Academic literature on the topic 'Lipoprotein kinetics'
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Journal articles on the topic "Lipoprotein kinetics"
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Levels, J. H. M., P. R. Abraham, A. van den Ende, and S. J. H. van Deventer. "Distribution and Kinetics of Lipoprotein-Bound Endotoxin." Infection and Immunity 69, no. 5 (2001): 2821–28. http://dx.doi.org/10.1128/iai.69.5.2821-2828.2001.
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ABSTRACT Lipopolysaccharide (LPS), the major glycolipid component of gram-negative bacterial outer membranes, is a potent endotoxin responsible for pathophysiological symptoms characteristic of infection. The observation that the majority of LPS is found in association with plasma lipoproteins has prompted the suggestion that sequestering of LPS by lipid particles may form an integral part of a humoral detoxification mechanism. Previous studies on the biological properties of isolated lipoproteins used differential ultracentrifugation to separate the major subclasses. To preserve the integrity of the lipoproteins, we have analyzed the LPS distribution, specificity, binding capacity, and kinetics of binding to lipoproteins in human whole blood or plasma by using high-performance gel permeation chromatography and fluorescent LPS of three different chemotypes. The average distribution of O111:B4, J5, or Re595 LPS in whole blood from 10 human volunteers was 60% (±8%) high-density lipoprotein (HDL), 25% (±7%) low-density lipoprotein, and 12% (±5%) very low density lipoprotein. The saturation capacity of lipoproteins for all three LPS chemotypes was in excess of 200 μg/ml. Kinetic analysis however, revealed a strict chemotype dependence. The binding of Re595 or J5 LPS was essentially complete within 10 min, and subsequent redistribution among the lipoprotein subclasses occurred to attain similar distributions as O111:B4 LPS at 40 min. We conclude that under simulated physiological conditions, the binding of LPS to lipoproteins is highly specific, HDL has the highest binding capacity for LPS, the saturation capacity of lipoproteins for endotoxin far exceeds the LPS concentrations measured in clinical situations, and the kinetics of LPS association with lipoproteins display chemotype-dependent differences.
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Levels, Johannes H. M., Philip R. Abraham, Erik P. van Barreveld, Joost C. M. Meijers, and Sander J. H. van Deventer. "Distribution and Kinetics of Lipoprotein-Bound Lipoteichoic Acid." Infection and Immunity 71, no. 6 (2003): 3280–84. http://dx.doi.org/10.1128/iai.71.6.3280-3284.2003.
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ABSTRACT Lipoteichoic acid (LTA), a major cell wall component of gram-positive bacteria, is an amphipathic anionic glycolipid with structural similarities to lipopolysaccharide (LPS) from gram-negative bacteria. LTA has been implicated as one of the primary immunostimulatory components that may trigger the systemic inflammatory response syndrome. Plasma lipoproteins have been shown to sequester LPS, which results in attenuation of the host response to infection, but little is known about the LTA binding characteristics of plasma lipid particles. In this study, we have examined the LTA binding capacities and association kinetics of the major lipoprotein classes under simulated physiological conditions in human whole blood (ex vivo) by using biologically active, fluorescently labeled LTA and high-performance gel permeation chromatography. The average distribution of an LTA preparation from Staphylococcus aureus in whole blood from 10 human volunteers revealed that >95% of the LTA was associated with total plasma lipoproteins in the following proportions: high-density lipoprotein (HDL), 68% ± 10%; low-density lipoprotein (LDL), 28% ± 8%; and very low density lipoprotein (VLDL), 4% ± 5%. The saturation capacity of lipoproteins for LTA was in excess of 150 μg/ml. The LTA distribution was temperature dependent, with an optimal binding between 22 and 37°C. The binding of LTA by lipoproteins was essentially complete within 10 min and was followed by a subsequent redistribution from HDL and VLDL to LDL. We conclude that HDL has the highest binding capacity for LTA and propose that the loading and redistribution of LTA among plasma lipoproteins is a specific process that closely resembles that previously described for LPS (J. H. M. Levels, P. R. Abraham, A. van den Ende, and S. J. H. van Deventer, Infect. Immun. 68:2821-2828, 2001).
