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Xiaoqian Yang - One of the best experts on this subject based on the ideXlab platform.
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the fucoidan a3 from the seaweed ascophyllum nodosum enhances rct related genes expression in hyperlipidemic c57Bl 6j mice
International Journal of Biological Macromolecules, 2019Co-Authors: Jin Wang, Jiayu Yin, Zixun Yang, Xiaoqian Yang, Bin Xia, Yufeng WangAbstract:ABstract Reverse cholesterol transport (RCT) has Been demonstrated to reduce hyperlipidemia, and fucoidans are found to possess hypolipidemic effect. This study was designed to investigate the lipid-lowering effect of the fucoidan from the Brown seaweed A. nodosum and whether it improves RCT-related genes expression in C57 BL/6J mice. Our results indicated that fucoidan A3 (100 mg/kg/day) intervention significantly reduced plasma total cholesterol (~23.2%), triglyceride (~48.7%) and fat pad index. This fucoidan significantly increased the mRNA expression of low-density lipoprotein <B>ReceptorB> (LDLR), <B>ScavengerB> <B>ReceptorB> B type 1 (SR-B1), cholesterol 7 alpha-hydroxylase A1 (CYP7A1), liver X <B>ReceptorB> (LXR) β, ATP-Binding cassette transporter (ABC) A1 and sterol regulatory element-Binding protein (SREBP) 1c, and decreased the expression of peroxisome proliferator-activated <B>ReceptorB> (PPAR) γ, however, it had no effect on the expression of proprotein convertase suBtilisin/kexin type 9, PPARα, LXRα, SREBP-2, ABCG1, ABCG8 and Niemann-Pick C1-like 1. These results demonstrated that this fucoidan improved lipid transfer from plasma to the liver By activating SR-B1 and LDLR, and up-regulated lipid metaBolism By activating LXRβ, ABCA1 and CYP7A1. In conclusion, this fucoidan lowers lipid By enhancing RCT-related genes expression, and it can Be explored as a potential candidate for prevention or treatment of lipid disorders.
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fucoidan a2 from the Brown seaweed ascophyllum nodosum lowers lipid By improving reverse cholesterol transport in c57Bl 6j mice fed a high fat diet
Journal of Agricultural and Food Chemistry, 2019Co-Authors: Zixun Yang, Jin Wang, Peng-bo Hou, Jiayu Yin, Xiaoqian Yang, Bin Xia, Yufeng Wang, Weiguo Song, Guanjun Liu, Shoudong GuoAbstract:Reverse cholesterol transport (RCT) is a physiological process, in which excess peripheral cholesterol is transported to the liver and further excreted into the Bile and then feces. Recently, fucoidans are reported to have a lipid-lowering effect. This study was designed to investigate whether fucoidan from the Brown seaweed Ascophyllum nodosum lowers lipid By modulating RCT in C57BL/6J mice fed a high-fat diet. Our results indicated that fucoidan intervention significantly reduced plasma triglyceride, total cholesterol, and fat pad index and markedly increased high-density lipoprotein cholesterol in a dose-dependent manner. In the liver, fucoidan significantly increased the expression of peroxisome proliferator-activated <B>ReceptorB> (PPAR)α, PPARγ, liver X <B>ReceptorB> (LXR)β, adenosine triphosphate (ATP) Binding cassette (ABC)A1, ABCG8, low-density lipoprotein <B>ReceptorB> (LDLR), <B>ScavengerB> <B>ReceptorB> B type 1 (SR-B1), and cholesterol 7-α-hydroxylase A1 (CYP7A1) and decreased the triglyceride level and expression of proprotein convertase suBtilisin/kexin type 9 (PCSK9) and PPARβ But had no effect on LXRα, ABCG1, and ABCG5. In the small intestine, the fucoidan treatment significantly reduced the expression of Niemann-Pick C1-like 1 (NPC1L1) and improved ABCG5 and ABCG8. These results demonstrated that fucoidan can improve lipid transfer from plasma to the liver By activating SR-B1 and LDLR and inactivating PCSK9 and upregulate lipid metaBolism By activating PPARα, LXRβ, ABC transporters, and CYP7A1. In the small intestine, this fucoidan can decrease cholesterol aBsorption and increase cholesterol excretion By activating NPC1L1 and ABCG5 and ABCG8, respectively. In conclusion, fucoidan from A. nodosum may lower lipids By modulating RCT-related protein expression and can Be explored as a potential compound for prevention or treatment of hyperlipidemia-related diseases.
