-release niacin effectively lowers plasma TG levels and raises plasma high-density lipoproteins (HDL) cholesterol levels, but the mechanisms responsible for these effects are unclear.
Methods and Results—We examined the effects of extended-release niacin (2 g/d) and extended-release niacin (2 g/d) plus lovastatin (40 mg/d), relative to placebo, on the kinetics of apolipoprotein (apo) A-I and apoA-II in HDL, apoB-100 in TG-rich lipoproteins (TRL), intermediate-density lipoproteins (IDL) and low-density lipoproteins (LDL), and apoB-48 in TRL in 5 men with combined hyperlipidemia. Niacin significantly increased HDL cholesterol and apoA-I concentrations, associated with a significant increase in apoA-I production rate (PR) and no change in fractional catabolic rate (FCR). Plasma TRL apoB-100 levels were significantly lowered by niacin, accompanied by a trend toward an increase in FCR and no change in PR. Niacin treatment significantly increased TRL apoB-48 FCR but had no effect on apoB-48 PR. No effects of niacin on concentrations or kinetic parameters of IDL and LDL apoB-100 and HDL apoA-II were noted. The addition of lovastatin to niacin promoted a lowering in LDL apoB-100 attributable to increased LDL apoB-100 FCR.
Conclusion—Niacin treatment was associated with significant increases in HDL apoA-I concentrations and production, as well as enhanced clearance of TRL apoB-100 and apoB-48.
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