Relevant bibliographies by topics / Chylomicron

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  2. Dissertations / Theses
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Academic literature on the topic 'Chylomicron'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Chylomicron"

1

Redgrave, T. G. "Chylomicron metabolism." Biochemical Society Transactions 32, no. 1 (February 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 appropriately formulated emulsions are providing valuable new information.
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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 recipients. Lymph apolipoprotein (apo) B48, apo B100, and apo E were measured using sodium dodecyl sulfate–polyacrylamide gradient gel electrophoresis. Mean blood sugar of the diabetic donors and diabetic recipients were 19.7 ± 2.3 and 17.2 ± 3.2 mmol/L. Diabetic rabbits had significantly raised plasma triglyceride (10.8 ± 13.9 versus 0.8 ± 0.5 mmol/L,P< 0.02). There was a large increase in apo B48 in lymph chylomicrons in the diabetic donor animals (0.19 ± 0.10 versus 0.04 ± 0.02 mg/h,P< 0.01) and apo B100 (0.22 ± 0.15 versus 0.07 ± 0.07 mg/h,P< 0.05) and a reduction in apo E on the lymph chylomicron particle (0.27 ± 0.01 versus 0.62 ± 0.07 mg/mg apo B,P< 0.001). Diabetic recipients cleared both control and diabetic chylomicron triglyceride significantly more slowly than control recipients (P< 0.05). Clearance of control chylomicron cholesterol was delayed when injected into diabetic recipients compared to when these chylomicrons were injected into control recipients (P< 0.005). Clearance of diabetic chylomicron cholesterol was significantly slower when injected into control animals compared to control chylomicron injected into control animals (P< 0.02). In this animal model of atherosclerosis, we have demonstrated that diabetes leads to the production of an increased number of lipid and apo E–deficient chylomicron particles. Chylomicron particles from the control animals were cleared more slowly by the diabetic recipient (both triglyceride and cholesterol). The chylomicron particles obtained from the diabetic animals were cleared even more slowly when injected into the diabetic recipient. Although there was an initial delay in clearance of chylomicron triglyceride from the diabetic particle when injected into the control animals, the clearance over the first 15 minutes was not significantly different when compared to the control chylomicron injected into the control animal. On the other hand, the cholesterol clearance was significantly delayed. Thus, diabetes resulted in the production of an increased number of lipid- and apo E–deficient chylomicron particles. These alterations account, in part, for the delay in clearance of these particles.
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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 (April 1, 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 matrix (study B), and finally in rats with a dehydrated matrix (study C). The chylomicron appearance times were 11.7, 13.6, and 21.7 min for the rats from studies A-C, respectively. Thus, the data obtained from this study indicate that the matrix hydration may exert a more significant influence on chylomicron movement than lymph flow per se. In conclusion, the reduced chylomicron appearance time produced by expansion of the mucosal interstitium results from a diminished resistance of the interstitial matrix to chylomicron movement rather than a decreased transit time due to an enhanced convective flux of chylomicrons.
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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 (March 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 greater relevance to arterial exposure than postprandial fluctuations. Insulin critically regulates the metabolism of very low density lipoprotein (VLDL) and hence it would be expected that the hormone is also involved in the regulation of chylomicron metabolism. Impaired insulin action may therefore be responsible for the associated hyperchylomicronaemia. In this review we examine the hypothesis that insulin chronically modulates chylomicron metabolism and present evidence suggesting that hyperchylomicronaemia primarily results from impaired chylomicron production.
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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 (July 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 that lymph flow has a profound effect on intestinal chylomicron transport. As lymph flow increased, the chylomicron appearance time (time between the placement of radioactive fatty acid into the intestinal lumen to the appearance of radioactive lipid in the central lacteal) was reduced. When lymph flow exceeded 40 microliter/min, the chylomicron appearance time reached a minimum value of 13.6 min. This minimum chylomicron appearance time probably represents the time required for assembly of absorbed lipid, formation of chylomicrons, and their subsequent discharge into the lymphatics. The chylomicron appearance time lengthened as lymph flow fell. The results of this study underscore the necessity of using steady-state lymphatic lipid output data to assess factors affecting the cellular packaging and release of chylomicrons in the small intestine.
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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 (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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Milan, Amber M., Anu Nuora, Shikha Pundir, Chantal A. Pileggi, James F. Markworth, Kaisa M. Linderborg, and David Cameron-Smith. "Older adults have an altered chylomicron response to a high-fat meal." British Journal of Nutrition 115, no. 5 (January 15, 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, circulating chylomicron particle size was smaller (P<0·05), with greater apoB content (P<0·05) at all postprandial time points. However, total chylomicron TAG concentration between the groups was unaltered post-meal. Compared with younger subjects, the older subjects exhibited a greater proportion of oleic acid in the TAG and phospholipid (PL) fraction (P<0·05), plus lower proportions of linoleic acid in the TAG fraction of the chylomicrons (P<0·01). Thus, following the ingestion of a high-fat meal, older individuals demonstrate both smaller, more numerous chylomicrons, with a greater total MUFA and lower PUFA contents. These data suggest that the increased postprandial lipaemia of ageing cannot be attributed to increased chylomicron TAG. Rather, ageing is associated with changes in chylomicron particle size, apoB content and fatty acid composition of the chylomicron TAG and PL fractions.
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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 (September 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 fats also predominated in their respective chylomicrons, but their proportions were reduced during the processes leading to their formation. Endogenous contributions of linoleic, eicosapentaenoic, and docosahexaenoic acids were particularly noted when these fatty acids were not well-represented in the original oils and fats, suggesting that they may be obligatory constituents in the formation of chylomicrons. The conversion of chylomicrons to remnants further attenuated the extremes in fatty acid composition of the dietary oils and fats. These results indicate that following an acute intake of oil or fat, the resulting chylomicrons and chylomicron remnants presented to the tissues contain a more balanced distribution of saturated, mono-and polyunsaturated fatty acids than the oils and fats from which they were derived.
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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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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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Dissertations / Theses on the topic "Chylomicron"

