Scavenger receptor BI (SR-BI) is known to mediate the selective uptake of high density lipoprotein (HDL) cholesteryl ester (CE) in liver and steroidogenic tissues. To evaluate the role of SR-BI in plasma lipoprotein metabolism, we have generated transgenic mice with liver-specific overexpression of murine SR-BI. On a chow diet SR-BI transgenic (SR-BI Tg) mice have decreased HDL-CE, apoA-I, and apoA-II levels; plasma triglycerides, low density lipoprotein (LDL) cholesterol, and very low density lipoprotein (VLDL) and LDL apoB were also decreased, compared with control mice. Turnover studies using non-degradable CE and protein labels showed markedly increased total and selective uptake of HDL-CE in the liver and increased HDL protein catabolism in both liver and kidney. To evaluate the changes in apoB further, mice were challenged with high fat, high cholesterol diets. In SR-BI Tg mice plasma apoB levels were only 3–15% of control levels, and the dietary increase in VLDL and LDL apoB was virtually abolished. These studies show that steady state overexpression of hepatic SR-BI reduces HDL levels and increases reverse cholesterol transport. They also indicate that SR-BI can play a role in the metabolism of apoB-containing lipoproteins. The dual effects of increased reverse cholesterol transport and lowering of apoB-containing lipoproteins that result from hepatic SR-BI overexpression could have anti-atherogenic consequences. Scavenger receptor BI (SR-BI) is known to mediate the selective uptake of high density lipoprotein (HDL) cholesteryl ester (CE) in liver and steroidogenic tissues. To evaluate the role of SR-BI in plasma lipoprotein metabolism, we have generated transgenic mice with liver-specific overexpression of murine SR-BI. On a chow diet SR-BI transgenic (SR-BI Tg) mice have decreased HDL-CE, apoA-I, and apoA-II levels; plasma triglycerides, low density lipoprotein (LDL) cholesterol, and very low density lipoprotein (VLDL) and LDL apoB were also decreased, compared with control mice. Turnover studies using non-degradable CE and protein labels showed markedly increased total and selective uptake of HDL-CE in the liver and increased HDL protein catabolism in both liver and kidney. To evaluate the changes in apoB further, mice were challenged with high fat, high cholesterol diets. In SR-BI Tg mice plasma apoB levels were only 3–15% of control levels, and the dietary increase in VLDL and LDL apoB was virtually abolished. These studies show that steady state overexpression of hepatic SR-BI reduces HDL levels and increases reverse cholesterol transport. They also indicate that SR-BI can play a role in the metabolism of apoB-containing lipoproteins. The dual effects of increased reverse cholesterol transport and lowering of apoB-containing lipoproteins that result from hepatic SR-BI overexpression could have anti-atherogenic consequences. free cholesterol cholesteryl ester cholesteryl oleyl ether HDL cholesteryl ester fractional catabolic rate lecithin:cholesterol acyltransferase scavenger receptor class B type I transgenic apolipoprotein A-I apolipoprotein A-II apolipoprotein B apolipoprotein E high density lipoprotein low density lipoprotein intermediate density lipoprotein very low density lipoprotein phospholipids 125I-N-methyltyramine cellobiose polyacrylamide gel electrophoresis fast protein liquid chromatography. The risk of coronary heart disease is inversely correlated with the levels of plasma high density lipoproteins (HDL)1 (1Gordon D.J. Rifkind B.M. N. Engl. J. Med. 1989; 321: 1311-1316Crossref PubMed Scopus (1412) Google Scholar, 2Tall A.R. Breslow J.L. Fuster V. Ross R. Topol E.J. Atherosclerosis and Coronary Artery Disease. Lippincott-Raven Publishers, Philadelphia1996: 105-128Google Scholar). HDL appears to transport cholesterol from peripheral tissues to the liver for catabolism and secretion (reverse cholesterol transport) (3Eisenberg S. J. Lipid Res. 1984; 25: 1017-1058Abstract Full Text PDF PubMed Google Scholar, 4Tall A.R. J. Clin. Invest. 