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Journal articles on the topic 'Chylomicron remnant'

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Published: 4 June 2021
Last updated: 6 February 2022

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1

Bowler, A., T. G. Redgrave, and J. C. L. Mamo. "Chylomicron-remnant clearance in homozygote and heterozygote Watanabe-heritable-hyperlipidaemic rabbits is defective. Lack of evidence for an independent chylomicron-remnant receptor." Biochemical Journal 276, no. 2 (June 1, 1991): 381–86. http://dx.doi.org/10.1042/bj2760381.

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Lymph chylomicrons radiolabelled in triacylglycerol and cholesteryl ester were injected into control and Watanabe heritable-hyperlipidaemic (WHHL) rabbits. Clearance of chylomicrons was slower in heterozygote and homozygote WHHL rabbits. Slower remnant clearance in WHHL rabbits was confirmed by monitoring the clearance from plasma of preformed chylomicron remnants. Use of chylomicron-like lipid emulsions injected into control and WHHL rabbits also confirmed the defect in remnant clearance in heterozygote WHHL and homozygote WHHL groups. Clearance from plasma of emulsion triolein was delayed in both WHHL groups compared with controls, owing to slower remnant clearance. The clearance from plasma of radioiodinated rabbit low-density lipoproteins (LDL) in heterozygote WHHL rabbits was the same as control rabbits. Defective chylomicron-remnant removal but normal LDL clearance in the heterozygote WHHL corresponded to elevated concentrations of plasma triacylglycerol and normal concentrations of plasma cholesterol. Receptor versus non-receptor clearances of chylomicron remnants were studied by comparing the clearance of emulsions with and without unesterified cholesterol respectively. Unlike control rabbits, there were no significant differences in the clearances of the two emulsion types in either the homozygote or heterozygote WHHL rabbits, indicating that the apolipoprotein-B100/E receptor is the primary route for clearance of chylomicron remnants from plasma.
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2

Mansbach, C. M., and R. F. Dowell. "Role of the intestine in chylomicron remnant clearance." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 1 (July 1, 1995): G144—G152. http://dx.doi.org/10.1152/ajpgi.1995.269.1.g144.

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When 810 mumol of [3H]glyceryl trioleate (TO) were infused intraduodenally over 6 h into rats, 29% of the triacylglycerol (TG) acyl groups in the mucosa were not from the infusate. We tested the hypothesis that chylomicron remnants contribute to the mucosal pool of nondietary TG acyl groups, since the acyl group composition of the chylomicron remnants was 58% oleate, compared with 90% in their parent chylomicrons. Purified 3H-labeled remnants were generated from chylomicrons formed in rats receiving TO intraduodenally, with 95% of the remnant disintegrations per minute (dpm) being in TG. The 3H-remnants were infused intravenously into rats receiving either saline or 135 mumol/h TO intraduodenally. In the saline-infused rats, 32% of the infused 3H dpm were in the proximal and 19% in the distal intestine and 32% were in the liver. In the fat-infused rats, 12% of the infused 3H dpm were in the proximal and 5% were in the distal gut and 29% were in the liver. When [3H]cholesterol-labeled remnants were infused intravenously and saline was infused intraduodenally, the percentage uptake into the mucosa was nearly the same as with the TG label, but comparable uptake by the liver increased. We conclude that the intestine competes with the liver for chylomicron remnant TG and cholesterol.
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3

YU, Kenneth C. W., and John C. L. MAMO. "Chylomicron-remnant-induced foam cell formation and cytotoxicity: a possible mechanism of cell death in atherosclerosis." Clinical Science 98, no. 2 (January 11, 2000): 183–92. http://dx.doi.org/10.1042/cs0980183.

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The effects of chylomicron remnants on cytoplasmic lipid loading and cell viability were assessed in cultures of human monocyte-derived macrophages and rabbit arterial smooth muscle cells. At a cholesterol concentration of 150 μg/ml, chylomicron remnants induced substantial cytoplasmic lipid loading of macrophages, but not of smooth muscle cells, within 6 h of exposure. Chylomicron remnants were found to be cytotoxic to macrophages and smooth muscle cells, although the latter were generally more resistant. Chylomicron remnants contained no detectable oxysterols (> 1 ng) and contained less non-esterified (‘free’) fatty acids than non-lipolysed nascent chylomicrons. Chylomicron-remnant-induced cytotoxicity appeared to be time- and dose-dependent. Macrophage and smooth muscle cell viability were inversely related to the production of superoxide free radicals and were significantly improved in the combined presence of superoxide dismutase and catalase. Collectively, our data suggest that, in macrophages, cell viability is compromised as a consequence of superoxide free radical production following uptake of chylomicron remnants. We would suggest that, in arterial smooth muscle cells, chylomicron-remnant-induced cell death also occurs as a consequence of superoxide free radical production. Our observations in the present study suggest that macrophage foam cells in atherosclerotic plaques might be derived from the cellular uptake of chylomicron remnants. Furthermore, arterial accumulation of chylomicron remnants might contribute to plaque destabilization as a consequence of cell death following superoxide free radical production by macrophages and smooth muscle cells.
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4

Soued, M., and C. M. Mansbach. "Chylomicron remnant uptake by enterocytes is receptor dependent." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 1 (January 1, 1996): G203—G212. http://dx.doi.org/10.1152/ajpgi.1996.270.1.g203.

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During glyceryl trioleate absorption in the rat, mucosal triacylglycerol (TG) fatty acids have been shown to consist of only 71% exogenous oleate. Chylomicron remnants are enriched with endogenous TG fatty acids, compared with their parent chylomicrons, which consist primarily of exogenous TG fatty acids. Because enterocytes have the apolipoprotein B-100/E receptor, this study was directed at determining whether the cells can take up and metabolize chylomicron remnants and, if so, whether this was receptor mediated. Isolated enterocytes were incubated with purified 3H-labeled chylomicron remnants. The remnants were shown to be taken up by the basolateral membrane, not the apical membrane. Remnant uptake was proportional to time and number of enterocytes, and saturation kinetics were observed. Nonradiolabeled remnants, human low-density lipoprotein (LDL), anti-LDL receptor antibody, and receptor-associated protein, an LDL-related receptor inhibitor, were all shown to compete for or reduce 3H-remnant uptake. Remnants taken up by the enterocytes could not be removed on incubation with excess human LDL. Uptake was shown to be greatest in the villus tips of the proximal intestine. These studies suggest that enterocytes take up chylomicron remnants by a receptor-mediated process from their basolateral membranes and that the remnants could provide a source of endogenous TG fatty acids for the enterocytes.
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5

Irawati, Deasy, John C. L. Mamo, Karin M. Slivkoff-Clark, Mario J. Soares, and Anthony P. James. "Dietary fat and physiological determinants of plasma chylomicron remnant homoeostasis in normolipidaemic subjects: insight into atherogenic risk." British Journal of Nutrition 117, no. 3 (February 14, 2017): 403–12. http://dx.doi.org/10.1017/s0007114517000150.