Anna Schwendeman - One of the best experts on this subject based on the ideXlab platform.
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effect of size and pegylation of liposomes and peptide Based synthetic lipoproteins on tumor targeting
Nanomedicine: Nanotechnology Biology and Medicine, 2017Co-Authors: Jie Tang, Rui Kuai, Wenmin Yuan, Lindsey R. Drake, James J. Moon, Anna SchwendemanAbstract:Synthetic high-density lipoprotein nanoparticles (sHDL) are a valuaBle class of nanomedicines with estaBlished animal safety profile, clinical toleraBility and therapeutic efficacy for cardiovascular applications. In this study we examined how the <B>ScavengerB> <B>ReceptorB> B-I-mediated (SR-BI) tumor-targeting aBility of sHDL, long plasma circulation half-life, and small particle size (9.6±0.2nm) impacted sHDL accumulation in SR-BI positive colorectal carcinoma cells, 3D tumor spheroids, and in vivo xenografts. We compared tumor accumulation of sHDL with that of liposomes (LIP, 130.7±0.8nm), pegylated liposomes (PEG-LIP, 101±2nm), and pegylated sHDL (12.1±0.1nm), all prepared with the same lipid components. sHDL penetrated deep (210μm) into tumor spheroids and exhiBited 12- and 3-fold higher in vivo solid tumor accumulation, compared with LIP (p<0.01) and PEG-LIP (p<0.05), respectively. These results suggest that sHDL with estaBlished human safety possess promising intrinsic tumor-targeted properties.
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Synthetic high-density lipoproteins for delivery of 10-hydroxycamptothecin
International journal of nanomedicine, 2016Co-Authors: Yue Yuan, Jie Tang, Anna Schwendeman, Jian Wen, Qiming Kan, Rose Ackermann, Karl F. OlsenAbstract:The purpose of this study was to develop a novel synthetic high-density lipoprotein (sHDL) nanoparticle delivery system for 10-hydroxycamptothecin (HCPT) for treatment of colon carcinoma. HDL is recognized By <B>ScavengerB> <B>ReceptorB> B-I (SR-BI) over-expressed in colon carcinomas 5- to 35-fold relative to the human fiBroBlasts. The sHDL nanoparticles were composed of apolipoprotein A-I mimic peptide (5A) and contained 0.5%-1.5% (w/w) of HCPT. An optimized HCPT-sHDL formulation exhiBited 0.7% HCPT loading with 70% efficiency with an average size of 10-12 nm. Partitioning of HCPT in the sHDL lipid memBrane enhanced drug staBility in its active lactone form, increased soluBilization, and enaBled slow release. Cytotoxicity studies in HT29 colon carcinoma cells revealed that the IC50 of HCPT-sHDL was approximately 3-fold lower than that of free HCPT. Pharmacokinetics in rats following intravenous administration showed that the area under the serum concentration-time curve (AUC0-t) and Cmax of HCPT-HDL were 2.7- and 6.5-fold higher relative to the values for the free HCPT, respectively. These results suggest that sHDL-Based formulations of hydrophoBic drugs are useful for future evaluation in treatment of SR-BI-positive tumors.
Zixun Yang - One of the best experts on this subject based on the ideXlab platform.