1990; 86: 379-384Crossref PubMed Scopus (586) Google Scholar). A putative cell-surface receptor for this process has been identified (5Acton S. Rigotti A. Landschulz K.T. Xu S. Hobbs H.H. Krieger M. Science. 1996; 271: 518-520Crossref PubMed Scopus (2011) Google Scholar). This receptor, scavenger receptor BI (SR-BI), mediates high affinity binding of HDL and the selective uptake of HDL cholesteryl ester (CE) (5Acton S. Rigotti A. Landschulz K.T. Xu S. Hobbs H.H. Krieger M. Science. 1996; 271: 518-520Crossref PubMed Scopus (2011) Google Scholar), a process for delivery of cholesteryl ester into cells without degradation of HDL proteins (6Glass C. Pittman R.C. Weinstein D.B. Steinberg D. Proc. Natl. Acad. Sci. U. S. A. 1983; 80: 5435-5439Crossref PubMed Scopus (423) Google Scholar). Furthermore, SR-BI mRNA and protein levels are highest in adrenal gland, ovary, testis, and liver, tissues that display greatest selective cholesteryl ester uptake from HDL (7Cao G. Garcia C.K. Wyne K.L. Schultz R.A. Parker K.L. Hobbs H.H. J. Biol. Chem. 1997; 272: 33068-33076Abstract Full Text Full Text PDF PubMed Scopus (234) Google Scholar, 8Wang N. Weng W. Breslow J.L. Tall A.R. J. Biol. Chem. 1996; 271: 21001-21004Abstract Full Text Full Text PDF PubMed Scopus (192) Google Scholar, 9Landschultz K.T. Pathak R.K. Rigotti A. Krieger M. Hobbs H.H. J. Clin. Invest. 1996; 98: 984-995Crossref PubMed Scopus (470) Google Scholar). SR-BI expression in steroidogenic cells is regulated by hormones and mutations that alter cholesterol supply or metabolism in those tissues in vivo (8Wang N. Weng W. Breslow J.L. Tall A.R. J. Biol. Chem. 1996; 271: 21001-21004Abstract Full Text Full Text PDF PubMed Scopus (192) Google Scholar, 9Landschultz K.T. Pathak R.K. Rigotti A. Krieger M. Hobbs H.H. J. Clin. Invest. 1996; 98: 984-995Crossref PubMed Scopus (470) Google Scholar, 10Rigotti A. Edelman E.R. Seifert P. Iqbal S.N. DeMattos R.B. Temel R.E. Krieger M. William D.L. J. Biol. Chem. 1996; 271: 33545-33549Abstract Full Text Full Text PDF PubMed Scopus (205) Google Scholar, 11Ng D.S. Francone O.L. Forte T.M. Zhang J. Haghpassand M. Rubin E.M. J. Biol. Chem. 1997; 272: 15777-15781Abstract Full Text Full Text PDF PubMed Scopus (124) Google Scholar). More recently, strong support for the role of SR-BI in HDL metabolism has been provided by studies of mice with a targeted mutation resulting in decreased SR-BI gene expression (12Rigotti A. Trigatti B.L. Penman M. Rayburn H. Herz J. Krieger M. Proc. Natl. Acad. Sci. U. S. A. 1997; 94: 12610-12615Crossref PubMed Scopus (761) Google Scholar, 13Varban M.L. Rinninger F. Wang N. Huntress V.F. Dunmore J.H. Fang Q. Gosselin M.L. Dixon K.L. Deeds J.D. Acton S.L. Tall A.R. Huszar D. Proc. Natl. Acad. Sci. U. S. A. 1998; 95: 4619-4624Crossref PubMed Scopus (269) Google Scholar). These mice demonstrate increased plasma HDL cholesterol, decreased adrenal cholesterol content (12Rigotti A. Trigatti B.L. Penman M. Rayburn H. Herz J. Krieger M. Proc. Natl. Acad. Sci. U. S. A. 1997; 94: 12610-12615Crossref PubMed Scopus (761) Google Scholar, 13Varban M.L. Rinninger F. Wang N. Huntress V.F. Dunmore J.H. Fang Q. Gosselin M.L. Dixon K.L. Deeds J.D. Acton S.L. Tall A.R. Huszar D. Proc. Natl. Acad. Sci. U. S. A. 1998; 95: 4619-4624Crossref PubMed Scopus (269) Google Scholar), and