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AbstractTAG depleted remnants of postprandial chylomicrons are a risk factor for atherosclerosis. Recent studies have demonstrated that in the fasted state, the majority of chylomicrons are small enough for transcytosis to arterial subendothelial space and accelerate atherogenesis. However, the size distribution of chylomicrons in the absorptive state is unclear. This study explored in normolipidaemic subjects the postprandial distribution of the chylomicron marker, apoB-48, in a TAG-rich lipoprotein plasma fraction (Svedberg flotation rate (Sf>400), in partially hydrolysed remnants (Sf 20–400) and in a TAG-deplete fraction (Sf<20), following ingestion of isoenergetic meals with either palm oil (PO), rice bran or coconut oil. Results from this study show that the majority of fasting chylomicrons are within the potentially pro-atherogenic Sf<20 fraction (70–75 %). Following the ingestion of test meals, chylomicronaemia was also principally distributed within the Sf<20 fraction. However, approximately 40 % of subjects demonstrated exaggerated postprandial lipaemia specifically in response to the SFA-rich PO meal, with a transient shift to more buoyant chylomicron fractions. The latter demonstrates that heterogeneity in the magnitude and duration of hyper-remnantaemia is dependent on both the nature of the meal fatty acids ingested and possible metabolic determinants that influence chylomicron metabolism. The study findings reiterate that fasting plasma TAG is a poor indicator of atherogenic chylomicron remnant homoeostasis and emphasises the merits of considering specifically, chylomicron remnant abundance and kinetics in the context of atherogenic risk. Few studies address the latter, despite the majority of life being spent in the postprandial and absorptive state.
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6

Tsai, Michael Y., Angeliki Georgopoulos, James D. Otvos, Jose M. Ordovas, Naomi Q. Hanson, James M. Peacock, and Donna K. Arnett. "Comparison of Ultracentrifugation and Nuclear Magnetic Resonance Spectroscopy in the Quantification of Triglyceride-Rich Lipoproteins after an Oral Fat Load." Clinical Chemistry 50, no. 7 (July 1, 2004): 1201–4. http://dx.doi.org/10.1373/clinchem.2004.032938.

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Abstract Background: The measurement of triglyceride (TG)-rich particles after an oral fat challenge has been used to provide a measure of risk for coronary artery disease independent of the fasting plasma triglyceride concentration. The analytical “gold standard” for measuring TG-rich lipoproteins uses density gradient ultracentrifugation; however, this technique is labor-intensive. Because of our need to perform numerous postprandial analyses of TG-rich lipoproteins for a large interventional study (Genetics of Lipid Lowering Drugs and Diet Network), we evaluated the use of nuclear magnetic resonance (NMR) spectroscopy for measuring TG-rich particles. Methods: EDTA-blood samples were obtained 0, 3.5, 6, and 8 h after ingestion of an oral fat meal (89% of calories from fat) in 20 apparently healthy individuals. The plasma TG concentrations of chylomicron and chylomicron remnant/VLDL fractions were analyzed by ultracentrifugation and NMR spectroscopy. Results: Comparison of all values (n = 78) by ultracentrifugation (x) and NMR (y) produced a linear regression equation of y = 0.979x − 0.035 mmol/L (R2 = 0.90) for chylomicrons and y = 1.398x + 0.067 mmol/L (R2 = 0.96) for the fraction containing chylomicron remnants and VLDL. Postprandial response of chylomicrons and chylomicron remnant/VLDL was similar, with maximum response occurring between 3.5 to 6 h regardless of method of measurement. Conclusion: Chylomicron and chylomicron remnant/VLDL fraction measurements obtained by NMR have a high degree of correlation with results produced by ultracentrifugation. NMR may therefore be suitable as an alternative method for the measurement of postprandial TG-rich lipoproteins in individuals consuming a high-fat meal.
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7

van Dijk, M. C. M., G. J. Ziere, W. Boers, C. Linthorst, M. K. Bijsterbosch, and T. J. C. van Berkel. "Recognition of chylomicron remnants and β-migrating very-low-density lipoproteins by the remnant receptor of parenchymal liver cells is distinct from the liver α2-macroglobulin-recognition site." Biochemical Journal 279, no. 3 (November 1, 1991): 863–70. http://dx.doi.org/10.1042/bj2790863.

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The uptake in vivo of chylomicrons and beta-migrating very-low-density lipoprotein (beta-VLDL) by rat liver, which is primarily carried out by parenchymal cells, is inhibited, 5 min after injection, to respectively 35 and 8% of the control values after preinjection of lactoferrin. The decrease in the uptake of lipoproteins by the liver caused by lactoferrin is a specific inhibition of uptake by parenchymal cells. Competition studies in vitro demonstrate that chylomicron remnants and beta-VLDL compete for the same recognition site on parenchymal cells. Data obtained in vivo together with the competition studies performed in vitro indicate that chylomicron remnants and beta-VLDL interact specifically with the same remnant receptor. Hepatic uptake of 125I-labelled-alpha 2-macroglobulin in vivo, mediated equally by parenchymal and endothelial cells, is not decreased by preinjection of lactoferrin and no effect on the parenchymal-cell-mediated uptake is found. In vitro, alpha 2-macroglobulin and chylomicron remnants or beta-VLDL show no cross-competition. Culturing of parenchymal cells for 24-48 h leads to a decrease in the cell association of alpha 2-macroglobulin to 26% of the initial value, while the cell association of beta-VLDL with the remnant receptor is not influenced. It is concluded that beta-VLDL and chylomicron remnants are recognized by a specific remnant receptor on parenchymal liver cells, while uptake of alpha 2-macroglobulin by liver is carried out by a specific receptor system (presumably involving the LDL-receptor-related protein) which shows properties that are distinct from those of the remnant receptor.
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8

Borensztajn, J., and T. J. Kotlar. "Phospholipids as modulators of hepatic recognition of chylomicron remnants. Observations with emulsified lipoprotein lipids." Biochemical Journal 269, no. 2 (July 15, 1990): 539–42. http://dx.doi.org/10.1042/bj2690539.

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The lipids extracted from chylomicrons, chylomicron remnants generated in vivo and hepatic-lipase-treated chylomicrons were emulsified by sonication. These emulsified particles retained the capacity of the native lipoproteins to be differentiated by the liver in vivo, i.e. only the particles derived from remnant and hepatic-lipase-treated chylomicron lipids were efficiently taken up by the liver. To investigate the role of phospholipids in this differentiation process, the phospholipids of all three lipoprotein preparations were separated from the remaining lipids by silicic acid chromatography. The phospholipid-free lipid fraction of chylomicrons was then emulsified with the phospholipids derived from each of the three lipoprotein preparations. Only the particles emulsified with phospholipids derived from remnants and hepatic-lipase-treated chylomicrons were efficiently taken up by the liver in vivo. These results support the proposition that phospholipids modulate the hepatic differentiation between chylomicrons and remnants in vivo.
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9

ELSEGOOD, Caryn L., Sebely PAL, Paul D. ROACH, and John C. L. MAMO. "Binding and uptake of chylomicron remnants by primary and THP-1 human monocyte-derived macrophages: determination of binding proteins." Clinical Science 101, no. 2 (June 18, 2001): 111–19. http://dx.doi.org/10.1042/cs1010111.

