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Joachim Herz - One of the best experts on this subject based on the ideXlab platform.
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inhibition of hepatic Chylomicron Remnant uptake by gene transfer of a receptor antagonist
Science, 1994Co-Authors: Thomas E Willnow, Shun Ishibashi, Zeqi Sheng, Joachim HerzAbstract:The low density lipoprotein receptor-related protein (LRP) has been proposed to mediate in concert with the LDL receptor (LDLR) the uptake of dietary lipoproteins into the hepatocytes. This hypothesis was tested by transient inactivation of LRP in vivo. Receptor-associated protein (RAP), a dominant negative regulator of LRP function, was transferred by an adenoviral vector to the livers of mice lacking LDLR (LDLR-/-). The inactivation of LRP by RAP was associated with a marked accumulation of Chylomicron Remnants in LDLR-/- mice and to a lesser degree in normal mice, suggesting that both LDLR and LRP are involved in Remnant clearance.
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low density lipoprotein receptor related protein and gp330 bind similar ligands including plasminogen activator inhibitor complexes and lactoferrin an inhibitor of Chylomicron Remnant clearance
Journal of Biological Chemistry, 1992Co-Authors: Thomas E Willnow, Joseph L Goldstein, Kim Orth, Michael S Brown, Joachim HerzAbstract:The low density lipoprotein receptor-related protein/alpha 2-macroglobulin receptor (LRP) and gp330, two members of the low density lipoprotein receptor gene family, share a multitude of cysteine-rich repeats. LRP has been shown to act as an endocytosis-mediating receptor for several ligands, including protease-antiprotease complexes and plasma lipoproteins. The former include alpha 2-macroglobulin-protease complexes and plasminogen activator inhibitor-activator complexes. The latter include Chylomicron Remnant-like particles designated beta-very low density lipoproteins (beta-VLDL) complexed with apoprotein E or lipoprotein lipase. The binding specificity of gp330 is unknown. In the current studies we show that gp330 from rat kidney membranes binds several of these ligands on nitrocellulose blots. We also show that both LRP and gp330 bind an additional ligand, bovine lactoferrin, which is known to inhibit the hepatic clearance of Chylomicron Remnants. Lactoferrin blocked the LRP-dependent stimulation of cholesteryl ester synthesis in cultured human fibroblasts elicited by apoprotein E-beta-VLDL or lipoprotein lipase-beta-VLDL complexes. Cross-competition experiments in fibroblasts showed that the multiple ligands recognize at least three distinct, but partially overlapping sites on the LRP molecule. Binding of all ligands to LRP and gp330 was inhibited by the 39-kDa protein, which co-purifies with the two receptors, suggesting that the 39-kDa protein is a universal regulator of ligand binding to both receptors. The correlation of the inhibitory effects of lactoferrin in vivo and in vitro support the notion that LRP functions as a Chylomicron Remnant receptor in liver. LRP and gp330 share a multiplicity of binding sites, and both may function as endocytosis-mediating receptors for a large number of ligands in different organs.
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low density lipoprotein receptor related protein and gp330 bind similar ligands including plasminogen activator inhibitor complexes and lactoferrin an inhibitor of Chylomicron Remnant clearance
Journal of Biological Chemistry, 1992Co-Authors: Thomas E Willnow, Joseph L Goldstein, Kim Orth, Michael S Brown, Joachim HerzAbstract:Abstract The low density lipoprotein receptor-related protein/alpha 2-macroglobulin receptor (LRP) and gp330, two members of the low density lipoprotein receptor gene family, share a multitude of cysteine-rich repeats. LRP has been shown to act as an endocytosis-mediating receptor for several ligands, including protease-antiprotease complexes and plasma lipoproteins. The former include alpha 2-macroglobulin-protease complexes and plasminogen activator inhibitor-activator complexes. The latter include Chylomicron Remnant-like particles designated beta-very low density lipoproteins (beta-VLDL) complexed with apoprotein E or lipoprotein lipase. The binding specificity of gp330 is unknown. In the current studies we show that gp330 from rat kidney membranes binds several of these ligands on nitrocellulose blots. We also show that both LRP and gp330 bind an additional ligand, bovine lactoferrin, which is known to inhibit the hepatic clearance of Chylomicron Remnants. Lactoferrin blocked the LRP-dependent stimulation of cholesteryl ester synthesis in cultured human fibroblasts elicited by apoprotein E-beta-VLDL or lipoprotein lipase-beta-VLDL complexes. Cross-competition experiments in fibroblasts showed that the multiple ligands recognize at least three distinct, but partially overlapping sites on the LRP molecule. Binding of all ligands to LRP and gp330 was inhibited by the 39-kDa protein, which co-purifies with the two receptors, suggesting that the 39-kDa protein is a universal regulator of ligand binding to both receptors. The correlation of the inhibitory effects of lactoferrin in vivo and in vitro support the notion that LRP functions as a Chylomicron Remnant receptor in liver. LRP and gp330 share a multiplicity of binding sites, and both may function as endocytosis-mediating receptors for a large number of ligands in different organs.
