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Journal articles on the topic 'Chylomicron'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

Redgrave, T. G. "Chylomicron metabolism." Biochemical Society Transactions 32, no. 1 (2004): 79–82. http://dx.doi.org/10.1042/bst0320079.

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Chylomicrons are the ‘orphans’ of the lipoprotein family. Difficulty of measurement has impeded understanding of their metabolism. Plasma concentrations of chylomicrons and chylomicron remnants give no insight into the magnitude of substrate flux through these pathways. A defect in clearance of chylomicron remnants is probably an indication of a more generalized defect in lipoprotein metabolism. Accumulating evidence supports a relationship between abnormalities in the clearance from plasma of chylomicron remnants and accelerated progression of atherosclerosis. Methods using stable isotopes in

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Phillips, Catherine, Claire Madigan, Daphne Owens, Patrick Collins, and Gerald H. Tomkin. "Defective Chylomicron Synthesis as a Cause of Delayed Particle Clearance in Diabetes?" International Journal of Experimental Diabetes Research 3, no. 3 (2002): 171–78. http://dx.doi.org/10.1080/15604280214277.

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Chylomicron metabolism is abnormal in diabetes and the chylomicron particle may play a very important role in atherosclerosis. The aim of this study was to examine the effect of diabetes on the metabolism of chylomicrons in cholesterol-fed alloxan diabetic and nondiabetic rabbits. Five diabetic rabbits and 5 control rabbits were given [C14]linoleic acid and [H3]cholesterol by gavage. Lymph was collected following cannulation of the lymph duct and radiolabelled chylomicrons were isolated by ultracentrifugation. The chylomicrons from each animal were injected into paired control and diabetic rec

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Tso, P., J. A. Barrowman, and D. N. Granger. "Importance of interstitial matrix hydration in intestinal chylomicron transport." American Journal of Physiology-Gastrointestinal and Liver Physiology 250, no. 4 (1986): G497—G500. http://dx.doi.org/10.1152/ajpgi.1986.250.4.g497.

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We have shown previously that lymph flow has a profound effect on intestinal chylomicron transport. However, since lymph flow both determines the rate of convective movement of chylomicrons within the interstitium and reflects the degree of hydration of the interstitial matrix, we were unable to determine which factor was more important for the inverse relation between the chylomicron appearance time and lymph flow. In this investigation, we measured the chylomicron appearance time in rats with a normal lymph flow and expanded matrix (study A), in rats with a reduced lymph flow but expanded ma

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James, AP, K. Slivkoff-Clark, and JCL Mamo. "New Insights into Cardiovascular Disease Risk in Subjects with Visceral Obesity." Asia Pacific Journal of Public Health 15, no. 1_suppl (2003): S37—S40. http://dx.doi.org/10.1177/101053950301500s10.

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Obese insulin resistant individuals often present with a dyslipidemic phenotype characterised by hypertriglyceridemia, low HDL cholesterol levels, essentially normal total- and LDL-cholesterol, but a propensity for smaller, denser LDL particles. We have reported that concentrations of chylomicrons are two to three folds greater than in age-matched lean controls. We have recently observed that in lean free-living subjects the flux of chylomicrons over a 12h period was just 25% greater in these subjects than basal chylomicron production. Constitutive secretion of chylomicrons appears to be of gr

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Tso, P., V. Pitts, and D. N. Granger. "Role of lymph flow in intestinal chylomicron transport." American Journal of Physiology-Gastrointestinal and Liver Physiology 249, no. 1 (1985): G21—G28. http://dx.doi.org/10.1152/ajpgi.1985.249.1.g21.