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The binding and uptake of chylomicron remnants by human macrophages was studied in order to resolve paradoxical observations that have described the putative mechanisms by which postprandial lipoproteins induce foam cell formation. Chylomicron remnants bound to human monocyte-derived macrophages (HMMs) and to the transformed monocytic cell line THP-1 with high affinity (Kd of approx. 5.5 µg of chylomicron remnant protein/ml). Binding was found to be saturable for both cell types, and was strongly inhibited in the presence of unlabelled chylomicron remnants. Ligand blot studies with colloidal-gold-labelled chylomicron remnants identified two cell surface binding sites on both HMMs and THP-1 cells, with molecular masses of approx. 128 kDa and 43 kDa. The high-molecular-mass binding site was found to be the low-density lipoprotein (LDL) receptor, based on the strong inhibition of chylomicron remnant binding in the presence of unlabelled LDL, Fab2 antibody fragments to the LDL receptor or calcium chelators. Competition studies suggested that, in HMMs, the LDL receptor appeared to facilitate approximately half of the total chylomicron remnant uptake. In contrast, the LDL receptor was not significantly involved in macrophage uptake of chylomicron remnants by THP-1 cells. The identity of the 43 kDa binding site is presently unknown, but, importantly, expression was not inhibited as a consequence of sterol loading, which was induced by incubating HMMs and THP-1 cells with 25-hydroxycholesterol. In contrast, the expression of the LDL receptor was substantially attenuated following lipid loading. Collectively, our data suggest that, while the macrophage LDL receptor can bind chylomicron remnants and facilitate uptake in non-lipid-loaded HMMs, other sterol-insensitive sites are responsible for the unabated uptake of chylomicron remnants by macrophages. We propose that the 43 kDa macrophage chylomicron remnant binding protein may be a candidate for the sterol loading of macrophages.
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10

Mahley, Robert W., and M. Mahmood Hussain. "Chylomicron and chylomicron remnant catabolism." Current Opinion in Lipidology 2, no. 3 (June 1991): 170–76. http://dx.doi.org/10.1097/00041433-199106000-00005.

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11

Windler, E. E. T., J. Greeve, W. H. Daerr, and H. Greten. "Binding of rat chylomicrons and their remnants to the hepatic low-density-lipoprotein receptor and its role in remnant removal." Biochemical Journal 252, no. 2 (June 1, 1988): 553–61. http://dx.doi.org/10.1042/bj2520553.

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Binding and uptake of rat chylomicrons of different metabolic stages by the hepatic low-density-lipoprotein (LDL) receptor were studied. Pure chylomicrons, characterized by apolipoprotein B-48 devoid of contaminating B-100, were labelled in their cholesteryl esters. Lymph chylomicrons and serum chylomicrons, enriched in apolipoprotein E and the C-apolipoproteins, bound poorly to rat hepatic membranes. In contrast, chylomicron remnants, containing the apolipoproteins B-48 and E, bound with high affinity. Specific binding of remnants was virtually completely competed for by LDL free of apolipoprotein E. In addition, in ligand blots both remnants and LDL associated with the same protein with an Mr characteristic of the LDL receptor. Uptake of remnants during a single pass through isolated perfused rat livers was decreased to about 50% by an excess of LDL. It is concluded that rat chylomicron remnants are a ligand of the hepatic LDL receptor. The much higher affinity as compared with LDL is mediated by apolipoprotein E but not B-48, and is inhibited by the C-apolipoproteins. This explains why serum chylomicrons are not taken up by the liver, whereas remnants are rapidly removed from the circulation. Results from experiments in vivo suggest that the LDL receptor makes an important contribution to the hepatic uptake of remnants and may be the principal binding site of the liver responsible for remnant removal.
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12

Karpe, F., T. Olivecrona, A. Hamsten, and M. Hultin. "Chylomicron/chylomicron remnant turnover in humans: evidence for margination of chylomicrons and poor conversion of larger to smaller chylomicron remnants." Journal of Lipid Research 38, no. 5 (May 1997): 949–61. http://dx.doi.org/10.1016/s0022-2275(20)37219-9.

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13

Lambert, Marc S., Michael A. Avella, Kathleen M. Botham, and Peter A. Mayes. "Comparison of short- and long-term effects of different dietary fats on the hepatic uptake and metabolism of chylomicron remnants in rats." British Journal of Nutrition 79, no. 2 (February 1998): 203–11. http://dx.doi.org/10.1079/bjn19980032.

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The uptake and metabolism of [14C]oleate-labelled chylomicron remnants derived from olive oil, maize oil, palm oil, fish oil or butter fat was investigated using perfused livers from rats fed on the corresponding fat-supplemented diet (providing 40 % of the dietary energy) or a low-fat diet for 21 d. The percentage of added [14C]oleate-labelled remnant removed from the perfusate was similar for livers from rats fed on the fat-supplemented diets irrespective of the type of fat fed, whereas livers from rats fed on the low-fat diet removed more labelled fish oil and butter fat remnants than olive, maize or palm oil remnants. Following hepatic uptake in the fat-supplemented groups, the oxidation of [14C]oleate-labelled remnant lipid from maize oil, fish oil, and butter fat remnants was greater than that of the lipids from olive and palm oil remnants, although only the oxidation of lipids from maize and palm oil remnants was increased by prior fat-supplementation of the diet. In addition, the livers from rats fed on the fish-oil-supplemented diet incorporated more [14C]oleate-labelled remnant lipid into phospholipid compared with the livers from rats fed on the other fat-supplemented diets or the low-fat diets. These investigations show that both prior fat feeding and the composition of the fat fed, as well as the fatty acid composition of the chylomicron remnant particles themselves, influence the uptake and metabolism of chylomicron remnants by the liver.
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14

WATTS, G. F., D. C. F. CHAN, P. H. R. BARRETT, I. J. MARTINS, and T. G. REDGRAVE. "Preliminary experience with a new stable isotope breath test for chylomicron remnant metabolism: a study in central obesity." Clinical Science 101, no. 6 (November 20, 2001): 683–90. http://dx.doi.org/10.1042/cs1010683.

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We aimed to investigate the metabolism of chylomicron remnants in the postabsorptive state employing a new stable isotope breath test in centrally obese men without overt hyperlipidaemia. Groups of 12 centrally obese and 12 non-obese men of similar age and with similar plasma cholesterol and triacylglycerol (triglyceride) levels were studied. The catabolism of chylomicron remnants was measured using an intravenous injection of a remnant-like emulsion containing cholesteryl [13C]oleate. Isotopic enrichment of 13CO2 in breath was determined using isotope-ratio mass spectrometry, and a multi-compartmental model (SAAM II program) was used to estimate the fractional catabolic rate (FCR) of the chylomicron remnant-like particles. The plasma concentrations of low-density lipoprotein (LDL)-cholesterol, non-high-density lipoprotein (HDL)-cholesterol and insulin were significantly higher (P < 0.05) in the obese than the control subjects. The obese subjects had significantly lower HDL-cholesterol (P < 0.05) and, in particular, a decreased FCR of the remnant-like particles compared with lean subjects (0.061±0.014 and 0.201±0.048pools/h respectively; P = 0.016). In the obese group, the FCR of remnant-like particles was inversely associated with the waist/hip ratio, and with plasma triacylglycerol, cholesterol, LDL-cholesterol and non-HDL-cholesterol levels. In multiple regression analysis, the waist/hip ratio was the best predictor of the FCR of the emulsion. In conclusion, this new test suggests that postabsorptive chylomicron remnant catabolism is impaired in centrally obese subjects without overt hyperlipidaemia. This defect may be due to the degree of adiposity.
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15

Sakr, Sana W., N. Attia, M. Haourigui, J. L. Paul, T. Soni, D. Vacher, and A. Girard-Globa. "Fatty acid composition of an oral load affects chylomicron size in human subjects." British Journal of Nutrition 77, no. 1 (January 1997): 19–31. http://dx.doi.org/10.1017/s0007114500002853.

