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J. Biol. Chem., Vol. 281, Issue 11, 7214-7219, March 17, 2006

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Accelerated Lipid Absorption in Mice Overexpressing Intestinal SR-BI^*

Florence Bietrix¹, Daoguang Yan², Michel Nauze, Corinne Rolland, Justine Bertrand-Michel, Christine Coméra, Stephane Schaak, Ronald Barbaras, Albert K. Groen, Bertrand Perret, François Tercé, and Xavier Collet³

From the INSERM U 563, Centre de Physiopathologie de Toulouse Purpan, Département Lipoprotéines et Médiateurs Lipidiques, IFR30 and Université Paul Sabatier, 31024 Toulouse Cedex 3, France and Academic Medical Center, Liver Center, Meibergdreef 69-71, 1105 BK Amsterdam, The Netherlands

Dietary cholesterol absorption contributes to a large part of the circulating cholesterol. However, the mechanism of sterol intestinal uptake is not clearly elucidated. Scavenger receptor class B type I (SR-BI), major component in the control of cholesterol homeostasis, is expressed in the intestine, but its role in this organ remains unclear. We have generated transgenic mice overexpressing SR-BI primarily in the intestine by using the mouse SR-BI gene under the control of intestinal specific "apoC-III enhancer coupled with apoA-IV promoter." We found SR-BI overexpression with respect to the natural protein along the intestine and at the top of the villosities. After a meal containing [¹⁴C]cholesterol and [³H]triolein, SR-BI transgenic mice presented a rise in intestinal absorption of both lipids that was not due to a defect in chylomicron clearance nor to a change in the bile flow or the bile acid content. Nevertheless, SR-BI transgenic mice showed a decrease of total cholesterol but an increase of triglyceride content in plasma without any change in the high density lipoprotein apoA-I level. Thus, we described for the first time a functional role in vivo for SR-BI in cholesterol but also in triglyceride intestinal absorption.

Received for publication, August 11, 2005 , and in revised form, January 17, 2006.

^* This work was supported in part by AIC Nutrition INSERM/INRA (ER 66) and ANRS Grant R03038BS and by Genopole Toulouse Midi-Pyrénées/Platforms of Physiopathological Exploration of Genome/Experimental Histopathology Technical Plateau and Lipid Mediator Analysis Technical Facilities. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Supported by a doctoral fellowship from the French Atherosclerosis Society and the French Nutrition Society.

² Supported by a postdoctoral fellowship from the French government.

³ To whom correspondence should be addressed: INSERM U563, CPTP Bt C, Hôpital Purpan, BP 3028 31024 Toulouse Cedex 3, France. Tel.: 33-5-61-77-94-76; Fax: 33-5-61-77-94-01; E-mail: xcollet{at}toulouse.inserm.fr.

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