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In this study we investigated the influence of lymph flow on chylomicron transport. We examined the effects of varying the hydration of the interstitial matrix on chylomicron appearance time and on lymphatic lipid transport rate when a lipid test meal containing oleic acid and 1-monoolein was infused intraduodenally at a constant rate. The three groups of rats tested were control rats (normal interstitial hydration), rats receiving intravenous saline infusion (expanded interstitial matrix), and rats with an attenuated water absorption rate (dehydrated interstitial matrix). This study shows tha

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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 (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–

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Milan, Amber M., Anu Nuora, Shikha Pundir, et al. "Older adults have an altered chylomicron response to a high-fat meal." British Journal of Nutrition 115, no. 5 (2016): 791–99. http://dx.doi.org/10.1017/s000711451500505x.

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AbstractAgeing is associated with a prolonged and exaggerated postprandial lipaemia. This study aimed to examine the contribution of alterations in chylomicron synthesis, size and lipid composition to increased lipaemia. Healthy older (60–75 years; n 15) and younger (20–25 years; n 15) subjects consumed a high-fat breakfast. Chylomicron dynamics and fatty acid composition were analysed for 5 h in the postprandial state. Plasma TAG levels were elevated following the meal in the older subjects, relative to younger subjects (P<0·01). For older subjects compared with younger subjects, circulati

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8

Lambert, Marc S., Kathleen M. Botham, and Peter A. Mayes. "Modification of the fatty acid composition of dietary oils and fats on incorporation into chylomicrons and chylomicron remnants." British Journal of Nutrition 76, no. 3 (1996): 435–45. http://dx.doi.org/10.1079/bjn19960048.

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Possible changes in the fatty acid composition of dietary fats and oils which might occur during digestion, absorption and formation of chylomicrons and chylomicron remnants were investigated. Chylomicrons were collected from the thoracic duct of rats tube-fed with olive, maize, palm or fish oil or butter fat, and their fatty acid composition was determined and compared with that of their parent lipids. In turn, these lipoproteins were converted to chylomicron remnants infunctionally hepatectomized rats and their composition re-determined. The predominant fatty acids in each of the oils and fa

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9

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 (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

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Tsai, Michael Y., Angeliki Georgopoulos, James D. Otvos, et al. "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 (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

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Mansbach, C. M., and A. Arnold. "Steady-state kinetic analysis of triacylglycerol delivery into mesenteric lymph." American Journal of Physiology-Gastrointestinal and Liver Physiology 251, no. 2 (1986): G263—G269. http://dx.doi.org/10.1152/ajpgi.1986.251.2.g263.

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The output of triacylglycerol in chylomicrons can be increased 60% by prefeeding rats with a 20% fat diet or 110% by including phosphatidylcholine in a lipid infusion. The present study was designed to determine whether the increment was due to an expansion of the chylomicron triacylglycerol precursor pool or an increase in its fractional turnover rate. A steady-state kinetic model was established in rats receiving 135 mumol glyceryl trioleate/h. The decay in specific activity of triacylglycerol after removal of radiolabeled glyceryl trioleate from the duodenal infusate was followed for 4 h an

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Black, Dennis D. "Development and Physiological Regulation of Intestinal Lipid Absorption. I. Development of intestinal lipid absorption: cellular events in chylomicron assembly and secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 293, no. 3 (2007): G519—G524. http://dx.doi.org/10.1152/ajpgi.00189.2007.

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The newborn mammal must efficiently absorb dietary fat, predominantly as triacylglycerol, and produce chylomicrons to deliver this lipid to peripheral tissues. The cellular mechanisms involved in enterocyte chylomicron assembly have recently been elucidated, and data on their regulation in the immature gut are beginning to emerge. This review focuses on key proteins involved in chylomicron assembly: apolipoprotein B-48, microsomal triglyceride transfer protein, and apolipoproten A-IV. Recent studies support a role for apolipoprotein A-IV in enhancing chylomicron secretion by promoting producti

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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 (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 chromatograph

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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 (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 n

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Redgrave, T. G., H. L. Ly, E. C. R. Quintao, C. F. Ramberg, and R. C. Boston. "Clearance from plasma of triacylglycerol and cholesteryl ester after intravenous injection of chylomicron-like lipid emulsions in rats and man." Biochemical Journal 290, no. 3 (1993): 843–47. http://dx.doi.org/10.1042/bj2900843.

