HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: M600346-JLR200v1 47/12/2762    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Plat, J. Articles by Mensink, R. P. Search for Related Content PubMed PubMed Citation Articles by Plat, J. Articles by Mensink, R. P. Social Bookmarking                      What's this?

Journal of Lipid Research, Vol. 47, 2762-2771, December 2006
Copyright © 2006 by American Society for Biochemistry and Molecular Biology

Plant sterol or stanol esters retard lesion formation in LDL receptor-deficient mice independent of changes in serum plant sterols

Jogchum Plat^1,*, Ilona Beugels^*, Marion J. J. Gijbels^,, Menno P. J. de Winther and Ronald P. Mensink^*

^* Nutrition and Toxicology Research Institute Maastricht, Department of Human Biology, Maastricht University, 6229 ER, Maastricht, The Netherlands
Cardiovascular Research Institute Maastricht, Department of Molecular Genetics, Maastricht University, 6229 ER, Maastricht, The Netherlands
Cardiovascular Research Institute Maastricht, Department of Pathology, Maastricht University, 6229 ER, Maastricht, The Netherlands

Published, JLR Papers in Press, September 6, 2006.

¹ To whom correspondence should be addressed. e-mail: j.plat{at}hb.unimaas.nl

Statins do not always decrease coronary heart disease mortality, which was speculated based on increased serum plant sterols observed during statin treatment. To evaluate plant sterol atherogenicity, we fed low density lipoprotein-receptor deficient (LDLr^+/–) mice for 35 weeks with Western diets (control) alone or enriched with atorvastatin or atorvastatin plus plant sterols or stanols. Atorvastatin decreased serum cholesterol by 22% and lesion area by 57%. Adding plant sterols or stanols to atorvastatin decreased serum cholesterol by 39% and 41%. Cholesterol-standardized serum plant sterol concentrations increased by 4- to 11-fold during sterol plus atorvastatin treatment versus stanol plus atorvastatin treatment. However, lesion size decreased similarly in the sterol plus atorvastatin (–99% vs. control) and the stanol plus atorvastatin (–98%) groups, with comparable serum cholesterol levels, suggesting that increased plant sterol concentrations are not atherogenic. Our second study confirms this conclusion. Compared with lesions after a 33 week atherogenic period, lesion size further increased in controls (+97%) during 12 more weeks on the diet, whereas 12 weeks with the addition of plant sterols or stanols decreased lesion size (66% and 64%). These findings indicate that in LDLr^+/– mice 1) increased cholesterol-standardized serum plant sterol concentrations are not atherogenic, 2) adding plant sterols/stanols to atorvastatin further inhibits lesion formation, and 3) plant sterols/stanols inhibit the progression or even induce the regression of existing lesions.

Supplementary key words low density lipoprotein • atherosclerosis • nutrition

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				S. Helske, T. Miettinen, H. Gylling, M. Mayranpaa, J. Lommi, H. Turto, K. Werkkala, M. Kupari, and P. T. Kovanen Accumulation of cholesterol precursors and plant sterols in human stenotic aortic valves J. Lipid Res., July 1, 2008; 49(7): 1511 - 1518. [Abstract] [Full Text] [PDF]