Thomas E Willnow - One of the best experts on this subject based on the ideXlab platform.
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inhibition of hepatic Chylomicron Remnant uptake by gene transfer of a receptor antagonist
Science, 1994Co-Authors: Thomas E Willnow, Shun Ishibashi, Zeqi Sheng, Joachim HerzAbstract:The low density lipoprotein receptor-related protein (LRP) has been proposed to mediate in concert with the LDL receptor (LDLR) the uptake of dietary lipoproteins into the hepatocytes. This hypothesis was tested by transient inactivation of LRP in vivo. Receptor-associated protein (RAP), a dominant negative regulator of LRP function, was transferred by an adenoviral vector to the livers of mice lacking LDLR (LDLR-/-). The inactivation of LRP by RAP was associated with a marked accumulation of Chylomicron Remnants in LDLR-/- mice and to a lesser degree in normal mice, suggesting that both LDLR and LRP are involved in Remnant clearance.
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low density lipoprotein receptor related protein and gp330 bind similar ligands including plasminogen activator inhibitor complexes and lactoferrin an inhibitor of Chylomicron Remnant clearance
Journal of Biological Chemistry, 1992Co-Authors: Thomas E Willnow, Joseph L Goldstein, Kim Orth, Michael S Brown, Joachim HerzAbstract:The low density lipoprotein receptor-related protein/alpha 2-macroglobulin receptor (LRP) and gp330, two members of the low density lipoprotein receptor gene family, share a multitude of cysteine-rich repeats. LRP has been shown to act as an endocytosis-mediating receptor for several ligands, including protease-antiprotease complexes and plasma lipoproteins. The former include alpha 2-macroglobulin-protease complexes and plasminogen activator inhibitor-activator complexes. The latter include Chylomicron Remnant-like particles designated beta-very low density lipoproteins (beta-VLDL) complexed with apoprotein E or lipoprotein lipase. The binding specificity of gp330 is unknown. In the current studies we show that gp330 from rat kidney membranes binds several of these ligands on nitrocellulose blots. We also show that both LRP and gp330 bind an additional ligand, bovine lactoferrin, which is known to inhibit the hepatic clearance of Chylomicron Remnants. Lactoferrin blocked the LRP-dependent stimulation of cholesteryl ester synthesis in cultured human fibroblasts elicited by apoprotein E-beta-VLDL or lipoprotein lipase-beta-VLDL complexes. Cross-competition experiments in fibroblasts showed that the multiple ligands recognize at least three distinct, but partially overlapping sites on the LRP molecule. Binding of all ligands to LRP and gp330 was inhibited by the 39-kDa protein, which co-purifies with the two receptors, suggesting that the 39-kDa protein is a universal regulator of ligand binding to both receptors. The correlation of the inhibitory effects of lactoferrin in vivo and in vitro support the notion that LRP functions as a Chylomicron Remnant receptor in liver. LRP and gp330 share a multiplicity of binding sites, and both may function as endocytosis-mediating receptors for a large number of ligands in different organs.