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the fucoidan a3 from the seaweed ascophyllum nodosum enhances rct related genes expression in hyperlipidemic c57Bl 6j mice
International Journal of Biological Macromolecules, 2019Co-Authors: Jin Wang, Jiayu Yin, Zixun Yang, Xiaoqian Yang, Bin Xia, Yufeng WangAbstract:ABstract Reverse cholesterol transport (RCT) has Been demonstrated to reduce hyperlipidemia, and fucoidans are found to possess hypolipidemic effect. This study was designed to investigate the lipid-lowering effect of the fucoidan from the Brown seaweed A. nodosum and whether it improves RCT-related genes expression in C57 BL/6J mice. Our results indicated that fucoidan A3 (100 mg/kg/day) intervention significantly reduced plasma total cholesterol (~23.2%), triglyceride (~48.7%) and fat pad index. This fucoidan significantly increased the mRNA expression of low-density lipoprotein <B>ReceptorB> (LDLR), <B>ScavengerB> <B>ReceptorB> B type 1 (SR-B1), cholesterol 7 alpha-hydroxylase A1 (CYP7A1), liver X <B>ReceptorB> (LXR) β, ATP-Binding cassette transporter (ABC) A1 and sterol regulatory element-Binding protein (SREBP) 1c, and decreased the expression of peroxisome proliferator-activated <B>ReceptorB> (PPAR) γ, however, it had no effect on the expression of proprotein convertase suBtilisin/kexin type 9, PPARα, LXRα, SREBP-2, ABCG1, ABCG8 and Niemann-Pick C1-like 1. These results demonstrated that this fucoidan improved lipid transfer from plasma to the liver By activating SR-B1 and LDLR, and up-regulated lipid metaBolism By activating LXRβ, ABCA1 and CYP7A1. In conclusion, this fucoidan lowers lipid By enhancing RCT-related genes expression, and it can Be explored as a potential candidate for prevention or treatment of lipid disorders.
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fucoidan a2 from the Brown seaweed ascophyllum nodosum lowers lipid By improving reverse cholesterol transport in c57Bl 6j mice fed a high fat diet
Journal of Agricultural and Food Chemistry, 2019Co-Authors: Zixun Yang, Jin Wang, Peng-bo Hou, Jiayu Yin, Xiaoqian Yang, Bin Xia, Yufeng Wang, Weiguo Song, Guanjun Liu, Shoudong GuoAbstract:Reverse cholesterol transport (RCT) is a physiological process, in which excess peripheral cholesterol is transported to the liver and further excreted into the Bile and then feces. Recently, fucoidans are reported to have a lipid-lowering effect. This study was designed to investigate whether fucoidan from the Brown seaweed Ascophyllum nodosum lowers lipid By modulating RCT in C57BL/6J mice fed a high-fat diet. Our results indicated that fucoidan intervention significantly reduced plasma triglyceride, total cholesterol, and fat pad index and markedly increased high-density lipoprotein cholesterol in a dose-dependent manner. In the liver, fucoidan significantly increased the expression of peroxisome proliferator-activated <B>ReceptorB> (PPAR)α, PPARγ, liver X <B>ReceptorB> (LXR)β, adenosine triphosphate (ATP) Binding cassette (ABC)A1, ABCG8, low-density lipoprotein <B>ReceptorB> (LDLR), <B>ScavengerB> <B>ReceptorB> B type 1 (SR-B1), and cholesterol 7-α-hydroxylase A1 (CYP7A1) and decreased the triglyceride level and expression of proprotein convertase suBtilisin/kexin type 9 (PCSK9) and PPARβ But had no effect on LXRα, ABCG1, and ABCG5. In the small intestine, the fucoidan treatment significantly reduced the expression of Niemann-Pick C1-like 1 (NPC1L1) and improved ABCG5 and ABCG8. These results demonstrated that fucoidan can improve lipid transfer from plasma to the liver By activating SR-B1 and LDLR and inactivating PCSK9 and upregulate lipid metaBolism By activating PPARα, LXRβ, ABC transporters, and CYP7A1. In the small intestine, this fucoidan can decrease cholesterol aBsorption and increase cholesterol excretion By activating NPC1L1 and ABCG5 and ABCG8, respectively. In conclusion, fucoidan from A. nodosum may lower lipids By modulating RCT-related protein expression and can Be explored as a potential compound for prevention or treatment of hyperlipidemia-related diseases.