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HDL-phospholipids are determinants in reverse cholesterol transport. They are mostly derived from triacylglycerol (TG)-rich lipoproteins. Chylomicron size is important, therefore, because it is related to the ratio surface phospholipids: core TG and, thus, determines the availability of postprandial phospholipids for transfer to HDL. Eleven healthy young women each ingested four different fat loads supplemented with retinyl palmitate and containing 60 g sunflower oil (SO), oleic–sunflower oil (OSO), mixed oil (MO; (g/kg) linoleic acid 480, oleic acid 380, linolenic acid 13) or beef tallow (BT). At the peak of TG absorption for all loads (4 h) chylomicron diameters, determined by agarose-gel filtration, were larger after SO compared with OSO (P< 0·05) and BT (P= 0·06) and after MO compared with BT (P< 0·05). At 6 h chylomicron size was larger after the vegetable oils compared with BT (P< 0·05 in each case). After each fat load chylomicron size decreased at 6 and 8 h compared with that at 4 h (P< 0·05) except for OSO. Retinyl ester and TG concentrations were lower in chylomicrons after BT than after the other fats but not in the chylomicron-free serum (containing chylomicron remnants), suggesting absorption in the form of very small particles. Compared with the fasting value, the concentration of the Svedberg unit of flotation 20–400 fraction, which contains VLDL and chylomicron remnants, was lower 8 h after MO, the only fat to contain significant amounts of linolenic acid. We conclude that chylomicron size is dependent on the fatty acid composition of ingested fats and the time-course of digestion, being larger for polyunsaturated fatty acid-rich fats and in the early phase of digestion. On the basis of retinyl ester concentration there were no differences between fats in chylomicron-remnant clearance.
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16

Karpe, F., A. S. Bickerton, L. Hodson, B. A. Fielding, G. D. Tan, and K. N. Frayn. "Removal of triacylglycerols from chylomicrons and VLDL by capillary beds: the basis of lipoprotein remnant formation." Biochemical Society Transactions 35, no. 3 (May 22, 2007): 472–76. http://dx.doi.org/10.1042/bst0350472.

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The triacylglycerol content of chylomicrons and VLDL (very-low-density lipoprotein) compete for the same lipolytic pathway in the capillary beds. Although chylomicron triacylglycerols appear to be the favoured substrate for lipoprotein lipase, VLDL particles compete in numbers. Methods to quantify the specific triacylglycerol removal from VLDL and chylomicrons may involve endogenous labelling of the triacylglycerol substrate with stable isotopes in combination with arteriovenous blood sampling in humans. Arteriovenous quantification of remnant lipoproteins suggests that adipose tissue with its high lipoprotein lipase activity is a principal site for generation of remnant lipoproteins. Under circumstances of reduced efficiency in the removal of triacylglycerols from lipoproteins, there is accumulation of remnant lipoproteins, which are potentially atherogenic.
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17

Williams, Christine M. "Dietary interventions affecting chylomicron and chylomicron remnant clearance." Atherosclerosis 141 (December 1998): S87—S92. http://dx.doi.org/10.1016/s0021-9150(98)00224-x.

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18

Lambert, M. S., K. M. Botham, and P. A. Mayes. "Variations in composition of dietary fats affect hepatic uptake and metabolism of chylomicron remnants." Biochemical Journal 310, no. 3 (September 15, 1995): 845–52. http://dx.doi.org/10.1042/bj3100845.

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The hepatic metabolism of [1-14C]oleate- and [1,2-3H]cholesterol-dual-labelled chylomicron remnants derived from olive, corn, palm and fish oil and butter fat was compared by adding each lipoprotein separately to the perfusate of isolated livers from rats fed on a normal diet. Labelled remnants from butter fat and fish oil were removed more rapidly from the perfusate than remnants derived from olive, corn and palm oil. The oxidation of labelled remnant fatty acid from olive oil, fish oil or butter fat was four to seven times greater than that from corn and palm oil. Labelled fatty acid in fish oil remnants was incorporated into phospholipid significantly more efficiently than the labelled fatty acid in olive, corn or palm oil remnants, with butter fat giving an intermediate value. For all the remnants, there was a significant amount of hydrolysis of labelled esterified cholesterol by the liver which was dependent on the magnitude of hepatic uptake of each type of remnant. The recovery of remnant [3H]cholesterol label in the bile was 50% less with palm oil remnants than with all the other remnants studied. The results indicate that the fatty acid composition of chylomicron remnants has a major impact on their uptake and metabolism by the liver.
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19

Mamo, J. C. L., C. L. Elsegood, K. Yu, S. Schurmann, T. G. Redgrave, and Y. Umeda. "Chylomicron remnant metabolism by macrophages." Atherosclerosis 109, no. 1-2 (September 1994): 197–98. http://dx.doi.org/10.1016/0021-9150(94)93795-8.

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20

Bernik, Márcia MS, Joel C. Heimann, Edna R. Nakandakare, Patrícia M. Cazita, Valéria S. Nunes, Jussara C. Rocha, Mônica QTS Neves, and Eder CR Quintão. "Effects of hydrochlorothiazide and propranolol treatment on chylomicron metabolism in hypertensive subjects." Canadian Journal of Physiology and Pharmacology 83, no. 7 (July 1, 2005): 617–23. http://dx.doi.org/10.1139/y05-051.

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Modifications in chylomicron metabolism caused by antihypertensive drugs were investigated in hypertensive subjects because previous studies had indicated that diuretics and beta-blockers modify the plasma lipid concentrations through mechanisms that were not fully understood. A triglyceride-rich emulsion resembling lymph chylomicrons, labeled with (3H) triolein and (14C) cholesteryl oleate, was infused intravenously into mildly hypertensive patients after 8 weeks on placebo and subsequently on hydrochlorothiazide (n = 10) or propranolol (n = 8). The residence time of both radioactivities in plasma was utilized for the simultaneous calculation of the particle remnant removal rate and of the lipoprotein lipase activity expressed as a delipidation index = 1 – [(3H) triolein residence time/(14C) cholesteryl oleate residence time]. Treatment with hydrochlorothiazide diminished the delipidation rate value whereas propranolol mildly increased the removal rate of the remnant particle. These alterations of the chylomicron kinetics were not accompanied by changes in plasma triglycerides, glucose, and insulin concentration as measured in the fasting state. The impairment of the lipoprotein lipase activity by thiazides and the faster removal rate of the whole particle by propranolol could explain the reason why in previous clinical studies the simultaneous use of these drugs does not aggravate the hyperlipidemia known to be induced by thiazides alone. Key words: hydrochlorothiazide, propranolol, hypertension, plasma lipoproteins, chylomicron metabolism.
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21

Sultan, F., D. Lagrange, X. Le Liepvre, and S. Griglio. "Chylomicron-remnant uptake by freshly isolated hepatocytes. Effect of heparin and of hepatic triacylglycerol lipase." Biochemical Journal 258, no. 2 (March 1, 1989): 587–94. http://dx.doi.org/10.1042/bj2580587.