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low density lipoprotein receptor related protein and gp330 bind similar ligands including plasminogen activator inhibitor complexes and lactoferrin an inhibitor of Chylomicron Remnant clearance
Journal of Biological Chemistry, 1992Co-Authors: Thomas E Willnow, Joseph L Goldstein, Kim Orth, Michael S Brown, Joachim HerzAbstract:Abstract The low density lipoprotein receptor-related protein/alpha 2-macroglobulin receptor (LRP) and gp330, two members of the low density lipoprotein receptor gene family, share a multitude of cysteine-rich repeats. LRP has been shown to act as an endocytosis-mediating receptor for several ligands, including protease-antiprotease complexes and plasma lipoproteins. The former include alpha 2-macroglobulin-protease complexes and plasminogen activator inhibitor-activator complexes. The latter include Chylomicron Remnant-like particles designated beta-very low density lipoproteins (beta-VLDL) complexed with apoprotein E or lipoprotein lipase. The binding specificity of gp330 is unknown. In the current studies we show that gp330 from rat kidney membranes binds several of these ligands on nitrocellulose blots. We also show that both LRP and gp330 bind an additional ligand, bovine lactoferrin, which is known to inhibit the hepatic clearance of Chylomicron Remnants. Lactoferrin blocked the LRP-dependent stimulation of cholesteryl ester synthesis in cultured human fibroblasts elicited by apoprotein E-beta-VLDL or lipoprotein lipase-beta-VLDL complexes. Cross-competition experiments in fibroblasts showed that the multiple ligands recognize at least three distinct, but partially overlapping sites on the LRP molecule. Binding of all ligands to LRP and gp330 was inhibited by the 39-kDa protein, which co-purifies with the two receptors, suggesting that the 39-kDa protein is a universal regulator of ligand binding to both receptors. The correlation of the inhibitory effects of lactoferrin in vivo and in vitro support the notion that LRP functions as a Chylomicron Remnant receptor in liver. LRP and gp330 share a multiplicity of binding sites, and both may function as endocytosis-mediating receptors for a large number of ligands in different organs.
Fredrik Karpe - One of the best experts on this subject based on the ideXlab platform.
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the contribution of splanchnic fat to vldl triglyceride is greater in insulin resistant than insulin sensitive men and women studies in the postprandial state
Diabetes, 2007Co-Authors: Leanne Hodson, Fredrik Karpe, A Bickerton, S Mcquaid, Rachel Roberts, Keith N Frayn, Barbara A FieldingAbstract:OBJECTIVE— We aimed to determine differences in the postprandial contributions of different fatty acid sources to VLDL triglycerides (TGs) in healthy men and women with varying degrees of insulin resistance. RESEARCH DESIGN AND METHODS— Insulin-resistant ( n = 11) and insulin-sensitive ( n = 11) men and women ( n = 6) were given an intravenous infusion of [ 2 H 2 ]palmitic acid to investigate systemic nonesterified fatty acid (NEFA) incorporation into VLDL TGs. Participants were also fed a mixed meal containing [U- 13 C]palmitic acid to investigate the contribution of dietary fatty acids to VLDL TG production. Blood samples were taken over the following 6 h. Separation of VLDL was performed by density gradient ultracentrifugation and immunoaffinity techniques specific to apolipoprotein B-100. RESULTS— Insulin-resistant and insulin-sensitive men had similar postprandial Chylomicron and Chylomicron Remnant TG concentrations, but insulin-resistant men had higher postprandial VLDL TG concentrations (median [range]; area under the curve 485 μmol/l [123–992] vs. 287 μmol/l [162–510]; P P CONCLUSIONS— In the postprandial period, the only sources of fatty acids for VLDL TG production to differ in the insulin-resistant compared with the insulin-sensitive men are those derived from splanchnic sources.
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Chylomicron Chylomicron Remnant turnover in humans evidence for margination of Chylomicrons and poor conversion of larger to smaller Chylomicron Remnants
Journal of Lipid Research, 1997Co-Authors: Fredrik Karpe, Anders Hamsten, Thomas Olivecrona, Magnus HultinAbstract:The size of cholesterol-rich lipoprotein particles is a strong determinant of whether they may be deposited in the arterial wall and by this become potentially atherogenic. This study deals with th ...
