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J Lipid Res. 2014 Sep;55(9):1914-24. doi: 10.1194/jlr.M048819. Epub 2014 Jun 22.

High density lipoprotein metabolism in low density lipoprotein receptor-deficient mice.

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Department of Medicine, University Hospital Hamburg Eppendorf, 20246 Hamburg, Germany.
Department of Biochemistry and Molecular Cell Biology, University Hospital Hamburg Eppendorf, 20246 Hamburg, Germany.
Translational Laboratories in Genetic Medicine, Agency for Science, Technology and Research National University of Singapore, Singapore 117609 Department of Medicine, National University of Singapore, Singapore 117609.
Centre for Molecular Medicine and Therapeutics and Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia V5Z 4H4, Canada.
Department of Pediatrics, College of Physicians and Surgeons of Columbia University, New York, NY 10032.


The LDL receptor (LDLR) and scavenger receptor class B type I (SR-BI) play physiological roles in LDL and HDL metabolism in vivo. In this study, we explored HDL metabolism in LDLR-deficient mice in comparison with WT littermates. Murine HDL was radiolabeled in the protein ((125)I) and in the cholesteryl ester (CE) moiety ([(3)H]). The metabolism of (125)I-/[(3)H]HDL was investigated in plasma and in tissues of mice and in murine hepatocytes. In WT mice, liver and adrenals selectively take up HDL-associated CE ([(3)H]). In contrast, in LDLR(-/-) mice, selective HDL CE uptake is significantly reduced in liver and adrenals. In hepatocytes isolated from LDLR(-/-) mice, selective HDL CE uptake is substantially diminished compared with WT liver cells. Hepatic and adrenal protein expression of lipoprotein receptors SR-BI, cluster of differentiation 36 (CD36), and LDL receptor-related protein 1 (LRP1) was analyzed by immunoblots. The respective protein levels were identical both in hepatic and adrenal membranes prepared from WT or from LDLR(-/-) mice. In summary, an LDLR deficiency substantially decreases selective HDL CE uptake by liver and adrenals. This decrease is independent from regulation of receptor proteins like SR-BI, CD36, and LRP1. Thus, LDLR expression has a substantial impact on both HDL and LDL metabolism in mice.


cholesteryl ester; scavenger receptor class B type I; selective uptake

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