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Vergès, Bruno, Laurence Duvillard, Laurent Lagrost, et al. "Changes in Lipoprotein Kinetics Associated With Type 2 Diabetes Affect the Distribution of Lipopolysaccharides Among Lipoproteins." Journal of Clinical Endocrinology & Metabolism 99, no. 7 (2014): E1245—E1253. http://dx.doi.org/10.1210/jc.2013-3463.
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Context: Lipopolysaccharides (LPSs) are inflammatory components of the outer membrane of Gram-negative bacteria and, in plasma, are mostly associated with lipoproteins. This association is thought to promote their catabolism while reducing their proinflammatory effects. Objectives: Our aim was to determine the impact of lipoprotein kinetics on plasma LPS distribution and how it may affect patients with type 2 diabetes mellitus (T2DM). Design: We performed a kinetic study in 30 individuals (16 T2DM patients, 14 controls) and analyzed the impact of changes in lipoprotein kinetics on LPS distribution among lipoproteins. Results: Plasma LPS levels in T2DM patients were not different from those in controls, but LPS distribution in the two groups was different. Patients with T2DM had higher LPS-very low-density lipoprotein (VLDL; 31% ± 7% vs 22% ± 11%, P = .002), LPS-high-density lipoprotein (HDL; 29% ± 9% vs 19% ± 10%, P = .015), free (nonlipoprotein bound) LPS (10% ± 4% vs 7% ± 4%, P = .043) and lower LPS-low-density lipoprotein (LDL; 30% ± 13% vs 52% ± 16%, P = .001). In multivariable analysis, VLDL-LPS was associated with HDL-LPS (P < .0001); LDL-LPS was associated with VLDL-LPS (P = .004), and VLDL apolipoprotein (apo) B100 catabolism (P = .002); HDL-LPS was associated with free LPS (P < .0001) and VLDL-LPS (P = .033); free LPS was associated with HDL-LPS (P < .0001). In a patient featuring a dramatic decrease in VLDL catabolism due to apoA-V mutation, LDL-LPS was severely decreased (0.044 EU/mL vs 0.788 EU/mL in controls). The difference between T2DM patients and controls for LDL-LPS fraction was no longer significant after controlling for VLDL apoB100 total fractional catabolic rate. Conclusions: Our data suggest that in humans, free LPS transfers first to HDL and then to VLDL, whereas the LPS-bound LDL fraction is mainly derived from VLDL catabolism; the latter may hence represent a LPS catabolic pathway. T2DM patients show lower LDL-LPS secondary to reduced VLDL catabolism, which may represent an impaired catabolic pathway.
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Khalil, Abdelouahed, та Tamàs Fülöp. "A comparison of the kinetics of low-density lipoprotein oxidation induced by copper or by γ-rays: Influence of radiation dose-rate and copper concentration". Canadian Journal of Physiology and Pharmacology 79, № 2 (2001): 114–21. http://dx.doi.org/10.1139/y00-080.
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The oxidation of low-density lipoproteins is the first step in the complex process leading to atherosclerosis. The aim of our study was to compare the kinetics of low density lipoprotein oxidation induced by copper ions or by oxygen free radicals generated by60Co γ-rays. The effects of copper concentration and irradiation dose-rate on LDL peroxidation kinetics were also studied. The oxidation of LDL was followed by the measurement of conjugated diene, hydroperoxides, and thiobarbituric acid reactive substance formation as well as α-tocopherol disappearance. In the case of gamma irradiation, the lag-phase before the onset of lipid peroxidation was inversely correlated to the radiation dose-rate. The radiation chemical rates (v) increased with increasing dose-rate. Copper-induced LDL peroxidation followed two kinetic patterns: a slow kinetic for copper concentrations between 520 µM, and a fast kinetic for a copper concentration of 40 µM. The concentration-dependent oxidation kinetics suggest the existence of a saturable copper binding site on apo-B. When compared with γ-rays, copper ions act as drastic and powerful oxidants only at higher concentrations ([Formula: see text]40 µM).Key words: LDL, peroxidation, kinetics, copper, γ-radiolysis, dose-rate.
