title: Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte.
abstract: Although cellular uptake of vitamin E was initially described as a passive process, recent studies in the liver and brain have shown that SR-BI (scavenger receptor class B type I) is involved in this phenomenon. As SR-BI is expressed at high levels in the intestine, the present study addressed the involvement of SR-BI in vitamin E trafficking across enterocytes. Apical uptake and efflux of the main dietary forms of vitamin E were examined using Caco-2 TC-7 cell monolayers as a model of human intestinal epithelium. (R,R,R)-gamma-tocopherol bioavailability was compared between wild-type mice and mice overexpressing SR-BI in the intestine. The effect of vitamin E on enterocyte SR-BI mRNA levels was measured by real-time quantitative reverse transcription-PCR. Concentration-dependent curves for vitamin E uptake were similar for (R,R,R)-alpha-, (R,R,R)-gamma-, and dl-alpha-tocopherol. (R,R,R)-alpha-tocopherol transport was dependent on incubation temperature, with a 60% reduction in absorption at 4 degrees C compared with 37 degrees C (p < 0.05). Vitamin E flux in enterocytes was directed from the apical to the basal side, with a relative 10-fold reduction in the transfer process when measured in the opposite direction (p < 0.05). Co-incubation with cholesterol, gamma-tocopherol, or lutein significantly impaired alpha-tocopherol absorption. Anti-human SR-BI antibodies and BLT1 (a chemical inhibitor of lipid transport via SR-BI) blocked up to 80% of vitamin E uptake and up to 30% of apical vitamin E efflux (p < 0.05), and similar results were obtained for (R,R,R)-gamma-tocopherol. SR-BI mRNA levels were not significantly modified after a 24-h incubation of Caco-2 cells with vitamin E. Finally, (R,R,R)-gamma-tocopherol bioavailability was 2.7-fold higher in mice overexpressing SR-BI than in wild-type mice (p < 0.05). The present data show for the first time that vitamin E intestinal absorption is, at least in part, mediated by SR-BI.
authors.affiliation: INSERM U476, 27 boulevard Jean Moulin, 1260 Institut National de la Recherche Agronomique (INRA), Université AixMarseille, and Institut de Physiopathologie Humaine de Marseille (IPMH), Marseille F-13385, France.
authors.forename: Emmanuelle
authors.initials: E
authors.lastname: Reboul
authors.forename: Alexis
authors.initials: A
authors.lastname: Klein
authors.forename: Florence
authors.initials: F
authors.lastname: Bietrix
authors.forename: Béatrice
authors.initials: B
authors.lastname: Gleize
authors.forename: Christiane
authors.initials: C
authors.lastname: Malezet-Desmoulins
authors.forename: Martina
authors.initials: M
authors.lastname: Schneider
authors.forename: Alain
authors.initials: A
authors.lastname: Margotat
authors.forename: Laurent
authors.initials: L
authors.lastname: Lagrost
authors.forename: Xavier
authors.initials: X
authors.lastname: Collet
authors.forename: Patrick
authors.initials: P
authors.lastname: Borel
mesh_terms: D000042:Absorption; D000818:Animals; D001667:Binding, Competitive; D001692:Biological Transport; D018955:CD36 Antigens / Q000378:metabolism / Q000502:physiology*; D018938:Caco-2 Cells; D002454:Cell Differentiation; D002784:Cholesterol / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D020895:Enterocytes / Q000378:metabolism*; D004847:Epithelial Cells / Q000378:metabolism; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D008055:Lipids / Q000737:chemistry; D051379:Mice; D008822:Mice, Transgenic; D008823:Micelles; D012333:RNA, Messenger / Q000378:metabolism; D013696:Temperature; D013997:Time Factors; D024505:Tocopherols / Q000378:metabolism; D014810:Vitamin E / Q000378:metabolism*; D024502:alpha-Tocopherol / Q000378:metabolism; D024504:gamma-Tocopherol / Q000378:metabolism
chemical_list: D018955:CD36 Antigens; D008055:Lipids; D008823:Micelles; D012333:RNA, Messenger; D014810:Vitamin E; D024504:gamma-Tocopherol; D002784:Cholesterol; D024502:alpha-Tocopherol; D024505:Tocopherols