decreased hepatic fractional clearance rate (FCR) for HDL-CE (13Varban M.L. Rinninger F. Wang N. Huntress V.F. Dunmore J.H. Fang Q. Gosselin M.L. Dixon K.L. Deeds J.D. Acton S.L. Tall A.R. Huszar D. Proc. Natl. Acad. Sci. U. S. A. 1998; 95: 4619-4624Crossref PubMed Scopus (269) Google Scholar), suggesting that SR-BI is the major molecule mediating HDL-CE-selective uptake in the liver. By contrast, adenovirus-mediated, hepatic overexpression of SR-BI in mice results in depletion of plasma HDL and an increase in biliary cholesterol concentration (14Kozarsky K.F. Donahee M.H. Rigotti A. Iqbal S.N. Edelman E.R. Krieger M. Nature. 1997; 387: 414-417Crossref PubMed Scopus (631) Google Scholar). Although these studies nicely demonstrate the effect of acute overexpression of SR-BI on HDL levels (14Kozarsky K.F. Donahee M.H. Rigotti A. Iqbal S.N. Edelman E.R. Krieger M. Nature. 1997; 387: 414-417Crossref PubMed Scopus (631) Google Scholar), they do not necessarily demonstrate plasma lipoprotein changes that would accompany steady state overexpression of SR-BI. In this paper we report an in depth study of transgenic mice with hepatic overexpression of murine SR-BI. These studies were designed to understand better the role of SR-BI in HDL metabolism and reverse cholesterol transport. During the initial characterization of these animals on a chow diet, we observed decreased LDL cholesterol and apoB levels. Whereas the mouse model studies to date have focused on HDL changes, SR-BI was originally identified a receptor both and LDL S.L. Krieger M. J. Biol. Chem. Full Text PDF PubMed Google Scholar). studies were on high fat, high cholesterol in to the effects of SR-BI on plasma apoB levels. A of murine SR-BI Wang N. M. Tall A.R. J. Biol. Chem. 1997; 272: Full Text Full Text PDF PubMed Scopus Google was into the of the J. Wang J. A. Q. Proc. Natl. Acad. Sci. U. S. A. PubMed Scopus Google Scholar), provided by M. of of A of the the and of the of the the murine SR-BI and the and hepatic control of the gene was to transgenic mice by animals were to mice and transgenic mouse SR-BI and SR-BI were in this paper were using SR-BI or SR-BI or mice for both SR-BI and plasma total for the SR-BI studies of to high mice were a type diet and cholesterol or a very high cholesterol diet cholesterol, and for plasma cholesterol, free cholesterol, and were using (8Wang N. Weng W. Breslow J.L. Tall A.R. J. Biol. Chem. 1996; 271: 21001-21004Abstract Full Text Full Text PDF PubMed Scopus (192) Google Scholar). of plasma apoB levels was using an with an affinity murine VLDL LDL and HDL were by density of mouse In VLDL and LDL were polyacrylamide gel of lipoproteins was using from were with and the of was by HDL was in the density from plasma of type and and in the protein with 125I-N-methyltyramine cellobiose R.C. PubMed Scopus Google Scholar), and with oleyl ether F. Pittman R.C. J. Lipid Res. Full Text PDF PubMed Google Scholar). was in a and HDL using plasma cholesteryl ester The were from HDL by by to cholesteryl ester protein from the HDL the HDL was to plasma of both HDL and of uptake were F. Pittman R.C. J. Lipid Res. Full Text PDF PubMed Google Scholar, C. Pittman R.C. R.C. Steinberg D. J. Biol. Chem. Full Text PDF PubMed Google Scholar). was from control and SR-BI Tg mice and animals were the study free to HDL was in an and were from the of and were for and for F. Pittman R.C. J. Lipid Res. Full Text PDF PubMed Google Scholar). the animals were and with and were and content of was and that of was on plasma of both HDL plasma were using a model R. R.B. PubMed Scopus Google Scholar). the of the plasma of the HDL by an were the plasma of total in a F. Pittman R.C. J. Lipid Res. Full Text PDF PubMed Google Scholar, C. Pittman R.C. R.C. Steinberg D. J. Biol. Chem. Full Text PDF PubMed Google Scholar). for SR-BI and and were (8Wang N. Weng W. Breslow J.L. Tall A.R. J. Biol. Chem. 1996; 271: 21001-21004Abstract Full Text Full Text PDF PubMed Scopus (192) Google Scholar, Francone O.L. C. R. J. A. Breslow J.L. Tall A.R. J. Clin. Invest. 