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Exogenous supplement of N-acetylneuraminic acid improves macrophage reverse cholesterol transport in apolipoprotein E-deficient mice
BMC, 2019Co-Authors: Peng-bo Hou, Jin Wang, Jiayu Yin, Zixun Yang, Guanghai Zhou, Shoudong GuoAbstract:ABstract Background N-acetylneuraminic acid (NANA) is the major form of sialic acid in mammals, and the plasma NANA level is increased in patients with cardiovascular diseases. Exogenous supplement of NANA has Been demonstrated to reduce hyperlipidaemia and the formation of atherosclerotic lesions; however, the underlying mechanisms have not yet Been clarified. The aim of this study is to investigate whether exogenous supplement of NANA improves reverse cholesterol transprot (RCT) in vivo. Methods Apolipoprotein E-deficient mice fed a high-fat diet were used to investigate the effect of NANA on RCT By [3H]-cholesterol-loaded macrophages, and the underlying mechanism was further investigated By various molecular techniques using fenofiBrate as a positive control. Results Our novel results demonstrated that exogenous supplement of NANA significantly improved [3H]-cholesterol transfer from [3H]-cholesterol-loaded macrophages to the plasma (an increase of > 42.9%), liver (an increase of 35.8%), and finally to the feces (an increase of 50.4% from 0 to 24 h) for excretion in apolipoprotein E-deficient mice fed a high-fat diet. In addition, NANA up regulated the protein expression of ATP-Binding cassette (ABC) G1 and peroxisome proliferator-activated <B>ReceptorB> α (PPARα), But not the protein expression of ABCA1and <B>ScavengerB> <B>ReceptorB> B type 1 in the liver. Therefore, the underlying mechanism of NANA in improving RCT may Be partially due to the elevated protein levels of PPARα and ABCG1. Conclusion Exogenous supplement of NANA improves RCT in apolipoprotein E-deficient mice fed a high-fat diet mainly By improving the protein expression of PPARα and ABCG1. These results are helpful in explaining the lipid-lowering effect of NANA
Xavier Collet - One of the best experts on this subject based on the ideXlab platform.
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hepatic lipase structure function relationship synthesis and regulation
Journal of Lipid Research, 2002Co-Authors: Bertrand Perret, Ronald Barbaras, Laurence Mabile, Laurent O Martinez, Francois Terce, Xavier ColletAbstract:Hepatic lipase (HL) is a lipolytic enzyme, synthesized By hepatocytes and found localized at the surface of liver sinusoid capillaries. In humans, the enzyme is mostly Bound onto heparan-sulfate proteoglycans at the surface of hepatocytes and also of sinusoid endothelial cells. HL shares a numBer of functional domains with lipoprotein lipase and with other memBers of the lipase gene family. It is a secreted glycoprotein, and remodelling of the N-linked oligosaccharides appears to Be crucial for the secretion process, rather than for the acquisition of the catalytic activity. HL is also present in adrenals and ovaries, where it might promote delivery of lipoprotein cholesterol for steroidogenesis. However, evidence of a local synthesis is still controversial. HL activity is fairly regulated according to the cell cholesterol content and to the hormonal status. Coordinate regulations have Been reported for Both HL and the <B>ScavengerB>-<B>ReceptorB> B-I, suggesting complementary roles in cholesterol metaBolism. However, genetic variants largely contriBute to HL variaBility and their possiBle impact in the development of a dyslipidemic phenotype, or in a context of insulin-resistance, is discussed.
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remodeling of hdl By cetp in vivo and By cetp and hepatic lipase in vitro results in enhanced uptake of hdl ce By cells expressing <B>ScavengerB> <B>ReceptorB> B i
Journal of Lipid Research, 1999Co-Authors: Xavier Collet, Alan R. Tall, Humaira Serajuddin, Karim Guendouzi, Lori Royer, Helena C. F. Oliveira, Ronald Barbaras, Xian-cheng Jiang, Omar L. FranconeAbstract:The transport of HDL cholesteryl esters (CE) from plasma to the liver involves a direct uptake pathway, mediated By hepatic <B>ScavengerB> <B>ReceptorB> B-I (SR-BI), and an indirect pathway, involving the exchange of HDL CE for triglycerides (TG) of TG-rich lipoproteins By cholesteryl ester transfer protein (CETP). We carried out HDL CE turnover studies in mice expressing human CETP and/or human lecithin:cholesterol acyltransferase (LCAT) transgenes on a Background of human apoA-I expression. The fractional clearance of HDL CE By the liver was delayed By LCAT transgene, while the CETP transgene increased it. However, there was no incremental transfer of HDL CE radioactivity to the TG-rich lipoprotein fraction in mice expressing CETP, suggesting increased direct removal of HDL CE in the liver. To evaluate the possiBility that this might Be mediated By SR-BI, HDL isolated from plasma of the different groups of transgenic mice was incuBated with SR-BI transfected or control CHO cells. HDL isolated from mice expressing CETP showed a 2- to 4-fold increase in SR-BI-mediated HDL CE uptake, compared to HDL from mice lacking CETP. The addition of pure CETP to HDL in cell culture did not lead to increased selective uptake of HDL CE By cells. However, when human HDL was enriched with TG By incuBation with TG-rich lipoproteins in the presence of CETP, then treated with hepatic lipase, there was a significant enhancement of HDL CE uptake. Thus, the remodeling of human HDL By CETP, involving CE;-TG interchange, followed By the action of hepatic lipase (HL), leads to the enhanced uptake of HDL CE By cellular SR-BI. These oBservations suggest that in animals such as humans in which Both the selective uptake and CETP pathways are active, the two pathways could operate in a synergistic fashion to enhance reverse cholesterol transport.
