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Journal of Lipid Research, Vol. 49, 136-146, January 2008
Copyright © 2008 by American Society for Biochemistry and Molecular Biology

Scavenger receptor BI facilitates the metabolism of VLDL lipoproteins in vivo

Miranda Van Eck¹, Menno Hoekstra, Ruud Out, I. Sophie T. Bos, J. Kar Kruijt, Reeni B. Hildebrand and Theo J. C. Van Berkel

Divison of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, Gorlaeus Laboratories, Leiden University, P.O. Box 9502, 2300 RA Leiden, The Netherlands

Published, JLR Papers in Press, October 22, 2007.

¹ To whom correspondence should be addressed. e-mail: m.eck{at}LACDR.LeidenUniv.nl

Scavenger receptor class B type I (SR-BI) functions as an HDL receptor that promotes the selective uptake of cholesteryl esters (CEs). The physiological role of SR-BI in VLDL metabolism, however, is largely unknown. SR-BI deficiency resulted in elevated VLDL cholesterol levels, both on chow diet and upon challenge with high-cholesterol diets. To specifically elucidate the role of SR-BI in VLDL metabolism, the plasma clearance and hepatic uptake of ¹²⁵I-β-VLDL were studied in SR-BI^+/+ and SR-BI^–/– mice. At 20 min after injection, 66 ± 2% of the injected dose was taken up by the liver in SR-BI^+/+ mice, as compared with only 22 ± 4% (P = 0.0007) in SR-BI^–/– mice. In vitro studies established that the B_max of ¹²⁵I-β-VLDL binding was reduced from 469 ± 30 ng/mg in SR-BI^+/+ hepatocytes to 305 ± 20 ng/mg (P = 0.01) in SR-BI^–/– hepatocytes. Both in vivo and in vitro, limited to no selective uptake of CEs from β-VLDL was found. Interestingly, HDL effectively competed for the association of β-VLDL in the presence as well as in the absence of SR-BI, indicating a second common recognition site. In conclusion, SR-BI plays an important physiological role in the metabolism of VLDL (remnants).

Supplementary key words liver • hepatocytes • gene expression • mouse model

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