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Chylomicrons transport fat and cholesterol via lymphatic vessels from the intestine into the bloodstream. The understanding of the metabolism of chylomicrons in man has been slowed by the difficulty of obtaining lymph chylomicrons for experimental studies. Acceptable methods for the study of chylomicron clearance in man are required, because the metabolism of chylomicrons may be abnormal in diseases such as diabetes mellitus. Metabolism of chylomicrons may also play a role in the development of atherosclerosis. In the present work, lipid emulsions were used as a physical model of chylomicrons.

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Yu, Kenneth C. W., Darrin Smith, Akira Yamamoto, et al. "Phagocytic Degradation of Chylomicron Remnants by Fibroblasts from Subjects with Homozygous Familial Hypercholesterolemia." Clinical Science 92, no. 2 (1997): 197–203. http://dx.doi.org/10.1042/cs0920197.

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1. Familial hypercholesterolaemia is a common genetic abnormality in man characterized by premature atherogenesis as a consequence of disturbed lipoprotein metabolism. Chylomicrons, which represent intestinally derived lipoproteins, are cleared poorly in familial hypercholesterolaemia which may explain the increased retention of chylomicron remnants in arterial fatty lesions. However, cellular uptake of chylomicron remnants in familial hypercholesterolaemia remains unclear. This study determined the quantitative significance of non-low-density lipoprotein receptor-mediated uptake in fibroblast

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Sakr, Sana W., N. Attia, M. Haourigui, et al. "Fatty acid composition of an oral load affects chylomicron size in human subjects." British Journal of Nutrition 77, no. 1 (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)

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Tso, P., and J. A. Balint. "Formation and transport of chylomicrons by enterocytes to the lymphatics." American Journal of Physiology-Gastrointestinal and Liver Physiology 250, no. 6 (1986): G715—G726. http://dx.doi.org/10.1152/ajpgi.1986.250.6.g715.

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Digestion of triglyceride in the intestine results in the production of 2-monoglyceride and fatty acid. Phosphatidylcholine is hydrolyzed in the lumen to form lysophosphatidylcholine before its absorption. These digestion products are absorbed by the enterocytes through simple diffusion. In contrast, cholesterol absorption seems specific and is energy dependent. After entry into the enterocytes, these lipid digestion products migrate to the endoplasmic reticulum. Both fatty acid-binding protein and sterol carrier protein may be involved in the intracellular transport of fatty acid and choleste

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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 (1997): 949–61. http://dx.doi.org/10.1016/s0022-2275(20)37219-9.

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JUNG, Hye Rim, Scott M. TURNER, Richard A. NEESE, Steven G. YOUNG, and Marc K. HELLERSTEIN. "Metabolic adaptations to dietary fat malabsorption in chylomicron-deficient mice." Biochemical Journal 343, no. 2 (1999): 473–78. http://dx.doi.org/10.1042/bj3430473.

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A mouse model of chylomicron deficiency was recently developed; these mice express a human apolipoprotein (apo) B transgene in the liver but do not synthesize any apoB in the intestine. Despite severe intestinal fat malabsorption, the mice maintain normal concentrations of plasma lipids and liver-derived apoB 100-containing lipoproteins. We investigated the metabolic mechanisms by which plasma lipid levels are kept normal. De novo lipogenesis (DNL) and cholesterogenesis were measured by mass isotopomer distribution analysis (MIDA). Plasma non-esterified fatty acid (NEFA) fluxes and hepatic re-

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Park, Yongsoon, Wayne J. Grellner, William S. Harris, and John M. Miles. "A new method for the study of chylomicron kinetics in vivo." American Journal of Physiology-Endocrinology and Metabolism 279, no. 6 (2000): E1258—E1263. http://dx.doi.org/10.1152/ajpendo.2000.279.6.e1258.