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Remodeling of HDL By CETP in vivo and By CETP and hepatic lipase in vitro results in enhanced uptake of HDL CE By cells expressing <B>ScavengerB> <B>ReceptorB> B-I.
Journal of lipid research, 1999Co-Authors: Xavier Collet, Alan R. Tall, Humaira Serajuddin, Karim Guendouzi, Lori Royer, Helena C. F. Oliveira, Ronald Barbaras, Xian-cheng Jiang, Omar L. FranconeAbstract:ABstract The transport of HDL cholesteryl esters (CE) from plasma to the liver involves a direct uptake pathway, mediated By hepatic <B>ScavengerB> <B>ReceptorB> B-I (SR-BI), and an indirect pathway, involving the exchange of HDL CE for triglycerides (TG) of TG-rich lipoproteins By cholesteryl ester transfer protein (CETP). We carried out HDL CE turnover studies in mice expressing human CETP and/or human lecithin:cholesterol acyltransferase (LCAT) transgenes on a Background of human apoA-I expression. The fractional clearance of HDL CE By the liver was delayed By LCAT transgene, while the CETP transgene increased it. However, there was no incremental transfer of HDL CE radioactivity to the TG-rich lipoprotein fraction in mice expressing CETP, suggesting increased direct removal of HDL CE in the liver. To evaluate the possiBility that this might Be mediated By SR-BI, HDL isolated from plasma of the different groups of transgenic mice was incuBated with SR-BI transfected or control CHO cells. HDL isolated from mice expressing CETP showed a 2- to 4-fold increase in SR-BI-mediated HDL CE uptake, compared to HDL from mice lacking CETP. The addition of pure CETP to HDL in cell culture did not lead to increased selective uptake of HDL CE By cells. However, when human HDL was enriched with TG By incuBation with TG-rich lipoproteins in the presence of CETP, then treated with hepatic lipase, there was a significant enhancement of HDL CE uptake. Thus, the remodeling of human HDL By CETP, involving CE–TG interchange, followed By the action of hepatic lipase (HL), leads to the enhanced uptake of HDL CE By cellular SR-BI. These oBservations suggest that in animals such as humans in which Both the selective uptake and CETP pathways are active, the two pathways could operate in a synergistic fashion to enhance reverse cholesterol transport.—Collet, X., A. R. Tall, H. Serajuddin, K. Guendouzi, L. Royer, H. Oliveira, R. BarBaras, X-c. Jiang, and O. L. Francone. Remodeling of HDL By CETP in vivo and By CETP and hepatic lipase in vitro results in enhanced uptake of HDL CE By cells expressing <B>ScavengerB> <B>ReceptorB> B-I. J. Lipid Res. 1999. 40: 1185–1193.
Omar L. Francone - One of the best experts on this subject based on the ideXlab platform.