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Hu, Yuhong, and Bal Ram Singh. "Comparative Surface Adsorption Behavior of High- and Low-Density Lipoproteins as Analyzed by FT-IR/ATR Spectroscopy." Applied Spectroscopy 49, no. 9 (1995): 1356–60. http://dx.doi.org/10.1366/0003702953965290.
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The adsorption behavior of high-density lipoprotein (HDL) and low-density lipoprotein (LDL) onto a zinc selenide crystal surface and cholesterol-modified ZnSe crystal surface has been studied in terms of adsorption kinetics and isotherms with the use of the FT-IR/ATR technique. Adsorption kinetic plots indicated that the adsorption equilibrium of HDL and LDL is reached at 30–40 min, which is similar to the case for other proteins. From the adsorption isotherms of HDL and LDL, transitions from monolayer adsorption to multilayer adsorption were observed at around 10−5 M for both lipoproteins. We also observed that the binding of HDL and LDL to a cholesterol-modified ZnSe surface is less than that to an unmodified ZnSe surface. For example, monolayer adsorption density of HDL on the ZnSe surface was 0.23 pmoles/cm2, whereas it was 0.13 pmoles/cm2 on the cholesterol-modified ZnSe surface.
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Maugeais, C., S. Braschi, K. Ouguerram, et al. "Lipoprotein Kinetics in Patients With Analbuminemia." Arteriosclerosis, Thrombosis, and Vascular Biology 17, no. 7 (1997): 1369–75. http://dx.doi.org/10.1161/01.atv.17.7.1369.
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Netea, Mihai G., Natasja de Bont, Pierre N. M. Demacker, et al. "Lipoprotein(a) Inhibits Lipopolysaccharide-Induced Tumor Necrosis Factor Alpha Production by Human Mononuclear Cells." Infection and Immunity 66, no. 5 (1998): 2365–67. http://dx.doi.org/10.1128/iai.66.5.2365-2367.1998.
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ABSTRACT Lipoproteins can bind lipopolysaccharide (LPS) and decrease LPS-stimulated cytokine production. Lipoprotein(a) [Lp(a)] was as potent as low-density lipoproteins (LDL) in inhibiting LPS-stimulated tumor necrosis factor synthesis by human mononuclear cells. The kinetics of LPS inhibition by Lp(a) was similar to that of LDL. This suggests that circulating Lp(a) may be an important factor determining the amplitude of the response to LPS in humans.
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Murthy, V. N., C. A. Marzetta, L. L. Rudel, L. A. Zech, and D. M. Foster. "Hepatic apo B-100 lipoproteins and plasma LDL heterogeneity in African green monkeys." American Journal of Physiology-Endocrinology and Metabolism 258, no. 6 (1990): E1041—E1057. http://dx.doi.org/10.1152/ajpendo.1990.258.6.e1041.
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The contribution of hepatic apolipoprotein (apo) B-100 lipoproteins to plasma low-density lipoprotein (LDL) metabolic heterogeneity was examined in African green monkeys. Hepatic 3H-labeled very low-density lipoproteins (VLDL) (d less than 1.006, where d is density in g/ml) or hepatic 131I-labeled LDL (1.030 less than d less than 1.063) were isolated from perfused livers and injected simultaneously with autologous plasma 125I-LDL into African green monkeys. Serial blood samples were taken, and the distribution of radioactivity among various subfractions of apo B-100 lipoproteins was determined using density-gradient ultracentrifugation. Compartmental models were developed to describe simultaneously the kinetics of hepatic lipoproteins and plasma LDL. In five of seven studies, the metabolic behavior of LDL derived from radiolabeled hepatic lipoprotein precursors differed from the metabolic behavior of radiolabeled autologous plasma LDL. These differences could be described by different models supporting two hypotheses with different physiological interpretations: 1) lipoproteins of donor and recipient animals are kinetically distinct, and/or 2) plasma LDL derived from various potential sources are kinetically distinct. Compartmental modeling was used to test these hypotheses, which were not accessible to testing by conventional experimental methodologies. The kinetic analyses of these studies suggest that plasma LDL may be derived from a variety of precursors, including hepatic VLDL and hepatic LDL, with each source giving rise to metabolically distinct plasma LDL.