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Our understanding of the metabolism of chylomicrons, the lipoprotein that transports dietary fat from the intestine to peripheral tissues, is incomplete. The present studies were conducted to determine whether a labeled intravenous lipid emulsion could be used to estimate chylomicron triglyceride (TG) rate of appearance (Ra) and thereby quantify the rate of intestinal fat absorption. After an overnight fast, healthy volunteers ( n = 6) sipped a3H-labeled drink over 6.5 h at a rate of 175 mg fat · kg−1 · h−1. Beginning at hour 5, an HPLC-purified, 14C-labeled lipid emulsion was infused intraven

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Williams, C. M., P. A. Bateman, K. G. Jackson, and P. Yaqoob. "Dietary fatty acids and chylomicron synthesis and secretion." Biochemical Society Transactions 32, no. 1 (2004): 55–58. http://dx.doi.org/10.1042/bst0320055.

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There is currently considerable interest in potential atherogenic and thrombogenic consequences of elevated concentrations of triacylglycerols, especially in the post-prandial state. Despite this, there is limited information on the effects of dietary fatty acids on the synthesis, secretion and metabolism of chylomicrons, the large triacylglycerol-rich lipoproteins synthesized in the enterocyte following the digestion and absorption of dietary fat. This brief review considers current approaches to the investigation of chylomicron synthesis and summarizes some of the human, cell and animal stud

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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 (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 3

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Borensztajn, J., T. J. Kotlar, and S. Y. Chang. "Apoprotein-independent binding of chylomicron remnants to rat liver membranes." Biochemical Journal 279, no. 3 (1991): 769–73. http://dx.doi.org/10.1042/bj2790769.

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Rat lymph chylomicrons and chylomicron remnants were treated with trypsin or Pronase. The ability of the resulting apoprotein-free lipoproteins to be taken up by the isolated perfused rat liver, and to bind to isolated rat liver membranes, was examined. Compared with control lipoproteins, the apoprotein-free chylomicrons and remnants retained unaltered their capacity to be differentiated by the intact liver and by the isolated membranes. Further, control remnants and apoprotein-free remnants competed for binding to the isolated membranes. We conclude that apoproteins are not required for the h

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Orth, Matthias, Monika Hanisch, Gerd Kröning, Mustafa Porsch-Özcürümez, Heinrich Wieland, and Claus Luley. "Fluorometric determination of total retinyl esters in triglyceride-rich lipoproteins." Clinical Chemistry 44, no. 7 (1998): 1459–65. http://dx.doi.org/10.1093/clinchem/44.7.1459.

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Abstract A time-consuming sample preparation and measuring procedure is required for the quantitation of retinyl palmitate by HPLC. We developed a fluorometric method for the determination of total retinyl esters in chylomicrons, chylomicron remnants, and VLDL. This method is precise, sensitive, rapid, simple, and particularly useful for large-scale studies of postprandial lipid metabolism. Because the turbidity of postprandial lipemic samples interferes with the fluorescence measurement, all samples were incubated for 10 min with a clearing buffer containing esterase and detergents. This buff

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Hsieh, Joanne, Karin E. Trajcevski, Sarah L. Farr, et al. "Glucagon-Like Peptide 2 (GLP-2) Stimulates Postprandial Chylomicron Production and Postabsorptive Release of Intestinal Triglyceride Storage Pools via Induction of Nitric Oxide Signaling in Male Hamsters and Mice." Endocrinology 156, no. 10 (2015): 3538–47. http://dx.doi.org/10.1210/en.2015-1110.