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Guldur, Tayfun. "Metabolism of chylomicrons and chylomicron remnants." Thesis, Royal Veterinary College (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522548.

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Grieve, David James. "The role of chylomicrons and chylomicron remnants in the initiation of atherosclerotic lesions in the artery wall." Thesis, Royal Veterinary College (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522544.

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Silva, K. D. Renuka R. "Markers of chylomicron metabolism in man." Thesis, University of Reading, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394221.

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Cuerq, Charlotte. "Absorption de la vitamine E dans les hypocholestérolémies génétiques." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1086.

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Les hypocholestérolémies génétiques représentent un ensemble de pathologies héréditaires du métabolisme caractérisées par une hypocholestérolémie inférieure au 5ème percentile pour l'âge et le sexe. Elles sont majoritairement dues à un défaut d'assemblage et de sécrétion des lipoprotéines entraînant, dès la période néonatale, une malabsorption des lipides et des vitamines liposolubles. Les conséquences à long terme peuvent être dramatiques (complications ophtalmologiques et neurologiques graves) si un traitement par vitamines liposolubles, en particulier vitamine E à fortes doses, n'est pas instauré rapidement. Pour ces raisons, l'étude clinique princeps a comparé une formulation de vitamine E rendue hydrosoluble (tocofersolan) à l'acétate de tocophérol liposoluble et traditionnellement utilisé en thérapeutique chez ces patients. En parallèle, un travail sur modèle cellulaire Caco2, nous a permis d'étudier les mécanismes d'absorption/sécrétion de ces deux formulations de vitamine E afin de mieux appréhender les mécanismes mis en jeu. Deux études méthodologiques ont été menées en amont de cette étude clinique. La première visait à vérifier la stabilité des échantillons dans les conditions de transport imposées par l'étude princeps. Par ailleurs, les concentrations effondrées de lipoprotéines chez ces patients rendent difficile l'évaluation du statut en vitamine E par les simples dosages plasmatiques. Aussi, la seconde étude avait pour but d'établir les valeurs usuelles pour les concentrations en vitamine E dans les globules rouges et le tissu adipeux chez l'enfant sain comme outil d'aide au suivi des patients atteints d'hypocholestérolémie génétique. Grâce aux valeurs de référence établies dans ce travail, l'analyse de la vitamine E dans les globules rouges et le tissu adipeux permet de proposer une vue plus globale du statut en vitamine E chez ces patients
Abetalipoproteinemia (ABL) and chylomicron retention disease (CMRD) are rare recessive forms of hypobetalipoproteinemia characterized by an intestinal lipid malabsorption and a severe vitamin E deficiency leading to disabling neuro-ophtalmologic sequelae. Oral a- tocopherol supplementation with high doses has to be initiated as early as possible to prevent or halt progression of complications. The main aim of our work was to investigate the interest of tocofersolan, a water-soluble derivative of RRR-α-tocopherol, compared to a-tocopherol acetate in ABL and CMRD. In parallel, we investigated the mechanisms of absorption / secretion of tocofersolan and a- tocopheryl acetate on Caco2 cells for a better understanding of the mechanisms of their therapeutic efficacy. Two methodological studies were conducted prior to this clinical study. Firstly, we studied the stability of commonly measured vitamins and carotenoids in whole blood in the conditions of transport imposed by the clinical study. Secondly, we established the reference intervals for vitamin E concentrations in red blood cells and adipose tissue in healthy child as a tool to monitore treatment of children with ABL and CMRD with vitamin E. Indeed, the very reduced lipoprotein concentrations in these patients make difficult the assesment of vitamin E status based on plasma a-tocopherol concentrations. The references values established in this work allows us to propose a more comprehensive view of the vitamin E status in these patients
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Sethi, Sunil. "Chylomicron marker metabolism in health and disease." Thesis, University of Surrey, 1995. http://epubs.surrey.ac.uk/844052/.