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Chylomicron Chylomicron Remnant turnover in humans evidence for margination of Chylomicrons and poor conversion of larger to smaller Chylomicron Remnants
Journal of Lipid Research, 1997Co-Authors: Fredrik Karpe, Anders Hamsten, Thomas Olivecrona, Magnus HultinAbstract:The size of cholesterol-rich lipoprotein particles is a strong determinant of whether they may be deposited in the arterial wall and by this become potentially atherogenic. This study deals with the in vivo transformation of larger-sized Chylomicrons and Chylomicron Remnants to smaller-sized Remnants. Twelve healthy men aged 22 to 45 years were given a fatty meal to which retinyl palmitate (RP) had been added. Plasmapheresis was performed 4 1/2 h after meal intake to isolate approximately 400 ml plasma. The RP-rich plasma was re-injected to the subject 24 h later. The RP content was determined in whole plasma and in Svedberg flotation rate fractions (Sf) > 400, Sf 60-400 and Sf 20-60. A compartmental model was developed for the kinetic analysis. Lipoprotein fractions showed minimal signs of aggregation, thus arguing for well-preserved postprandial lipoproteins. Approximately a fourth [23% (4-68%)] of the RP-containing lipoproteins in the Sf > 400 pool was converted to smaller species (Sf 60-400). Conversion of material from the Sf 60-400 to the Sf 20-60 fraction could not be detected. In a second study a large bolus dose of a triglyceride emulsion (Intralipid) was injected to subjects shortly after the RP-labeled plasma to investigate the endothelial binding of the Chylomicron/Chylomicron Remnants. RP material in the Sf > 400 fraction rapidly returned to plasma, arguing for margination of Chylomicrons, whereas the corresponding effect was minimal in the Sf 60-400 and Sf 20-60 fractions. The formation of small Chylomicron Remnants from the larger Chylomicron/Chylomicron Remnant species is limited and large Chylomicron/Chylomicron Remnants are not evenly distributed in plasma, rather they show signs of being marginated to the vascular endothelium.
Hamsten A - One of the best experts on this subject based on the ideXlab platform.
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Postprandial enrichment of Remnant lipoproteins with apoC-I in healthy normolipidemic men with early asymptomatic atherosclerosis.
2002Co-Authors: Björkegren J, Karpe F, Boquist S, Tang R, Mg Bond, De Faire U, Silveira A, Hamsten AAbstract:OBJECTIVES: Recently, we reported that exaggerated postprandial triglyceridemia in normolipidemic patients with coronary artery disease is associated with enrichment of Remnant lipoproteins with apolipoprotein C-I (apoC-I). In this study, the number and composition of Chylomicron Remnants and very low density lipoproteins (VLDLs) were examined in 30 asymptomatic normolipidemic 50-year-old men with and without early carotid atherosclerotic lesions. METHODS AND RESULTS: Intima-media thickness of the far wall of the common carotid artery was determined by B-mode ultrasound. Triglyceride-rich lipoproteins were subfractionated by density gradient ultracentrifugation and separated into VLDL and Chylomicron Remnant fractions by immunoaffinity chromatography. The postprandial triglyceridemia and increase in triglyceride-rich lipoprotein particle number (ie, apolipoprotein B concentrations) were not exaggerated in men with early atherosclerosis. In contrast, their large (Svedberg flotation rate 60 to 400) and small (Svedberg flotation rate 20 to 60) Chylomicron Remnants and VLDL were greatly enriched with apoC-I, and their small Chylomicron Remnants and VLDL particles were relatively enriched with cholesterol. Moreover, the number of apoC-I molecules on small Chylomicron Remnants was strongly associated with the degree of atherosclerosis. CONCLUSIONS: Early asymptomatic atherosclerosis in normolipidemic men without exaggerated postprandial triglyceridemia is associated with the enrichment of postprandial Chylomicron and VLDL particles with apoC-I. Therefore, it is conceivable that the apoC-I content of lipoprotein Remnants may serve as an early marker of coronary artery disease risk
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Effects of atorvastatin on postprandial plasma lipoproteins in postinfarction patients with combined hyperlipidaemia.