1996; 98: PubMed Scopus Google Scholar). was with a of mouse apoB to hepatic apoB mRNA levels. and adrenal cholesterol were by A. N. H. Tall A.R. S. Breslow J.L. J. Lipid Res. 1997; Full Text PDF PubMed Google Scholar). was by of plasma free cholesterol to cholesteryl was using HDL was with the an initial of A. PubMed Scopus Google Scholar). HDL of and in a total of The was by the of plasma and for was by the of to of SR-BI Tg SR-BI and SR-BI were The SR-BI mice a of liver-specific overexpression of SR-BI mRNA was expression in the showed a increase in hepatic SR-BI levels in transgenic mice B and levels of expression were observed for both of SR-BI Tg mice. of plasma on a chow diet that SR-BI Tg mice a of plasma total cholesterol with in both free cholesterol and cholesteryl ester (CE) was also a in plasma phospholipids and results were for mice of control and SR-BI Tg the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for high the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for the control and SR-BI Tg animals on the diet by for was and were and The are and the control and SR-BI Tg animals on the diet by for in a was and were and The are and mice. plasma was by fast protein liquid of the CE and were in the HDL in the control mice on the chow diet A and By HDL-CE and were in SR-BI Tg mice. HDL phospholipids were also markedly decreased was also a in in VLDL and LDL these were also low in control mice. of apolipoprotein of lipoproteins by a of HDL apoA-I, and levels in SR-BI mice The VLDL and LDL apoB and levels also were The results were by using for murine apoA-I, and results were in of plasma from a total of SR-BI mice and control mice and were also in the SR-BI not The changes in HDL in SR-BI Tg mice these expression of SR-BI (14Kozarsky K.F. Donahee M.H. Rigotti A. Iqbal S.N. Edelman E.R. Krieger M. Nature. 1997; 387: 414-417Crossref PubMed Scopus (631) Google HDL was using and labels (14Kozarsky K.F. Donahee M.H. Rigotti A. Iqbal S.N. Edelman E.R. Krieger M. Nature. 1997; 387: 414-417Crossref PubMed Scopus (631) Google Scholar). we HDL studies using non-degradable R.C. PubMed Scopus Google Scholar, F. Pittman R.C. J. Lipid Res. Full Text PDF PubMed Google Scholar). In the control the rate of from plasma of the to protein selective uptake of HDL-CE was a rate of clearance for both in SR-BI Tg mice. The plasma from these showed a increase in protein catabolism and increase in catabolism The selective of HDL-CE from the CE and protein was increased by in SR-BI Tg mice. of uptake from HDL were and results are the The liver was the for both HDL and protein catabolism F. Pittman R.C. J. Lipid Res. Full Text PDF PubMed Google Scholar, C. Pittman R.C. R.C. Steinberg D. J. Biol. Chem. Full Text PDF PubMed Google Scholar). The liver for to selective uptake of HDL in the liver. In contrast, a was for this is a major for selective HDL protein catabolism C. Pittman R.C. R.C. Steinberg D. J. Biol. Chem. Full Text PDF PubMed Google Scholar). SR-BI Tg mice showed a increase in hepatic for both HDL protein and The of HDL proteins was also markedly increased in SR-BI Tg this to the clearance of HDL in type or SR-BI Tg mice. for HDL protein and were increased and the uptake of HDL-CE was increased This have an of