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The intestinal overproduction of apolipoprotein B48 (apoB48)-containing chylomicron particles is a common feature of diabetic dyslipidemia and contributes to cardiovascular risk in insulin resistant states. We previously reported that glucagon-like peptide-2 (GLP-2) is a key endocrine stimulator of enterocyte fat absorption and chylomicron output in the postprandial state. GLP-2's stimulatory effect on chylomicron production in the postabsorptive state has been confirmed in human studies. The mechanism by which GLP-2 regulates chylomicron production is unclear, because its receptor is not expr

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

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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 (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 apolipopr

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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 (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 remna

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KENDRICK, John S., Lawrence CHAN, and Joan A. HIGGINS. "Superior role of apolipoprotein B48 over apolipoprotein B100 in chylomicron assembly and fat absorption: an investigation of apobec-1 knock-out and wild-type mice." Biochemical Journal 356, no. 3 (2001): 821–27. http://dx.doi.org/10.1042/bj3560821.

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Editing of apolipoprotein (apo)-B100 mRNA to yield apo-B48 is a specific and developmentally regulated step in enterocytes of mammals. However, the functional significance of this step is not known. Since mice containing only apo-B100have not been documented to exhibit any difference in intestinal fat absorption from wild-type mice, the evolutionary advantage of apoB mRNA editing has been questioned. In the present study, we have compared fat absorption and chylomicron assembly in apobec-1 knock-out (KO) or wild-type (WT) mice subjected to different dietary manipulations: low-fat chow, a fat-e

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Lambert, Marc S., Michael A. Avell, Yoel Berhane, Elaine Shervill, and Kathleen M. Botham. "The differential hepatic uptake of chylomicron remnants of different fatty acid composition is not mediated by hepatic lipase." British Journal of Nutrition 85, no. 5 (2001): 575–82. http://dx.doi.org/10.1079/bjn2000328.

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The hypothesis that hepatic lipase mediates the differential hepatic uptake of chylomicron remnants of different fatty acid composition, demonstrated in previous work from our laboratory, was tested by investigating the effect of antibodies to the enzyme on the uptake of remnants enriched with saturated or n-3 polyunsaturated fatty acids by the perfused rat liver. After perfusion of rat livers with polyclonal antibodies to rat hepatic lipase raised in rabbits or with rabbit non-immune serum for 15 min, [3H]oleate-labelled chylomicron remnants, derived from chylomicrons of rats given a bolus of

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Mardy, Kai, Darrell D. Belke, and David L. Severson. "Chylomicron metabolism by the isolated perfused mouse heart." American Journal of Physiology-Endocrinology and Metabolism 281, no. 2 (2001): E357—E364. http://dx.doi.org/10.1152/ajpendo.2001.281.2.e357.

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The catabolism of rat chylomicrons, labeled in their triacylglycerol (TG) component, was investigated using perfused working mouse hearts. Perfusion of mouse hearts with heparin increased lipoprotein lipase (LPL) activity in the perfusate. This heparin-releasable LPL pool remained constant over a variety of experimental conditions, including workload and fatty acid concentrations, making the mouse heart a suitable model to study chylomicron catabolism. Endothelium-bound LPL hydrolyzed radiolabeled 3H-labeled chylomicrons (0.4 mM TG); the fate of LPL-derived 3H-labeled fatty acids was split eve

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Mansbach, Charles M., and Shahzad Siddiqi. "Control of chylomicron export from the intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 310, no. 9 (2016): G659—G668. http://dx.doi.org/10.1152/ajpgi.00228.2015.

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The control of chylomicron output by the intestine is a complex process whose outlines have only recently come into focus. In this review we will cover aspects of chylomicron formation and prechylomicron vesicle generation that elucidate potential control points. Substrate (dietary fatty acids and monoacylglycerols) availability is directly related to the output rate of chylomicrons. These substrates must be converted to triacylglycerol before packaging in prechylomicrons by a series of endoplasmic reticulum (ER)-localized acylating enzymes that rapidly convert fatty acids and monoacylglycerol

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CHANG, Suyi, Nobuyo MAEDA, and Jayme BORENSZTAJN. "The role of lipoprotein lipase and apoprotein E in the recognition of chylomicrons and chylomicron remnants by cultured isolated mouse hepatocytes." Biochemical Journal 318, no. 1 (1996): 29–34. http://dx.doi.org/10.1042/bj3180029.

