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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:1672.)
© 2008 American Heart Association, Inc.

Clinical and Population Studies

Extended-Release Niacin Alters the Metabolism of Plasma Apolipoprotein (Apo) A-I and ApoB-Containing Lipoproteins

Stefania Lamon-Fava; Margaret R. Diffenderfer; P. Hugh R. Barrett; Aaron Buchsbaum; Mawuli Nyaku; Katalin V. Horvath; Bela F. Asztalos; Seiko Otokozawa; Masumi Ai; Nirupa R. Matthan; Alice H. Lichtenstein; Gregory G. Dolnikowski; Ernst J. Schaefer

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.

Correspondence to Stefania Lamon-Fava, MD, PhD, Lipid Metabolism Laboratory, Jean Mayer USDA Human Nutrition Research, Center on Aging at Tufts University, 711 Washington Street, Boston, MA 02111. E-mail stefania.lamon-fava{at}tufts.edu

Abstract

Objectives— Extended-release niacin effectively lowers plasma TG levels and raises plasma high-density lipoprotein (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.

We investigated the effects of niacin (2 g/d), without or with lovastatin (40 mg/d) on apolipoprotein kinetics in 5 subjects. Niacin treatment significantly increased HDL apoA-I concentrations and production, as well as enhanced clearance of TG-rich lipoprotein apoB-100 and apoB-48. The addition of lovastatin to niacin further promoted an enhanced clearance of LDL apoB-100.

Key Words: apolipoprotein • high-density lipoprotein • kinetics • lipid-lowering medications • triglyceride

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