adrenal SR-BI expression to HDL levels and depletion of adrenal cholesterol and with to HDL and protein not display major changes in SR-BI Tg fractional catabolic HDL in the control and SR-BI Tg animals by for the control and SR-BI Tg animals by for the control and SR-BI Tg animals by for the control and SR-BI Tg animals by for the control and SR-BI Tg animals by for the control and SR-BI Tg animals by for the control and SR-BI Tg animals by for the control and SR-BI Tg animals by for the control and SR-BI Tg animals by for the control and SR-BI Tg animals by for the control and SR-BI Tg animals by for the control and SR-BI Tg animals by for the control and SR-BI Tg animals by for the control and SR-BI Tg animals by for were from control and SR-BI mice of were and The are of plasma and the control and SR-BI Tg animals by for in a were from control and SR-BI mice of were and The are of plasma and The HDL studies that the plasma HDL and were in to HDL catabolism in SR-BI Tg mice. also hepatic mRNA levels and the control and SR-BI Tg animals free cholesterol was increased by in SR-BI Tg mice By adrenal cholesteryl ester virtually in SR-BI Tg and free cholesterol was also decreased the decreased plasma HDL-CE levels that result from hepatic overexpression of SR-BI (8Wang N. Weng W. Breslow J.L. Tall A.R. J. Biol. Chem. 1996; 271: 21001-21004Abstract Full Text Full Text PDF PubMed Scopus (192) Google Scholar). was a increase in adrenal SR-BI protein to decreased adrenal cholesterol content (8Wang N. Weng W. Breslow J.L. Tall A.R. J. Biol. Chem. 1996; 271: 21001-21004Abstract Full Text Full Text PDF PubMed Scopus (192) Google Scholar). The hepatic LDL receptor mRNA levels in SR-BI Tg mice were not by using from liver not and adrenal cholesterol the control and SR-BI Tg animals by for the control and SR-BI Tg animals by for and adrenal and content were in SR-BI mice on a chow diet and and CE was by from The are of of the control and SR-BI Tg animals by for in a and adrenal and content were in SR-BI mice on a chow diet and and CE was by from The are of of in SR-BI Tg mice on the chow diet was the in LDL apoB levels To evaluate apoB changes further, mice were challenged with a type high diet and or a very high cholesterol diet cholesterol, for In to these VLDL and LDL apoB levels were increased in control changes in apoB were in SR-BI Tg mice and The in apoB was for SR-BI mice SR-BI mice. of plasma apoB levels by that plasma apoB levels were markedly by on the chow diet and on the high fat, high cholesterol in SR-BI Tg mice compared with control mice The in apoB to both and in VLDL and LDL apoB mRNA levels were not in SR-BI Tg mice to the control mice on the chow diet to the chow diet, levels were in SR-BI Tg mice the control mice on high fat, high cholesterol B and levels in HDL were not decreased on the high fat, high cholesterol apoB for was to the SR-BI Tg mice with the control mice on the high apoB levels were using and from mice of were for the A for was to the SR-BI Tg mice with the control mice on the in a apoB levels were using and from mice of were for the On the type diet plasma was decreased by and CE by in SR-BI Tg mice compared with control mice plasma was in SR-BI Tg mice in the control and phospholipids were only decreased were decreased in SR-BI Tg mice. On the very high cholesterol diet plasma and were decreased, the changes were on the chow diet in SR-BI Tg mice of plasma lipoprotein of mice on the type diet showed that HDL-CE, and were in SR-BI Tg mice cholesterol in the VLDL was markedly and free cholesterol in the was increased and CE in the VLDL was only increased in SR-BI Tg mice. free cholesterol