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Chylomicron remnants labelled biologically with [3H]cholesterol were efficiently taken up by freshly isolated hepatocytes during a 3 h incubation in Krebs bicarbonate medium. Their [3H]cholesteryl ester was hydrolysed (74% net hydrolysis), and 0.1 mM-chloroquine could partially inhibit this hydrolysis, provided that hepatocytes were first preincubated for 2 h 30 min at 37 degrees C. This hydrolysis was also measured in preincubated cells with remnants double-labelled (3H and 14C) on their free cholesterol moiety; [3H]cholesterol arising from [3H]cholesteryl ester hydrolysis was recovered in the free [3H]cholesterol pool. A dose-response study showed saturation of remnant uptake at 180 micrograms of remnant protein/10(7) cells. Heparin (10 units/ml) increased remnant uptake by 63% (P less than 0.01), [3H]cholesteryl ester accumulation in the cell pellet by 110% (P less than 0.025) and hepatic lipase activity secreted in the medium by 2.4-fold (P less than 0.01) and by 3.3-fold (P less than 0.01) at the end of the preincubation and incubation periods respectively. Addition of 100 munits of semi-purified hepatic lipase preparation/flask stimulated remnant uptake by 44-69%, and [3H]cholesteryl ester accumulation in the presence of chloroquine by 2.1-fold (P less than 0.025). When hepatic lipase was incubated solely with the remnants, it decreased their triacylglycerol and phospholipid contents by 24% and 26% respectively. Thus freshly isolated hepatocytes may be used to study chylomicron-remnant uptake. Hepatic lipase, which seems to underly the stimulating effect of heparin, facilitates remnant uptake in vitro, and this could be mediated by at least one (or both) of its hydrolytic properties.
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22

Staprans, I., X. M. Pan, J. H. Rapp, and K. R. Feingold. "Chylomicron and Chylomicron Remnant Metabolism in STZ-Induced Diabetic Rats." Diabetes 41, no. 3 (March 1, 1992): 325–33. http://dx.doi.org/10.2337/diab.41.3.325.

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23

Staprans, I., X. M. Pan, J. H. Rapp, and K. R. Feingold. "Chylomicron and chylomicron remnant metabolism in STZ-induced diabetic rats." Diabetes 41, no. 3 (March 1, 1992): 325–33. http://dx.doi.org/10.2337/diabetes.41.3.325.

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24

Lippiello, P. M., P. J. Sisson, and M. Waite. "The uptake and metabolism of chylomicron-remnant lipids by rat liver parenchymal and non-parenchymal cells in vitro." Biochemical Journal 232, no. 2 (December 1, 1985): 395–401. http://dx.doi.org/10.1042/bj2320395.

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The uptake and metabolism of chylomicron-remnant lipids by individual liver cell types was examined by incubating remnants with monolayer cultures of hepatocytes, Kupffer cells, and endothelial cells from rat liver. Remnants were prepared in vitro from radiolabelled mesenteric-lymph chylomicra, utilizing either purified lipoprotein lipase from bovine milk, or plasma isolated from heparinized rats. The resulting particles contained [3H]phosphatidylcholine and cholesterol, and [14C]oleate in the acylglycerol, phospholipid, fatty-acid and cholesterol-ester fractions. The capacities of the three cell types for uptake of both [3H]lipids and [14C]lipids were determined to be, on a per-cell basis, in the order: Kupffer greater than hepatocytes greater than endothelial. The relative proportions of [3H]phospholipid and total [3H]cholesterol taken up by hepatocytes and non-parenchymal cells remained constant with time. The uptake of [14C]oleoyl lipids by all three cell types was slightly greater than that of the total [3H]cholesterol and [3H]phospholipid components. There was evidence of cholesterol-ester hydrolysis and turnover of [14C]oleate in the phospholipid fraction in hepatocytes and Kupffer cells, but not endothelial cells, over the first 2 h. With both remnant preparations, these observations indicate that significant differences exist between the three major liver cell types with respect to the uptake and metabolism of remnant lipid components.
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25

Bravo, E., and M. Napolitano. "Mechanisms involved in chylomicron remnant lipid uptake by macrophages." Biochemical Society Transactions 35, no. 3 (May 22, 2007): 459–63. http://dx.doi.org/10.1042/bst0350459.

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Although it is clear that chylomicron remnants are atherogenic, events leading to their internalization by macrophages are still debated. The lack of apoE (apolipoprotein E) in CRLPs (chylomicron remnant-like particles) reduces macrophage TAG (triacylglycerol) content by approx. 50%, suggesting that, as well as apoE-mediated endocytic uptake, apoE receptor-independent mechanisms are involved in the induction of foam cells by chylomicron remnants. Evaluation of the radioactivity associated with macrophages after incubation with CRLPs containing radiolabelled lipids suggests that the TAG and cholesterol carried by the particles have different kinetics of internalization. In addition, inhibition-based experiments indicate that cholesteryl ester-selective uptake and the extracellular lipoprotein lipase hydrolysis of TAG contribute to cholesterol and TAG accumulation respectively. Thus plasma TAG and cholesterol carried by remnant particles have to be considered two independent and non-interchangeable risk factors for athero-related diseases. In addition, the interaction between CRLPs and macrophages is modulated by dietary oxidized lipids and other lipophilic components. The presence of oxidized lipids, such as 7β-hydroxycholesterol and 7-oxocholesterol, the major cholesterol oxidation products found in atherosclerotic lesions, in CRLPs interferes with the mechanisms of their internalization, but does not cause quantitative changes of accumulated lipids, while the presence of the plant carotenoid, lycopene, or the antioxidant drug, probucol, enhances lipid accumulation in macrophages by increasing the rate of uptake of the particles and raising the intracellular synthesis of TAG. In conclusion, several mechanisms contribute to the macrophage uptake of postprandial lipoproteins, however, little is known of the balance and modulation between the different pathways.
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26

Willnow, T. E. "Mechanisms of Hepatic Chylomicron Remnant Clearance." Diabetic Medicine 14, S3 (August 1997): S75—S80. http://dx.doi.org/10.1002/(sici)1096-9136(199708)14:3+3.0.co;2-9.

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27

Willnow, T. E. "Mechanisms of Hepatic Chylomicron Remnant Clearance." Diabetic Medicine 14, S3 (August 1997): S75—S80. http://dx.doi.org/10.1002/(sici)1096-9136(199708)14:3+3.3.co;2-0.

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28

Pan, X. M., I. Staprans, D. A. Hardman, and J. H. Rapp. "Exposure to cigarette smoke delays the plasma clearance of chylomicrons and chylomicron remnants in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 273, no. 1 (July 1, 1997): G158—G163. http://dx.doi.org/10.1152/ajpgi.1997.273.1.g158.

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We investigated the effects of cigarette smoke exposure on the clearance of chylomicrons (CM) and CM remnants in rats after administration of a fat-containing meal. There was a decrease in clearance of both postprandial CM and exogenous radiolabeled CM in smoke-exposed animals. For exogenous CM, clearance (t1/2) increased significantly for both triglyceride and cholesterol labels and correlated with the delay in liver uptake. This decrease in lipid clearance could not be explained by decreased lipoprotein lipase (LPL) activity because smoke exposure resulted in a significant increase in LPL activity. When the hydrolysis of CM by endothelial LPL was tested in a heart perfusion system, there was no difference in CM hydrolysis between the two groups. Hepatic lipase activity was also unchanged in smoke-exposed animals. However, there was a significant delay in the CM remnant uptake into livers isolated from smoke-exposed rats. Thus the delay in CM clearance in smoke-exposed animals cannot be attributed to reduced lipase activities but results from impaired hepatic uptake of CM remnants.
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29

Hussain, M. M., R. W. Mahley, J. K. Boyles, M. Fainaru, W. J. Brecht, and P. A. Lindquist. "Chylomicron-Chylomicron Remnant Clearance by Liver and Bone Marrow in Rabbits." Journal of Biological Chemistry 264, no. 16 (June 1989): 9571–82. http://dx.doi.org/10.1016/s0021-9258(18)60570-8.

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30

Kaysen, G. A., L. Mehendru, X. M. Pan, and I. Staprans. "Both peripheral chylomicron catabolism and hepatic uptake of remnants are defective in nephrosis." American Journal of Physiology-Renal Physiology 263, no. 2 (August 1, 1992): F335—F341. http://dx.doi.org/10.1152/ajprenal.1992.263.2.f335.