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In this thesis, chylomicron (CM) and CM-remnant (CM-R) metabolism in humans was studied by the application of unique markers which label these lipoprotein particles from the stage of production by the enterocyte until, removal by hepatic receptor mediated processes. Retinyl palmitate (RP) is a vitamin A ester, which labels the CM/CM-R by behaving like the cholesterol ester (CE) which is carried in the core of these particles. Development of a mono-specific antibody to apolipoprotein (apo) B-48 and application of an enzyme linked immunosorbant assay (ELISA) enabled quantification of this apolipoprotein which is specifically located on the surface of CM/CM-R. The postprandial lipaemic response for all parameters were determined by the area under the time response curve (AUC). Plasma was separated by flotation ultracentrifugation, overlayered with saline (d=1.006 g/ml), to separate the triacylglycerol-rich lipoprotein (TRL) and infranatant fractions. To examine the effects of habitual low intensity exercise on the postprandial CM response to meals of varying fat contents, triacylglycerol (TAG), apo B-48 and RP were measured in the TRL fraction. 14 young men were recruited and divided into two groups, active and inactive, depending on their habitual activity level. Active subjects were defined as those who undertook aerobic activity for at least 3 sessions a week and the inactive group took no regular exercise. In response to meals of 20 g, 40 g and 80 g fat content, the active subjects showed lower postprandial CM response as assessed by the TRL-apo B-48 AUC, by 35%, 58% and 66% (p < 0.05), respectively. The TRL-RP response to these meals was also lower by 67%, 54% and 49% (p < 0.01 in each case), in the active subjects. Plasma lipoprotein lipase (LPL) activity was 50% (p < 0.05) higher in the active group following the 80 g fat meal. The metabolism of CM/CM-R in the postprandial state was studied in 9 middle aged men with non-insulin dependent diabetes mellitus (NIDDM) and in 6 matched controls. The subjects were given a standardised meal containing 50 g fat, followed by a 12 hr postprandial study. NIDDM subjects, compared with the controls, showed exaggerated plasma postprandial responses of apo B-48, TAG and RP of 3696 vs 1796 ug.ml-1.min (p < 0.005), 2525 vs 1243 mmol.L-1.min (p < 0.05), and 3957 vs 2923 umol.L-1.min (p < 0.05), respectively. In the TRL fraction, apo B-48, TAG and RP AUCs were 1021 vs 473 ug.ml-1.min (p < 0.05), 1307 vs 527 mmol.L-1.min (p < 0.05), and 2707 vs 2158 umol.L-1.min (NS = not significant), respectively. There was no significant difference in plasma lipoprotein lipase (LPL) activity, between the groups. The effect of bezafibrate on postprandial lipoprotein metabolism was investigated in a 6-week placebo controlled, cross-over trial in the same 9 NIDDM subjects. Bezafibrate reduced the AUC for plasma apo B-48, TAG and RP by 45% (p , 0.005), 30% (p < 0.005) and 46% (p < 0.01). The corresponding reduction following bezafibrate therapy in TRL apo B-48, TAG and RP were 62% (p < 0.005), 54% ( p < 0.005) and 49% (p < 0.05), respectively. Plasma LPL activity was increased after bezafibrate therapy (p < 0.005). The effects of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors on postprandial lipoprotein metabolism, and in particular, CM-R metabolism, were investigated in 20 middle-aged subjects with primary hypercholesterolaemia. Subjects were given a high fat meal and the CM/CM-R markers, apo B-48 and RP, were measured in various fractions of plasma, obtained by cumulative flotation ultracentrifugation, using a linear salt gradient. The Sf 20-400 fraction of plasma, containing the majority of plasma CM-R was isolated. Reductions in TAG, CE, retinyl ester (RE) and apo B-48 AUC, in this fraction, following 4 weeks of HMG CoA reductase therapy, were 61% (p < 0.01), 20% (p < 0.01), 13 % (NS) and 23% (p < 0.01), respectively. Additionally, the smaller, potentially atherogenic CM-R, as measured by apo B-48 AUC in the Sf 60-100 and Sf 20-60 fractions of plasma were reduced by 15% (p < 0.05) and 22% (p < 0.05), respectively, following HMG CoA therapy. These studies have established that measurement of apo B-48 and RP are useful in the study of the metabolism of CM/CM-R in health and disease.
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Field, Polly Ann. "The effects of insulin resistance on chylomicron metabolism." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302120.