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Lipoprotein lipase (LPL) has been proposed to play a role in the uptake of chylomicron remnants by hepatocytes by mediating the binding of these lipoproteins to cell-surface glycosaminoglycans and to the low-density-lipoprotein receptor-related protein (LRP). This proposal is based on studies that examined the binding of chylomicrons to HepG2 cells, fibroblasts and Chinese hamster ovary cells in culture, in the presence of large amounts of LPL [Beisiegel (1995) Curr. Opin. Lipidol. 6, 117–122]. We have investigated whether LPL attached to the surface of chylomicrons enhances the binding and up

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Lo, Chun-Min, Brian K. Nordskog, Andromeda M. Nauli, et al. "Why does the gut choose apolipoprotein B48 but not B100 for chylomicron formation?" American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 1 (2008): G344—G352. http://dx.doi.org/10.1152/ajpgi.00123.2007.

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Chylomicrons produced by the human gut contain apolipoprotein (apo) B48, whereas very-low-density lipoproteins made by the liver contain apo B100. To study how these molecules function during lipid absorption, we examined the process as it occurs in apobec-1 knockout mice (able to produce only apo B100; KO) and in wild-type mice (of which the normally functioning intestine makes apo B48, WT). Using the lymph fistula model, we studied the process of lipid absorption when animals were intraduodenally infused with a lipid emulsion (4 or 6 μmol/h of triolein). KO mice transported triacylglycerol (

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van Dijk, M. C. M., G. J. Ziere, W. Boers, C. Linthorst, M. K. Bijsterbosch та 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, № 3 (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 co

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Orth, Matthias, Claus Luley, and Heinrich Wieland. "Effects of VLDL, chylomicrons, and chylomicron remnants on platelet aggregability." Thrombosis Research 79, no. 3 (1995): 297–305. http://dx.doi.org/10.1016/0049-3848(95)00116-9.

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Bernik, Márcia MS, Joel C. Heimann, Edna R. Nakandakare, et al. "Effects of hydrochlorothiazide and propranolol treatment on chylomicron metabolism in hypertensive subjects." Canadian Journal of Physiology and Pharmacology 83, no. 7 (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 p

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Hussain, M. M., R. W. Mahley, J. K. Boyles, P. A. Lindquist, W. J. Brecht, and T. L. Innerarity. "Chylomicron metabolism." Journal of Biological Chemistry 264, no. 30 (1989): 17931–38. http://dx.doi.org/10.1016/s0021-9258(19)84662-8.

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Beisiegel, U., and J. Heeren. "Chylomicron pathways." Atherosclerosis 144 (May 1999): 3. http://dx.doi.org/10.1016/s0021-9150(99)80003-3.

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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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de Bari, Ornella, Brent A. Neuschwander-Tetri, Min Liu, Piero Portincasa, and David Q. H. Wang. "Ezetimibe: Its Novel Effects on the Prevention and the Treatment of Cholesterol Gallstones and Nonalcoholic Fatty Liver Disease." Journal of Lipids 2012 (2012): 1–16. http://dx.doi.org/10.1155/2012/302847.

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The cholesterol absorption inhibitor ezetimibe can significantly reduce plasma cholesterol concentrations by inhibiting the Niemann-Pick C1-like 1 protein (NPC1L1), an intestinal sterol influx transporter that can actively facilitate the uptake of cholesterol for intestinal absorption. Unexpectedly, ezetimibe treatment also induces a complete resistance to cholesterol gallstone formation and nonalcoholic fatty liver disease (NAFLD) in addition to preventing hypercholesterolemia in mice on a Western diet. Because chylomicrons are the vehicles with which the enterocytes transport cholesterol and

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Borensztajn, J., T. J. Kotlar, and C. A. Matza. "Heparin-binding apoproteins. Effects on lipoprotein lipase and hepatic uptake of remnants." Biochemical Journal 233, no. 3 (1986): 909–12. http://dx.doi.org/10.1042/bj2330909.