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We showed previously that proteinuria caused delayed chylomicron (CM) clearance in the rat and postulated the existence of a primary defect in CM hydrolysis. It was possible that reduced CM clearance resulted from increased lipogenesis causing saturation of catabolic sites and not from a primary defect in CM catabolism. To clarify this point we measured kinetically the absolute rate of triglyceride (TG) uptake from CM in rats with Heymann nephritis (HN) and normal Sprague-Dawley rats (SD) and determined TG uptake in individual tissues using [3H]TG- and [14C]cholesterol-labeled CM. Hepatic [14C]cholesterol uptake was reduced in HN (69.3 +/- 6 vs. 7.2 +/- 2% of dose, P less than 0.001). TG uptake was reduced in HN measured kinetically (1.01 +/- 0.09 vs. 0.213 +/- 0.028 mg TG.min-1.100 g body wt-1, P less than 0.001) and reduced in all tissues (heart, skeletal muscle, fat, and liver). CM are catabolized on the vascular endothelium to atherogenic, cholesterol-rich remnant (CM remnant) particles, which are then rapidly taken up by the liver. We measured hepatic CM remnant uptake in SD and in HN using [14C]cholesterol-labeled CM remnant. CM remnant uptake was significantly reduced in HN (58 +/- 1.2 vs. 20 +/- 0.86% uptake, P less than 0.01). CM remnants were increased significantly in plasma of HN. Thus the nephrotic syndrome causes a primary defect in the uptake of TG from CM that is expressed in all tissues and a separate defect in hepatic CM remnant uptake. Although CM remnant generation is impaired because of defective CM hydrolysis, the defect in hepatic CM remnant uptake is so severe that these particles accumulate in blood, posing a potential risk for atherogenesis.
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31

GOULTER, Andrew B., Michael A. AVELLA, Jonathan ELLIOTT, and Kathleen M. BOTHAM. "Chylomicron-remnant-like particles inhibit receptor-mediated endothelium-dependent vasorelaxation in pig coronary arteries." Clinical Science 103, no. 5 (October 3, 2002): 451–60. http://dx.doi.org/10.1042/cs1030451.

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The influence of native and oxidized chylomicron-remnant-like particles (CMR-LPs) on endothelium-dependent relaxation in pig coronary arteries was studied. Artificial lipid particles of a size and lipid composition resembling chylomicron remnants and containing pig apolipoprotein E were used to investigate the effects of chylomicron remnants on the relaxation of isolated segments of pig coronary arteries in response to three endothelium dilators: 5-hydroxytryptamine (5-HT), bradykinin and the calcium ionophore A23187. CMR-LPs caused significant inhibition of the maximum relaxation response of the vessels to 5-HT, but not that to bradykinin or A23187 (P<0.05). In contrast, CMR-LPs that had been oxidized by incubation with 10μM CuSO4 (oxidized CMR-LPs) were found to significantly reduce maximal relaxation to bradykinin by 13% (P<0.05) and to reduce the sensitivity of the tissue to A23187 by 1.7-fold (P<0.05). In experiments in which either the L-arginine/nitric oxide (NO) pathway or the endothelium-derived hyperpolarizing factor (EDHF) pathway was selectively inhibited, leaving the other intact, the inhibitory effect of oxidized CMR-LPs was observed only in vessels in which the L-arginine/NO-mediated pathway was operative. Furthermore, the oxidized particles had no inhibitory effect on the relaxation of the vessel segments to the non-endothelium-dependent agonists S-nitro-N-acetylpenicillamine, 5'-(N-ethylcarboxamido)adenosine or pinacidil. These results demonstrate that CMR-LPs inhibit vascular relaxation in pig coronary arteries by an endothelium-dependent mechanism involving the L-arginine/NO pathway, but not the EDHF pathway, and provide evidence in support of a role for chylomicron remnants in the endothelial dysfunction associated with hypercholesterolaemia and atherogenesis.
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32

BOKU, Akitoshi, Atsuko YANADA, Tomio ONUMA, Masahiro TSUTSUI, Shigeru OCHIAI, and Kazuo TAKEBE. "Abnormalities of Chylomicron Remnant Metabolism in Diabetics." Journal of Japan Atherosclerosis Society 16, no. 1 (1988): 59–62. http://dx.doi.org/10.5551/jat1973.16.1_59.

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33

Cooper, Allen D., and David Coleman. "Chylomicron remnant and asialoglycoprotein metabolism are independent." Lipids 20, no. 10 (October 1985): 664–67. http://dx.doi.org/10.1007/bf02534384.

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34

Willnow, T. E., S. Ishibashi, and J. Herz. "Dissection of the chylomicron remnant clearance pathway." Atherosclerosis 109, no. 1-2 (September 1994): 81–82. http://dx.doi.org/10.1016/0021-9150(94)93342-1.

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35

Rebholz, Sandra L., Katie T. Burke, Qing Yang, Patrick Tso, and Laura A. Woollett. "Dietary fat impacts fetal growth and metabolism: uptake of chylomicron remnant core lipids by the placenta." American Journal of Physiology-Endocrinology and Metabolism 301, no. 2 (August 2011): E416—E425. http://dx.doi.org/10.1152/ajpendo.00619.2010.

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The fetus requires significant energy for growth and development. Although glucose is a major source of energy for the fetus, other maternal nutrients also appear to promote growth. Thus, the goal of these studies was to determine whether triglyceride-rich remnants are taken up by the placenta and whether maternal dietary lipids, independently of adiposity, can impact fetal growth. To accomplish our first goal, chylomicron particles were duallly labeled with cholesteryl ester and triglycerides. The placenta took up remnant particles/core lipids at rates greater than adipose tissue and skeletal muscle but less than the liver. Although the placenta expresses apoE receptors, uptake of chylomicron remnants and/or core lipids can occur independently of apoE. To determine the impact of dietary lipid on fetal growth, independent of maternal adiposity, females were fed high-fat diets (HFD) for 1 mo; there was no change in adiposity or leptin levels prior to or during pregnancy of dams fed HFD. Fetal masses were greater in dams fed HFD, and mRNA levels of proteins involved in fatty acid oxidation (CPT I, PPARα), but not glucose oxidation (pyruvate kinase) or other regulatory processes (HNF-4α, LXR), were increased with maternal dietary fat. There was also no change in mRNA levels of proteins involved in placental glucose and fatty acid transport, and GLUT1 protein levels in microvillous membranes were similar in placentas of dams fed either diet. Thus, the ability of the placenta to take up chylomicron remnant core lipids likely contributes to accelerated fetal growth in females fed high fat diets.
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36

Castro Cabezas, Manuel, Tjerk W. A. de Bruin, Luciënne A. W. Kock, Wouter Kortlandt, Margreet Van Linde-Sibenius Trip, Hans Jansen, and D. Willem Erkelens. "Simvastatin improves chylomicron remnant removal in familial combined hyperlipidemia without changing chylomicron conversion." Metabolism 42, no. 4 (April 1993): 497–503. http://dx.doi.org/10.1016/0026-0495(93)90109-2.

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37

Huettinger, Manfred, Helmut Retzek, Martina Eder, and Hans Goldenberg. "Characteristics of chylomicron remnant uptake into rat liver." Clinical Biochemistry 21, no. 2 (April 1988): 87–92. http://dx.doi.org/10.1016/s0009-9120(88)80093-6.