for of total VLDL cholesterol, total cholesterol free with these phospholipids in the VLDL and were also markedly increased in SR-BI Tg mice The high content of free cholesterol and low cholesteryl and low apoB that the lipoproteins of lipoprotein of Science. PubMed Scopus Google Scholar). SR-BI Tg mice were to have in on a high diet H. P. PubMed Scopus Google Scholar, Forte J. J. Clin. Invest. Scopus Google Scholar). The of HDL from plasma of mice on type diet is in In SR-BI Tg HDL was of cholesteryl was increased and the major were increased and was free of HDL from mice on the type HDL was from plasma of control or SR-BI mice by density and the of was and The are of HDL and are the of cholesteryl in a HDL was from plasma of control or SR-BI mice by density and the of was and The are of HDL and are the of cholesteryl The of and in VLDL and LDL on the type diet that SR-BI Tg mice have a in plasma CE to the markedly decreased HDL levels, has been in mice H. N. J. Lipid Res. Full Text PDF PubMed Google Scholar). we the plasma cholesteryl ester SR-BI Tg mice a markedly fractional plasma CE rate compared with the control animals on both chow and type diets. In SR-BI Tg the of plasma S. D. J. Biol. Chem. Full Text PDF PubMed Google Scholar). To evaluate the of decreased CE levels were using of to of This levels of in the control and SR-BI Tg plasma control and of to CE for SR-BI Tg and of to CE by with and of suggesting that the in plasma cholesterol is to the levels of SR-BI Tg mice to have to depletion of plasma (14Kozarsky K.F. Donahee M.H. Rigotti A. Iqbal S.N. Edelman E.R. Krieger M. Nature. 1997; 387: 414-417Crossref PubMed Scopus (631) Google showed that the acute overexpression of SR-BI in the liver in a in HDL cholesterol and levels, clearance of HDL protein from increased hepatic uptake of from and increased biliary cholesterol levels. studies show a major in HDL cholesterol, apoA-I, and apoA-II a result of hepatic overexpression of SR-BI in a transgenic mouse They demonstrate increased selective uptake of HDL-CE in the liver, and increased uptake of HDL protein in both liver and kidney. we observed a in VLDL and LDL CE and apoB levels in SR-BI Tg mice compared with and in of mice a to increase plasma apoB levels challenged with high fat, high cholesterol diets. This the in vivo that SR-BI can play a role in the of plasma lipoprotein apoB levels, and this that of hepatic SR-BI overexpression on VLDL and LDL metabolism that the of SR-BI was originally a receptor that both LDL and with high affinity S.L. Krieger M. J. Biol. Chem. Full Text PDF PubMed Google Scholar). the of has been to VLDL in to HDL and LDL D. D. Biol. 1997; PubMed Scopus Google Scholar). The of SR-BI to mediate the uptake and degradation of LDL and VLDL has not been and role in apoB vivo is for the in VLDL and LDL apoB in SR-BI Tg mice is that hepatic SR-BI mediates the of apoB-containing lipoproteins from are SR-BI overexpression could mediate increased binding of VLDL and LDL to and this to increased catabolism the LDL receptor or J. Clin. Invest. 1997; PubMed Scopus Google Scholar). is that SR-BI overexpression to decreased secretion of apoB from liver the transgenic mice have increased uptake of HDL cholesterol and into the liver would to increase apoB secretion J.L. J. Lipid Res. Full Text PDF PubMed Google Scholar). in apoB levels could the state of mice have apoB levels N. B.L. S. J. Biol. Chem. 1997; 272: Full Text Full Text PDF PubMed Scopus Google Scholar). the of apoB levels in mice with on a very high cholesterol diet N. B.L. S. J. Biol. Chem. 1997; 272: Full Text Full Text PDF PubMed Scopus Google is to the of apoB levels in