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Apoprotein-free heparin-binding and non-binding chylomicrons were used as substrates to test the effects on lipoprotein lipase activity of (a) chylomicron protein I; (b) the mixture of proteins I, II and apoprotein E and (c) human beta 2-glycoprotein I. No activation of the enzyme was observed with any of those apoproteins. When rats were injected simultaneously with [3H]cholesterol-labelled heparin-binding chylomicrons (containing proteins I and II) and [14C]cholesterol-labelled non-binding chylomicrons, no differences were detected between the rates of removal from circulation of those two t

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Felts, James M. "The quantitative separation of chylomicrons and chylomicron remnants by column chromatography." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 918, no. 1 (1987): 93–96. http://dx.doi.org/10.1016/0005-2760(87)90013-0.

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Levy, Emile. "The 1991 Borden Award Lecture. Selected aspects of intraluminal and intracellular phases of intestinal fat absorption." Canadian Journal of Physiology and Pharmacology 70, no. 4 (1992): 413–19. http://dx.doi.org/10.1139/y92-052.

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The recognition of chylomicrons as dietary lipid transporters dates back to more than 70 years and marks a milestone in lipoprotein history. Conventionally, three phases constitute the process of absorption of exogenous fat: intraluminal, intestinal, and delivery. The intraluminal phase includes chemical hydrolysis by lipolytic enzymes and the micellar solubilization of lipolytic products by bile acids. The intestinal phase comprises the diffusion of micelles through the unstirred water layer, passive diffusion across the microvillous membrane of the enterocyte, and the formation of lipid-carr

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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 (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

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Wathne, K. O., B. Carlander, K. R. Norum, and R. Blomhoff. "Uptake of retinyl ester in HL-60 cells via the low-density-lipoprotein-receptor pathway." Biochemical Journal 257, no. 1 (1989): 239–44. http://dx.doi.org/10.1042/bj2570239.

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Newly absorbed retinol is transported in association with chylomicrons and their remnants. In addition, after intake of high doses of retinol, significant amounts are also found in low-density lipoprotein (LDL). As both chylomicron remnants and LDL may be taken up by cells via the LDL receptor, and retinoids inhibit proliferation of some leukaemic cells, we have studied the uptake of retinol in leukaemic cells via the LDL-receptor pathway. HL-60 cells contain saturable binding sites for LDL. The binding of LDL to its receptor has a dissociation constant of about 3.2 x 10(-9) M, and the number

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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 (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-g

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Nauli, Andromeda M., Shuqin Zheng, Qing Yang, Ronggui Li, Ronald Jandacek, and Patrick Tso. "Intestinal alkaline phosphatase release is not associated with chylomicron formation." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 4 (2003): G583—G587. http://dx.doi.org/10.1152/ajpgi.00482.2002.

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Intestinal alkaline phosphatase (IAP) is one of the major sources of alkaline phosphatase in circulation. It is secreted into the intestinal lumen, serum, and lymph. After the ingestion of lipid, lymphatic alkaline phosphatase secretion increases significantly. We have found that the nonabsorbable fat olestra is unable to stimulate lymphatic alkaline phosphatase secretion. We also found that the hydrophobic surfactant Pluronic L-81, which blocks chylomicron formation, fails to inhibit this increase in lymphatic alkaline phosphatase secretion. These results suggest that it is the lipid uptake i

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Desaldeleer, Cécile, Sebastien Henno, Bertrand Bruneau, and Alain Dabadie. "Chylomicron retention disease." Digestive and Liver Disease 45, no. 2 (2013): e3. http://dx.doi.org/10.1016/j.dld.2012.08.003.

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