2002Co-Authors: Boquist S, Karpe F, Danell-toverud K, Hamsten AAbstract:Enhanced and prolonged postprandial lipaemia is implicated in coronary and carotid artery disease. This study assessed the effects of atorvastatin, a 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor, on postprandial plasma concentrations of triglyceride-rich lipoproteins (TRLs). Sixteen middle-aged men with combined hyperlipidaemia (baseline low density lipoprotein (LDL) cholesterol and plasma triglyceride concentrations (median (interquartile range) of 4.54 (4.17-5.26)) and 2.66 (2.04-3.20) mmol/l, respectively) and previous myocardial infarction were randomised to atorvastatin 40 mg or placebo once daily for 8 weeks in a double-blind, cross-over design. The apolipoprotein (apo) B-48 and B-100 contents were determined in subfractions of TRLs as a measure of Chylomicron Remnant and very low density lipoprotein (VLDL) particle concentrations (expressed as mg apo B-48 or apo B-100 per litre of plasma), in the fasting state and after intake of a mixed meal. Atorvastatin treatment reduced significantly the fasting plasma concentrations of VLDL cholesterol, LDL cholesterol and VLDL triglycerides (median% change) by 29, 44 and 27%, respectively, and increased high density lipoprotein (HDL) cholesterol by 19%, compared with baseline. The postprandial plasma concentrations of large (Svedberg flotation rate (Sf) 60-400) and small (Sf 20-60) VLDLs and Chylomicron Remnants were almost halved compared with baseline (mean 0-6 h plasma concentrations were reduced by 48% for Sf 60-400 apo B-100, by 46% for Sf 60-400 apo B-48, by 46% for Sf 20-60 apo B-100 and by 27% for Sf 20-60 apo B-48), and the postprandial triglyceridaemia was reduced by 23% during active treatment. In conclusion, atorvastatin 40 mg once daily causes profound reductions of postprandial plasma concentrations of all TRLs in combined hyperlipidaemic patients with premature coronary artery disease
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Insulin and non-esterified fatty acid relations to alimentary lipaemia and plasma concentrations of postprandial triglyceride-rich lipoproteins in healthy middle-aged men.
'Springer Science and Business Media LLC', 2000Co-Authors: Boquist S, Karpe F, Hamsten A, Ruotolo GAbstract:AIMS/HYPOTHESIS: Enhanced and prolonged postprandial lipaemia is related to cardiovascular disease but how postprandial lipaemia is regulated is poorly known. We therefore determined the relations of fasting insulin concentrations to fasting and postprandial lipids, lipoproteins and non-esterified fatty acids in middle-aged men. METHODS: The subjects, 99 healthy 50-year-old men with an apolipoprotein E3/3 genotype, ate a mixed meal. The apolipoprotein B-48 and B-100 contents were determined in triglyceride-rich lipoproteins as a measure of Chylomicron Remnant and very low density lipoprotein particle concentrations. RESULTS: Fasting plasma insulin was associated with the triglyceride response to the test meal, independently of body mass index, waist-to-hip circumference ratio, blood glucose and the insulin effect on fasting plasma triglycerides. Exaggerated and prolonged postprandial lipaemia in subjects in the upper quartile of the plasma insulin distribution was largely accounted for by large (Svedberg flotation rate > 60) very low density lipoproteins and Chylomicron Remnants. Insulin relations to large postprandial triglyceride-rich lipoproteins exclusively reflected the association between plasma insulin and the fasting plasma concentrations of these lipoprotein species, whereas plasma insulin and late postprandial plasma concentrations of small (Svedberg flotation rate 20-60) Chylomicron Remnants were related, independently of insulin influences on fasting concentrations. Strong positive relations were found between the late increases in large triglyceride-rich lipoproteins and plasma non-esterified fatty acid concentrations after 6 h. CONCLUSION/INTERPRETATION: The degree of insulin sensitivity is a major determinant of postprandial lipaemia in healthy middle-aged men and could add to the regulation of the basal production of large triglyceride-rich lipoproteins
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Alimentary lipemia, postprandial triglyceride-rich lipoproteins, and common carotid intima-media thickness in healthy, middle-aged men.
'Ovid Technologies (Wolters Kluwer Health)', 1999Co-Authors: Boquist S, Karpe F, Ruotolo G, Tang R, Björkegren J, Mg Bond, De Faire U, Hamsten AAbstract:BACKGROUND: Alimentary lipemia has been associated with coronary heart disease and common carotid artery intima-media thickness (IMT). This study was designed to investigate the relations of subclasses of postprandial triglyceride-rich lipoproteins (TRLs) with IMT. METHODS AND RESULTS: Ninety-six healthy 50-year-old men with an apolipoprotein (apo) E3/E3 genotype underwent an oral fat tolerance test and B-mode carotid ultrasound examination. The apo B-48 and apo B-100 contents of each fraction of TRLs were determined as a measure of Chylomicron Remnant and VLDL particle concentrations. In the fasting state, LDL cholesterol (P
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Alimentary lipemia, postprandial triglyceride-rich lipoproteins, and common carotid intima-media thickness in healthy, middle-aged men.