SR-BI Tg mice The changes in apoB were observed in the of overexpression of SR-BI in the liver. In contrast, mice with decreased SR-BI expression in the liver, a result of of SR-BI gene do not display increased apoB in plasma lipoproteins compared with type mice on chow (13Varban M.L. Rinninger F. Wang N. Huntress V.F. Dunmore J.H. Fang Q. Gosselin M.L. Dixon K.L. Deeds J.D. Acton S.L. Tall A.R. Huszar D. Proc. Natl. Acad. Sci. U. S. A. 1998; 95: 4619-4624Crossref PubMed Scopus (269) Google Scholar). In the mice is that decreased SR-BI expression is by LDL receptor The in VLDL and LDL CE in SR-BI Tg mice both to increased selective uptake of from VLDL and LDL and to increased plasma levels and VLDL and LDL CE and apoB levels were decreased, SR-BI Tg mice showed increases in VLDL and LDL free cholesterol on type In to overexpression of SR-BI (14Kozarsky K.F. Donahee M.H. Rigotti A. Iqbal S.N. Edelman E.R. Krieger M. Nature. 1997; 387: 414-417Crossref PubMed Scopus (631) Google Scholar), was also a increase in VLDL and LDL cholesterol levels, the of HDL A for these was provided by that mice with hepatic SR-BI overexpression have plasma cholesteryl ester and On the type diet the in VLDL were to free cholesterol and phospholipids and to of cholesteryl and they are to lipoprotein that are lipoproteins that in animals with in to high they of lipoproteins H. P. PubMed Scopus Google Scholar, Forte J. J. Clin. Invest. Scopus Google Scholar). is not these were on the type diet the very high cholesterol diet, could to a in plasma Tg levels on the type diet of study was the of uptake of HDL cholesteryl and using non-degradable and to the is that the results could the markedly decreased of HDL in the SR-BI Tg mice. of HDL in mice not the fractional catabolism of HDL-CE A. N. H. Tall A.R. S. Breslow J.L. J. Lipid Res. 1997; Full Text PDF PubMed Google Scholar). that overexpression of SR-BI in the liver to a increase in selective uptake of HDL-CE in the a increased selective uptake in the liver (13Varban M.L. Rinninger F. Wang N. Huntress V.F. Dunmore J.H. Fang Q. Gosselin M.L. Dixon K.L. Deeds J.D. Acton S.L. Tall A.R. Huszar D. Proc. Natl. Acad. Sci. U. S. A. 1998; 95: 4619-4624Crossref PubMed Scopus (269) Google Scholar). The SR-BI transgenic mice also have increased biliary free cholesterol content and decreased dietary cholesterol N. A. R. and J. we also observed an increase in HDL protein uptake in both liver and In the was expression of SR-BI these changes of HDL or that result from overexpression of SR-BI in the liver. SR-BI Tg mice was HDL to a of HDL changes by These results with decreased expression of SR-BI were changes in HDL protein uptake in the liver (13Varban M.L. Rinninger F. Wang N. Huntress V.F. Dunmore J.H. Fang Q. Gosselin M.L. Dixon K.L. Deeds J.D. Acton S.L. Tall A.R. Huszar D. Proc. Natl. Acad. Sci. U. S. A. 1998; 95: 4619-4624Crossref PubMed Scopus (269) Google Scholar). Although SR-BI overexpression could for increased uptake of HDL proteins in the liver, we that the of HDL to increased SR-BI to of HDL into HDL protein catabolic that are in the liver and kidney. studies show that in to reverse cholesterol SR-BI overexpression to in VLDL and LDL CE and apoB levels. an of the role of SR-BI in the of apoB from plasma studies with SR-BI overexpression of SR-BI is to have to transgenic overexpression of SR-BI. The results of reverse cholesterol transport by SR-BI overexpression are they also to HDL levels. that in plasma apoB levels the in VLDL and LDL have anti-atherogenic J. Lipid Res. 1998; Full Text Full Text PDF PubMed Google Scholar). for the
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