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remodeling of hdl By cetp in vivo and By cetp and hepatic lipase in vitro results in enhanced uptake of hdl ce By cells expressing <B>ScavengerB> <B>ReceptorB> B i
Journal of Lipid Research, 1999Co-Authors: Xavier Collet, Alan R. Tall, Humaira Serajuddin, Karim Guendouzi, Lori Royer, Helena C. F. Oliveira, Ronald Barbaras, Xian-cheng Jiang, Omar L. FranconeAbstract:The transport of HDL cholesteryl esters (CE) from plasma to the liver involves a direct uptake pathway, mediated By hepatic <B>ScavengerB> <B>ReceptorB> B-I (SR-BI), and an indirect pathway, involving the exchange of HDL CE for triglycerides (TG) of TG-rich lipoproteins By cholesteryl ester transfer protein (CETP). We carried out HDL CE turnover studies in mice expressing human CETP and/or human lecithin:cholesterol acyltransferase (LCAT) transgenes on a Background of human apoA-I expression. The fractional clearance of HDL CE By the liver was delayed By LCAT transgene, while the CETP transgene increased it. However, there was no incremental transfer of HDL CE radioactivity to the TG-rich lipoprotein fraction in mice expressing CETP, suggesting increased direct removal of HDL CE in the liver. To evaluate the possiBility that this might Be mediated By SR-BI, HDL isolated from plasma of the different groups of transgenic mice was incuBated with SR-BI transfected or control CHO cells. HDL isolated from mice expressing CETP showed a 2- to 4-fold increase in SR-BI-mediated HDL CE uptake, compared to HDL from mice lacking CETP. The addition of pure CETP to HDL in cell culture did not lead to increased selective uptake of HDL CE By cells. However, when human HDL was enriched with TG By incuBation with TG-rich lipoproteins in the presence of CETP, then treated with hepatic lipase, there was a significant enhancement of HDL CE uptake. Thus, the remodeling of human HDL By CETP, involving CE;-TG interchange, followed By the action of hepatic lipase (HL), leads to the enhanced uptake of HDL CE By cellular SR-BI. These oBservations suggest that in animals such as humans in which Both the selective uptake and CETP pathways are active, the two pathways could operate in a synergistic fashion to enhance reverse cholesterol transport.
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Remodeling of HDL By CETP in vivo and By CETP and hepatic lipase in vitro results in enhanced uptake of HDL CE By cells expressing <B>ScavengerB> <B>ReceptorB> B-I.
Journal of lipid research, 1999Co-Authors: Xavier Collet, Alan R. Tall, Humaira Serajuddin, Karim Guendouzi, Lori Royer, Helena C. F. Oliveira, Ronald Barbaras, Xian-cheng Jiang, Omar L. FranconeAbstract:ABstract The transport of HDL cholesteryl esters (CE) from plasma to the liver involves a direct uptake pathway, mediated By hepatic <B>ScavengerB> <B>ReceptorB> B-I (SR-BI), and an indirect pathway, involving the exchange of HDL CE for triglycerides (TG) of TG-rich lipoproteins By cholesteryl ester transfer protein (CETP). We carried out HDL CE turnover studies in mice expressing human CETP and/or human lecithin:cholesterol acyltransferase (LCAT) transgenes on a Background of human apoA-I expression. The fractional clearance of HDL CE By the liver was delayed By LCAT transgene, while the CETP transgene increased it. However, there was no incremental transfer of HDL CE radioactivity to the TG-rich lipoprotein fraction in mice expressing CETP, suggesting increased direct removal of HDL CE in the liver. To evaluate the possiBility that this might Be mediated By SR-BI, HDL isolated from plasma of the different groups of transgenic mice was incuBated with SR-BI transfected or control CHO cells. HDL isolated from mice expressing CETP showed a 2- to 4-fold increase in SR-BI-mediated HDL CE uptake, compared to HDL from mice lacking CETP. The addition of pure CETP to HDL in cell culture did not lead to increased selective uptake of HDL CE By cells. However, when human HDL was enriched with TG By incuBation with TG-rich lipoproteins in the presence of CETP, then treated with hepatic lipase, there was a significant enhancement of HDL CE uptake. Thus, the remodeling of human HDL By CETP, involving CE–TG interchange, followed By the action of hepatic lipase (HL), leads to the enhanced uptake of HDL CE By cellular SR-BI. These oBservations suggest that in animals such as humans in which Both the selective uptake and CETP pathways are active, the two pathways could operate in a synergistic fashion to enhance reverse cholesterol transport.—Collet, X., A. R. Tall, H. Serajuddin, K. Guendouzi, L. Royer, H. Oliveira, R. BarBaras, X-c. Jiang, and O. L. Francone. Remodeling of HDL By CETP in vivo and By CETP and hepatic lipase in vitro results in enhanced uptake of HDL CE By cells expressing <B>ScavengerB> <B>ReceptorB> B-I. J. Lipid Res. 1999. 40: 1185–1193.