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38

Cabezas, M. C., T. W. de Bruin, H. Jansen, L. A. Kock, W. Kortlandt, and D. W. Erkelens. "Impaired chylomicron remnant clearance in familial combined hyperlipidemia." Arteriosclerosis and Thrombosis: A Journal of Vascular Biology 13, no. 6 (June 1993): 804–14. http://dx.doi.org/10.1161/01.atv.13.6.804.

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39

KAWASAKI, SATORU, TAKAHIRO TANIGUCHI, YOSHIO FUJIOKA, AKIHIRO TAKAHASHI, TOMOSABURO TAKAHASHI, KOJI DOMOTO, MASAKO TAGUCHI, YUICHI ISHIKAWA, and MITSUHIRO YOKOYAMA. "Chylomicron Remnant Induces Apoptosis in Vascular Endothelial Cells." Annals of the New York Academy of Sciences 902, no. 1 (January 25, 2006): 336–41. http://dx.doi.org/10.1111/j.1749-6632.2000.tb06334.x.

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40

Windler, E., J. Greeve, S. Ja¨ckle, F. Rinninger, and H. Greten. "Mechanisms regulating hepatic chylomicron remnant uptake and metabolism." Atherosclerosis 109, no. 1-2 (September 1994): 173–74. http://dx.doi.org/10.1016/0021-9150(94)93699-4.

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41

Zilversmit, D. B. "Atherogenic nature of triglycerides, postprandial lipidemia, and triglyceride-rich remnant lipoproteins." Clinical Chemistry 41, no. 1 (January 1, 1995): 153–58. http://dx.doi.org/10.1093/clinchem/41.1.153.

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Abstract In addition to low-density lipoproteins, plasma chylomicrons and very-low-density lipoproteins (VLDL) contribute to atherogenesis. When triglyceride-rich particles bind to arterial endothelium and to deendothelialized areas, locally present lipoprotein lipase initiates triglyceride hydrolysis and decreases the size of the adhering particles. Additional changes in composition are brought about by the exchange of lipids between chylomicron/VLDL remnants and the cholesteryl ester-rich low- and high-density lipoproteins. These exchanges are mediated by lipid transfer proteins in plasma. Animal studies with doubly labeled lipoproteins show that the size of lipoprotein particles determines their rate of entering the artery and contributes to the formation of lesions. This model supports epidemiologic studies that have identified plasma triglycerides as a risk factor for atherogenesis. The model for a causal role of pre- and postprandial triglyceride-rich lipoproteins in atherogenesis suggests that measuring them may improve the assessment of cardiovascular risk factors.
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42

Szanto, A., S. Balasubramaniam, P. D. Roach, and P. J. Nestel. "Modulation of the low-density-lipoprotein-receptor-related protein and its relevance to chylomicron-remnant metabolism." Biochemical Journal 288, no. 3 (December 15, 1992): 791–94. http://dx.doi.org/10.1042/bj2880791.

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Hepatic levels of the low-density-lipoprotein (LDL)-receptor-related protein (LRP) and the LDL receptor were measured in rats subjected to treatments known to affect the expression of the LDL receptor. Propylthiouracil decreased both hepatic LRP and LDL receptor expression by 30-40%. Thyroxine treatment increased LDL receptor levels by 3-fold without altering LRP levels. In contrast, 17 alpha-ethinyloestradiol decreased LRP by 50%, whereas the LDL receptor was increased 5-fold. Plasma chylomicrons and their remnants were decreased to insignificant levels with this treatment. In rats fed with cholesterol there was a significant increase in these particles in plasma (1.21 +/- 0.4 versus 5.71 +/- 0.4 mg/dl), whereas the expression of LRP was unaltered. In Watanabe heritable hyperlipidaemic and cholesterol-fed rabbits, in which the LDL receptor expression is absent or decreased, the expression of LRP was not significantly different from that in normal rabbits. These results suggest that the expression of hepatic LRP can be modulated by changes in the hormonal status of the rat and that this modulation is not tightly co-ordinated with that of the LDL receptor. Moreover, LRP does not appear to have a significant role in chylomicron-remnant clearance, whereas the LDL receptor is actively involved in this process.
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43

Chan, Dick C., Gerald F. Watts, P. Hugh Barrett, John CL Mamo, and Trevor G. Redgrave. "Markers of Triglyceride-rich Lipoprotein Remnant Metabolism in Visceral Obesity." Clinical Chemistry 48, no. 2 (February 1, 2002): 278–83. http://dx.doi.org/10.1093/clinchem/48.2.278.

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Abstract Background: Triglyceride-rich lipoprotein remnants are atherogenic, and this may be particularly important in visceral obesity. We investigated remnant metabolism in obese men by measuring remnant-like particle-cholesterol (RLP-C), apolipoprotein (apo) B-48, apoC-III, and the clearance of a labeled remnant-like emulsion. Methods: Fasting RLP-C, apoB-48, and apoC-III concentrations were measured in 48 viscerally obese men and 10 lean controls. RLP-C was determined by immunoseparation assay, apoB-48 by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and enhanced chemiluminescence, and apoC-III by immunoturbidimetric assay. The catabolism of chylomicron remnants was measured by intravenous injection of a remnant-like emulsion containing cholesteryl [13C]oleate, with isotopic enrichment of 13CO2 in breath determined by isotope-ratio mass spectrometry and a multicompartmental model to estimate fractional catabolic rate (FCR) of the emulsion. Results: Compared with controls, obese men had significantly increased plasma concentrations of RLP-C, apoB-48, and apoC-III (P &lt;0.001 for all). Plasma total apoB-100, non-HDL-cholesterol, LDL-cholesterol, triglycerides, and insulin resistance (HOMA score) were also significantly higher in the obese group (P &lt;0.001 for all). Obese men had a significantly lower FCR of the remnant-like emulsion compared with controls (P = 0.020). Conclusions: Viscerally obese individuals have insulin resistance and increased plasma concentrations of triglyceride-rich lipoprotein remnants, which may be attributable to decreased catabolism of these particles.
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44

Lopez-Soldado, I., M. Avella, and K. M. Botham. "Comparison of the effects of dietary saturated, mono-unsaturated and polyunsaturated fatty acids on very-low-density lipoprotein secretion when delivered to hepatocytes in chylomicron remnant-like particles." Biochemical Society Transactions 35, no. 3 (May 22, 2007): 440–41. http://dx.doi.org/10.1042/bst0350440.

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The effect of chylomicron remnant-like particles (CRLPs) enriched in saturated, mono-unsaturated or n−6 polyunsaturated fatty acids (derived from palm, olive or corn oil, respectively) on the secretion of VLDL (very-low-density lipoprotein) by rat hepatocytes in culture was investigated. CRLPs were incubated with cultured hepatocytes for 5 h. The medium was then removed and the secretion of cholesterol and triacylglycerol (TAG) into the whole medium during the following 16 h was determined. After exposure of the cells to olive oil as compared with corn and palm oil CRLPs, secretion of TAG into the medium was decreased. The TAG content of the cells was also lower in experiments with olive oil as compared with corn oil CRLPs. The levels of apoB48 (apolipoprotein B48) found in the medium remained unchanged after the exposure of the cells to the different types of remnants. These findings indicate that the type of fat in the diet directly affects VLDL lipid secretion on delivery to the liver in chylomicron remnants.
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45

GOULTER, Andrew B., Michael AVELLA, Kathleen M. BOTHAM, and Jonathan ELLIOTT. "Chylomicron-remnant-like particles inhibit the basal nitric oxide pathway in porcine coronary artery and aortic endothelial cells." Clinical Science 105, no. 3 (September 1, 2003): 363–71. http://dx.doi.org/10.1042/cs20030039.

