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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:1892.)
© 2008 American Heart Association, Inc.

Editorials

Of Mice and Men

Blowing Away the Cobwebs From the Mechanism of Action of Niacin on HDL Metabolism

G.F. Watts; D.C. Chan

From the Metabolic Research Centre, School of Medicine and Pharmacology, University of Western Australia, Perth, Australia.

Correspondence to Professor Gerald F. Watts, School of Medicine and Pharmacology, University of Western Australia, Royal Perth Hospital, Australia. E-mail gerald.watts@uwa.edu.au

An extract of the first 250 words of the full text is provided, because this article has no abstract.

IAn increasing body of evidence suggests that disturbed HDL metabolism increases the risk of cardiovascular disease (CVD).¹ HDL metabolism is central to reverse cholesterol transport (RCT), in which excess cholesterol from peripheral tissue is returned to the liver for extracorporeal elimination. HDLs also have non-RCT functions including antiinflammatory, antioxidant, and antithrombotic properties. These may relate collectively to the apoA-I content of HDL particles. A number of therapeutic approaches that target HDL metabolism may be useful in preventing and regressing atherosclerosis and coronary disease.^2–3

See accompanying article on page 2016

Among lipid-regulators, niacin (nicotinic acid, vitamin B3, pyridine-3-carboxylic acid) is the most effective therapeutic agent presently available for elevating HDL-cholesterol and apoA-I. Notwithstanding issues with tolerability, niacin has long been available for treating atherogenic dyslipidemias. Data from several clinical trials collectively demonstrate that niacin alone or in combination with other agents, including statins, can reduce cardiovascular events and progression of coronary atherosclerosis.⁴ The precise therapeutic mechanism(s) of action of niacin remains unclear, but may largely involve a favorable regulation of HDL metabolism. But exactly how it mediates this effect has not yet been elucidated.

In this issue of Atherosclerosis, Thrombosis and Vascular Biology, van der Hoorn et al present data in a new animal model on the mechanism of the effect of niacin on HDL metabolism.⁵ First, they demonstrated that niacin increased plasma HDL-cholesterol concentration in the APOE*3Leiden.CETP (E3L.CETP) mouse model (ie, E3L mice crossbred with human CETP-expressing mice) but not in the E3L model alone. . . . [Full Text of this Article]

Related Article:

Niacin Increases HDL by Reducing Hepatic Expression and Plasma Levels of Cholesteryl Ester Transfer Protein in APOE*3Leiden.CETP Mice

José W.A. van der Hoorn, Willeke de Haan, Jimmy F.P. Berbée, Louis M. Havekes, J. Wouter Jukema, Patrick C.N. Rensen, and Hans M.G. Princen
Arterioscler Thromb Vasc Biol 2008 28: 2016-2022. [Abstract] [Full Text] [PDF]

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