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Siddiq, Ajmal 1963. "Modeling the distribution of chylomicron cholesterol in the body." Thesis, The University of Arizona, 1991. http://hdl.handle.net/10150/277981.

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A physiologically-based multi-compartment model has been developed which makes a priori predictions of the chylomicron cholesterol distribution in the body of a rat. The model considers each organ to be a separate compartment which interacts with all the other organs/compartments through the blood stream. A particle approach has been used since chylomicron cholesterol distribution is regulated more by the particle concentrations than cholesterol concentrations. The chylomicron cholesterol distribution is coupled to the triglyceride contents of the particle. Unsteady nonlinear differential equations have been developed by making mass balances over all the compartments, and the numerical solution of these dynamic model equations is outlined. Finally, this multi-compartment model was used to predict the distribution of chylomicron cholesterol after a bolus injection of chylomicrons or their continuous infusion into the blood. The model results were then compared with the existing literature data points for such systems.
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Nauli, Andromeda Margono. "Intestinal Lipid Uptake and Secretion of VLDL and Chylomicron." University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1123866425.

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Sun, Yuxi. "Development of in vitro Chylomicron Assay Using Caco-2 Cells." Digital Commons @ East Tennessee State University, 2013. https://dc.etsu.edu/etd/1781.

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Dietary fats are mainly transported by the intestine in lipoproteins: chylomicrons (CMs) and very low density lipoproteins (VLDLs). Unfortunately, studies of the intestinal absorption of dietary fat have been hampered by the lack of an adequate in vitro model system. As an in vitro model Caco-2 cells are able to secrete lipoproteins. We investigated the possible factors that may affect the secretion of CMs through the ultracentrifugation technique. The dose-dependent effects of oleic acid, mono-olein, egg lecithin, collagen matrix, and the effect of cell differentiation on CM secretion were then tested. We found that oleic acid, lecithin, and cell differentiation are critical for CM secretion by Caco-2 cells. To further confirm that our optimal condition is, in fact, favorable for efficient CM production, we compared it with control groups. We observed that our condition led to more efficient CM secretion as determined by the TGs, ApoB, and TEM analysis.
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Goulter, Andrew Barry. "Effects of chylomicron remnants on porcine coronary artery endothelial cell function." Thesis, Royal Veterinary College (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522537.

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Books on the topic "Chylomicron"

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Brahm, Amanda J., and Robert A. Hegele. Monogenic Chylomicronemia: Deficiency of Lipoprotein Lipase and Related Factors. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0033.

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Monogenic chylomicronemia is an autosomal recessive condition characterized by severely elevated fasting triglyceride that carries lifelong elevated risk of developing pancreatitis. The majority of cases are caused by mutations in the LPL gene encoding lipoprotein lipase, the enzyme primarily responsible for chylomicron clearance. Mutations in genes encoding associated proteins (APOC2, APOA5, GPIHBP1 and LMF1) may also present with a very similar phenotype. Current management, which includes restriction of dietary fat intake and standard pharmacologic interventions, has met with limited success, but new therapies under development may prove to be more effective.
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Skoutas, Demetrios. Responses of the chylomicron remnant marker, retinyl ester and apolipoprotein B-48 to meals ofvarying monousaturated fatty acid content in middle aged men. 1995.