1999Co-Authors: Boquist S, Karpe F, Ruotolo G, Tang R, Björkegren J, Mg Bond, De Faire U, Hamsten AAbstract:BACKGROUND: Alimentary lipemia has been associated with coronary heart disease and common carotid artery intima-media thickness (IMT). This study was designed to investigate the relations of subclasses of postprandial triglyceride-rich lipoproteins (TRLs) with IMT. METHODS AND RESULTS: Ninety-six healthy 50-year-old men with an apolipoprotein (apo) E3/E3 genotype underwent an oral fat tolerance test and B-mode carotid ultrasound examination. The apo B-48 and apo B-100 contents of each fraction of TRLs were determined as a measure of Chylomicron Remnant and VLDL particle concentrations. In the fasting state, LDL cholesterol (P<0.05) and basal proinsulin (P<0. 05) were significantly related to IMT, whereas HDL cholesterol, plasma triglycerides, and insulin were not. In the postprandial state, plasma triglycerides at 1 to 4 hours (P<0.01 at 2 hours), total triglyceride area under the curve (AUC) (P<0.05), incremental triglyceride AUC (P<0.01), and the large VLDL (Sf 60 to 400 apo B-100) concentration at 3 hours (P<0.05) were significantly related to IMT. Multivariate analyses showed that plasma triglycerides at 2 hours, LDL cholesterol, and basal proinsulin were consistently and independently related to IMT when cumulative tobacco consumption, alcohol intake, waist-to-hip circumference ratio, and systolic blood pressure were included as confounders. CONCLUSIONS: These results provide further evidence for postprandial triglyceridemia as an independent risk factor for early atherosclerosis and also suggest that the postprandial triglyceridemia is a better predictor of IMT than particle concentrations of individual TRLs
Magnus Hultin - One of the best experts on this subject based on the ideXlab platform.
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Chylomicron Chylomicron Remnant turnover in humans evidence for margination of Chylomicrons and poor conversion of larger to smaller Chylomicron Remnants
Journal of Lipid Research, 1997Co-Authors: Fredrik Karpe, Anders Hamsten, Thomas Olivecrona, Magnus HultinAbstract:The size of cholesterol-rich lipoprotein particles is a strong determinant of whether they may be deposited in the arterial wall and by this become potentially atherogenic. This study deals with th ...
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Chylomicron Chylomicron Remnant turnover in humans evidence for margination of Chylomicrons and poor conversion of larger to smaller Chylomicron Remnants
Journal of Lipid Research, 1997Co-Authors: Fredrik Karpe, Anders Hamsten, Thomas Olivecrona, Magnus HultinAbstract:The size of cholesterol-rich lipoprotein particles is a strong determinant of whether they may be deposited in the arterial wall and by this become potentially atherogenic. This study deals with the in vivo transformation of larger-sized Chylomicrons and Chylomicron Remnants to smaller-sized Remnants. Twelve healthy men aged 22 to 45 years were given a fatty meal to which retinyl palmitate (RP) had been added. Plasmapheresis was performed 4 1/2 h after meal intake to isolate approximately 400 ml plasma. The RP-rich plasma was re-injected to the subject 24 h later. The RP content was determined in whole plasma and in Svedberg flotation rate fractions (Sf) > 400, Sf 60-400 and Sf 20-60. A compartmental model was developed for the kinetic analysis. Lipoprotein fractions showed minimal signs of aggregation, thus arguing for well-preserved postprandial lipoproteins. Approximately a fourth [23% (4-68%)] of the RP-containing lipoproteins in the Sf > 400 pool was converted to smaller species (Sf 60-400). Conversion of material from the Sf 60-400 to the Sf 20-60 fraction could not be detected. In a second study a large bolus dose of a triglyceride emulsion (Intralipid) was injected to subjects shortly after the RP-labeled plasma to investigate the endothelial binding of the Chylomicron/Chylomicron Remnants. RP material in the Sf > 400 fraction rapidly returned to plasma, arguing for margination of Chylomicrons, whereas the corresponding effect was minimal in the Sf 60-400 and Sf 20-60 fractions. The formation of small Chylomicron Remnants from the larger Chylomicron/Chylomicron Remnant species is limited and large Chylomicron/Chylomicron Remnants are not evenly distributed in plasma, rather they show signs of being marginated to the vascular endothelium.