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The effects of chylomicron remnants on the activity of basally produced nitric oxide (NO) from porcine coronary artery rings and porcine aortic endothelial cells were studied by investigating the effects of chylomicron-remnant-like particles (CMR-LPs) containing porcine apolipoprotein E on the vessel tone of porcine coronary arteries and on cGMP release by aortic endothelial cells. CMR-LPs were oxidized by incubation with CuSO4 (10 μM) for 18 h at 37 °C. Nω-nitro-L-arginine (L-NOARG) and oxidized CMR-LPs (oxCMR-LPs), but not native CMR-LPs, increased the vessel tone of static porcine coronary artery rings (increase in tone as a percentage of the tone induced by depolarizing Krebs–;Henseleit solution: L-NOARG, 14.24±2.09; oxCMR-LPs, 4.98±0.88; and native CMR-LPs, 0.47±0.21). L-NOARG, endothelium removal and oxCMR-LPs also all significantly increased the maximum relaxation of the vessels to S-nitroso-N-acetyl-DL-penicillamine. In addition, oxCMR-LPs reduced the amounts of cGMP released by porcine aortic endothelial cells into the culture medium from 116±12.0 to 84.2±11.6 fmol/μg of cellular protein, mimicking the effects of L-NOARG. These results indicate that oxCMR-LPs, but not native CMR-LPs, inhibit the activity, production or release of NO from unstimulated porcine coronary and aortic endothelial cells. oxCMR-LPs mimicked the addition of L-NOARG and endothelium removal in these experimental systems, suggesting that the lipoproteins were interfering with the L-arginine/NO pathway. This study provides further evidence to support a role of chylomicron remnants in the development of atherosclerosis.
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Napolitano, Mariarosaria, Howard S. Kruth, and Elena Bravo. "Phospholipase A2 Mediates Apolipoprotein-Independent Uptake of Chylomicron Remnant-Like Particles by Human Macrophages." International Journal of Vascular Medicine 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/501954.

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Apolipoprotein E-receptor-mediated pathways are the main routes by which macrophages take up chylomicron remnants, but uptake may also be mediated by receptor-independent routes. To investigate these mechanisms, triacylglycerol (TG) accumulation induced by apolipoprotein-free chylomicron remnant-like particles (CRLPw/o) in human monocyte-derived macrophages was evaluated. Macrophage TG content increased about 5-fold after incubation with CRLPw/o, and this effect was not reduced by the inhibition of phagocytosis, macropinocytosis, apolipoprotein E function, or proteoglycan bridging. The role of lipases, including lipoprotein lipase, cholesteryl ester hydrolase, and secretory (sPLA2) and cytosolic phospholipase A2, was studied using [3H]TG-labelled CRLPw/o. Total cell radioactivity after incubation with [3H]TG CRLPw/o was reduced by 15–30% by inhibitors of lipoprotein lipase and cholesteryl ester hydrolase and by about 45% by inhibitors of sPLA2 and cytosolic PLA2. These results suggest that macrophage lipolytic enzymes mediate the internalization of postprandial TG-rich lipoproteins and that sPLA2and cytosolic PLA2, play a more important role than extracellular lipoprotein lipase-mediated TG hydrolysis.
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47

Van Berkel, Th J. C., M. C. M. Van Dijk, G. J. Ziere, M. N. Pieters, and J. K. Kruyt. "Chylomicron-remnant recognition and biliary secretion of dietary cholesterol." Atherosclerosis 109, no. 1-2 (September 1994): 174. http://dx.doi.org/10.1016/0021-9150(94)93700-1.

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48

Evans, M., Y. Berhane, K. M. Botham, J. Elliott, and C. P. D. Wheeler-Jones. "Chylomicron-remnant-like particles modify production of vasoactive mediators by endothelial cells." Biochemical Society Transactions 32, no. 1 (February 1, 2004): 110–12. http://dx.doi.org/10.1042/bst0320110.

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Endothelial-cell dysfunction is a critical initiating event in the pathogenesis of atherosclerosis. Although there is evidence to suggest that chylomicron remnants (CMRs), lipoproteins derived from the diet, influence endothelial-cell function to generate a pro-atherogenic phenotype, the mechanisms involved remain undefined. We have examined the effects of CMR-like particles (CMR-LPs) on human endothelial-cell function, focusing on the cyclo-oxygenase (COX) and nitric oxide synthase (NOS) pathways. CMR-LPs strongly enhanced the expression of the inducible cyclo-oxygenase COX-2 and increased prostacyclin synthesis in a biphasic manner. Studies with the COX-2-selective inhibitor NS-398 confirmed the COX-2 dependency of the later increase in prostanoid production. Pre-incubation with CMR-LPs reduced basal and thrombin-stimulated cGMP generation, whereas expression of endothelial NOS was not modified by remnant treatment.
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Redgrave, T. G., G. F. Watts, I. J. Martins, P. H. R. Barrett, J. C. L. Mamo, S. B. Dimmitt, and A. D. Marais. "Chylomicron remnant metabolism in familial dyslipidemias studied with a remnant-like emulsion breath test." Journal of Lipid Research 42, no. 5 (May 2001): 710–15. http://dx.doi.org/10.1016/s0022-2275(20)31632-1.

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NAPOLITANO, Mariarosaria, Kelly V. BATT, Michael AVELLA, Elena BRAVO, and Kathleen M. BOTHAM. "Lipid synthesis in macrophages derived from the human cell line THP-1: modulation of the effects of native and oxidized chylomicron-remnant-like particles by oestrogen." Clinical Science 101, no. 4 (September 14, 2001): 403–13. http://dx.doi.org/10.1042/cs1010403.

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Abstract:
The effects of native and oxidized chylomicron remnants on the synthesis of cholesteryl ester and triacylglycerol in macrophages, and the way that this is influenced by exposure of the cells to oestrogen, was investigated using the human monocyte cell line THP-1 and chylomicron-remnant-like particles containing human apolipoprotein E (CRLPs). Synthesis of the lipids was measured by the incorporation of [3H]oleate into cholesteryl ester and triacylglycerol. CRLPs (5-40μg of cholesterol/ml) containing either trilinolein or triolein as the triacylglycerol component caused a dose-dependent decrease in cholesteryl ester formation, while triacylglycerol production was unchanged. After oxidation of the CRLPs, the level of thiobarbituric acid-reactive substances was increased by 6.3-fold and 2.2-fold in particles containing trilinolein and triolein respectively. Furthermore, CRLPs containing oxidized trilinolein lost their ability to down-regulate cholesterol esterification, while CRLPs containing oxidized triolein did not. Both types of oxidized CRLPs decreased triacylglycerol synthesis. Treatment of the macrophages with 17β-oestradiol caused increases of approx. 94% and 34% in the synthesis of cholesteryl ester and triacylglycerol respectively in the absence of CRLPs. The differences between control and oestrogen-treated cells were abolished, however, when CRLPs (40μg of cholesterol/ml) were added to the incubations. In addition, in contrast with their lack of effect in control cells, CRLPs containing oxidized trilinolein decreased cholesterol esterification in oestrogen-treated cells by approx. 48%. These findings with CRLPs suggest that chylomicron remnants have significant effects on cholesteryl ester and triacylglycerol synthesis in macrophages, which may be modulated both by the oxidation state of the particles and by oestrogen.
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