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Wiklund, Olov, and Jan Borén. Pathogenesis of atherosclerosis: lipid metabolism. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0011.

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Lipids are carried in plasma as microparticles, lipoproteins, composed of a core of hydrophobic lipids and a surface of amphipathic lipids. In addition, the particles carry proteins (i.e. apolipoproteins). The proteins have key functions in the metabolism as receptor ligands, enzymes or activators. Lipoproteins are classified based on density into: chylomicrons, VLDL, IDL, LDL, and HDL. Retention of apoB-containing lipoproteins (LDL, IDL, and VLDL) in the arterial intima is the initiating event in the development of atherosclerosis. Retention is mediated by binding of apoB to structural proteoglycans in the intima. Increased plasma concentration of apoB-containing lipoproteins is the main risk factor for atherosclerotic cardiovascular disease (CVD) and the causative role of LDL has been demonstrated in several studies. Lp(a) is a subclass of LDL and elevated Lp(a) is an independent risk-factor, primarily genetically mediated. Genetic data support that high Lp(a) causes atherosclerosis. Elevated triglycerides in plasma are associated with increased risk for CVD. Whether triglycerides directly induce atherogenesis is still unclear, but current data strongly support that remnant particles from triglyceride-rich lipoproteins are causal. HDL are lipoproteins that have been considered to be important for reversed cholesterol transport. Low HDL is a strong risk-factor for CVD. However, the causative role of HDL is debated and intervention studies to raise HDL have not been successful. Reduction of LDL is the main target for prevention and treatment, using drugs that inhibit the enzyme HMG-CoA reductase, i.e. statins. Other drugs for LDL reduction and to modify other lipoproteins may further reduce risk, and new therapeutic targets are explored.
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Book chapters on the topic "Chylomicron"

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Gooch, Jan W. "Chylomicron." In Encyclopedic Dictionary of Polymers, 882. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13397.

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Peters, Nils, Martin Dichgans, Sankar Surendran, Josep M. Argilés, Francisco J. López-Soriano, Sílvia Busquets, Klaus Dittmann, et al. "Chylomicron Retention Disease." In Encyclopedia of Molecular Mechanisms of Disease, 359–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_352.

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Rodgers, John B. "Inhibitors of Chylomicron Formation and Secretion." In Intestinal Lipid Metabolism, 335–49. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1195-3_18.

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Windler, E., and H. Greten. "Chylomicron Catabolism and Uptake by the Liver." In Expanding Horizons in Atherosclerosis Research, 197–203. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71753-6_26.

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Beisiegel, Ulrike, Annette Krapp, Jörg Heeren, and Wilfried Weber. "In Vitro Studies on Human Chylomicron Catabolism." In Drugs Affecting Lipid Metabolism, 649–55. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0311-1_76.

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Windier, Eberhard E. T. "The Uptake of Chylomicron Remnants by the Liver." In Advances in Experimental Medicine and Biology, 131–35. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1268-0_19.

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Harris, W. S. "ω3 Fatty Acids and Human Chylomicron Metabolism." In Fatty Acids and Lipids - New Findings, 163–67. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000059777.

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Wickham, Nicholas, J. Cormak, G. M. Vercellotti, D. E. Hammerschmidt, and H. S. Jacob. "Post-Prandial Chylomicron Creaming, C-Reactive Protein and Enhanced Complement Activation." In Vascular Endothelium, 215–16. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2437-3_55.

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Torbet, J. "Magnetic Birefringence Study of Fibrin Formation and Chylomicron Behaviour in Human Blood Plasma." In Springer Proceedings in Physics, 23–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71526-6_5.

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Sultan, Fabrice, Dominique Lagrange, and Sabine Griglio. "In Vitro Binding and in Vivo Uptake of Chylomicron Remnants after their Hydrolysis by Hepatic Lipase." In Hypercholesterolemia, Hypocholesterolemia, Hypertriglyceridemia, in Vivo Kinetics, 311–17. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5904-3_37.

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Conference papers on the topic "Chylomicron"

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Dixon, J. Brandon. "Engineering Tools for Studying the Interplay Between Mechanics and Biology in Lymphatic Lipid Transport." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19364.

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The lymphatic vasculature extends through most tissues of the body and plays an essential role in maintaining fluid balance, immune cell trafficking, and lipid transport. Nearly all dietary lipid is transported from the intestine to the circulation via the lymphatic system in the form of triglyceride-rich lipoproteins called chylomicrons. This process can be described through two different mechanisms: 1) entry of the chylomicron into the initial lymphatic vessels of the small intestine, known as lacteals, and 2) the transport of these chylomicrons through the larger collecting lymphatics by a complex and coordinated system of individual contracting vessel units (lymphangions) and valve leaflets. We describe here a set of in vitro and in vivo tools we have developed to study the mechanisms that modulate lipid transport under these two different paradigms and show how these tools are uncovering important biological features involved in these mechanisms. Lymphatic pump function is known to be sensitive to the mechanical load on the vessel as the contractility of isolated vessels has been shown to be both shear and stretch sensitive [1], yet whether these mechanisms are important in regulating contractile function in vivo remains uncertain.
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Marcato, Larissa A., Diego V. S. Carvalho, Margarida M. Hamada, Carmen G. Vinagre, Raul C. Maranhão, Carlos H. de Mesquita, and Vito R. Vanin. "Internal Dosimetry of a Chylomicron-like Emulsion Labeled with [sup 14]C-CE in Humans." In XXXIII BRAZILIAN WORKSHOP ON NUCLEAR PHYSICS. AIP, 2011. http://dx.doi.org/10.1063/1.3608989.

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Chamulitrat, W., J. Seeßle, B. Javaheri-Haghighi, S. Döring, X. Zhu, S. Tuma-Kellner, H. Gan-Schreier, et al. "Intestinal deletion of fatty acid transport protein 4 in mice increases blood chylomicrons." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402169.

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Ruf, Horst, and Barry J. Gould. "Use of dynamic light scattering for the determination of size distributions of chylomicrons from human lymph." In BiOS '97, Part of Photonics West, edited by Alexander V. Priezzhev, Toshimitsu Asakura, and Robert C. Leif. SPIE, 1997. http://dx.doi.org/10.1117/12.273655.

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Surya, I. E., and J. W. N. Akkerman. "HUMAN PLASMA PAF-ACETYLHYDROLASE, NORMALLY PRESENT IN LOW DENSITY LIPOPROTEINS, IS ASSOCIATED WITH HIGH DENSITY LIPOPROTEINS IN A PATIENT WITH LDL DEFICIENCY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642882.

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Platelet Activating Factor (l-0-alkyl-2-acetyl-sn-glycerol-3-phosphocholine; PAF) plays an important role in allergic and inflammatory reactions and activates platelets in the nanomolar range. One of the main factors that controls PAF activity in blood is an enzyme that hydrolyzes the acetyl-chain thereby converting PAF to biologically inactive lyso-PAF. The enzyme is acid labile and normally associated with apo B-containing low density lipoproteins (LDL, density 1,006-1,063 g/ml).We investigated whether a deficiency in LDL would affect the enzyme activity. PAF-inactivating activity was measured in plasma from a patient with abetalipoproteinemia, a rare autosomal recessive disorder, characterized by the absence of apo B and apo B-containing lipoproteins (chylomicrons, VLDL and LDL). Plasma triglyceride was 0,2 mmol/1 (normal 1,40-2,20 mmol/1) and cholesterol 1,3 mmol/1 (normal 5,60-7,70 mmol/1). Separation of lipoproteins by density gradient centrifugation revealed a slightly decreased HDL content whereas VLDL and LDL were below the detection limit (0,20 mmol/1; based on cholesterol content).Despite the absence of LDL, PAF-inactivating activity in plasma of the patient (measured by (1) the decrease in aggregation inducing activity of PAF after incubation, (ii) the conversion of 3H-acyl-PAF to lysa PAF, separated on TLC, (iii) the liberation of 3H-label from 3H-acetyl PAF) was present and even slightly higher than in normal plasma (hydrolysis of 3 3H-PAF after 20 minutes incubation was 78 ± 4% and 65 ± 6% in patient and normals, respectively, n = 4). Subfractionation revealed that the enzyme activity was present in fractions with densities of 1,065-1,214 g/ml, which are typical for HDL.These results indicate that PAF-acetylhydrolase, although normally present in LDL, binds to HDL in a patient with extreme LDL-deficiency.Supported by the Dutch Heart Foundation (grant 85082)
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