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Ooi, E., D. Sprecher, E. Schaefer, M. Diffenderfer, N. Matthan, and H. Barrett. "Abstract: 139 LIPOPROTEIN KINETICS IN SUBJECTS WITH LIPOPROTEIN LIPASE (LPL) GENE MUTATIONS." Atherosclerosis Supplements 10, no. 2 (2009): e245. http://dx.doi.org/10.1016/s1567-5688(09)70249-1.
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Maugeais, Cyrille, Khadija Ouguerram, Regis Frénais, et al. "Effect of Low-Density Lipoprotein Apheresis on Kinetics of Apolipoprotein B in Heterozygous Familial Hypercholesterolemia1." Journal of Clinical Endocrinology & Metabolism 86, no. 4 (2001): 1679–86. http://dx.doi.org/10.1210/jcem.86.4.7428.
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The acute reduction of low-density lipoprotein (LDL) cholesterol obtained by LDL-apheresis allows the role of the high level of circulating LDL on lipoprotein metabolism in heterozygous familial hypercholesterolemia (heterozygous FH) to be addressed. We studied apolipoprotein B (apoB) kinetics in five heterozygous FH patients before and the day after an apheresis treatment using endogenous labeling with [2H3]leucine. Compared with younger control subjects, heterozygous FH patients before apheresis showed a significant decrease in the fractional catabolic rate of LDL (0.24 ± 0.08 vs. 0.65 ± 0.22 day−1; P < 0.01), and LDL production was increased in heterozygous FH patients (18.9 ± 7.0 vs. 9.9 ± 4.2 mg/kg·day; P< 0.05). The modeling of postapheresis apoB kinetics was performed using a nonsteady state condition, taking into account the changing pool size of very low density lipoprotein (VLDL), intermediate density lipoprotein, and LDL apoB. The postapheresis kinetic parameters did not show statistical differences compared with preapheresis parameters in heterozygous FH patients; however, a trend for increases in fractional catabolic rate of LDL (0.24 ± 0.08 vs. 0.35± 0.09 day−1; P = 0.067) and the production of VLDL (13.7 ± 8.3 vs. 21.9 ± 1.6 mg/kg·day; P = 0.076) was observed. These results suggested that the marked decrease in plasma LDL obtained a short time after LDL-apheresis is able to stimulate LDL receptor activity and VLDL production in heterozygous FH.
Dissertations / Theses on the topic "Lipoprotein kinetics"
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Ooi, Esther M. M. "Regulation of lipoprotein transport in the metabolic syndrome : impact of statin therapy." University of Western Australia. School of Medicine and Pharmacology, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0125.
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[Truncated abstract] The metabolic syndrome is characterized by cardiovascular risk factors including dyslipidemia, insulin resistance, visceral obesity, hypertension and diabetes. The dyslipidemia of the metabolic syndrome includes elevated plasma triglyceride and apolipoprotein (apo) B levels, accumulation of small, dense low-density lipoprotein (LDL) particles and low high-density lipoprotein (HDL) cholesterol concentration. However, the precise mechanisms for this dyslipoproteinemia, specifically low plasma HDL cholesterol, are not well understood. This thesis therefore, focuses on HDL, its structure, function and metabolism. However, lipoprotein metabolism is a complex interconnected system, which includes forward and reverse cholesterol transport pathways. Hence, this thesis also examines and discusses the metabolism of apoB-containing lipoproteins. This thesis tests the general hypothesis that apolipoprotein kinetics are altered in the metabolic syndrome, and that lipid regulating therapies can improve these kinetic abnormalities. The aims were first, to compare and establish the clinical, metabolic and kinetic differences between metabolic syndrome and lean subjects; and second, to determine the regulatory effects of statin therapy, specifically, rosuvastatin on lipoprotein transport in the metabolic syndrome. Five observation statements were derived from the general hypothesis and examined in the studies described below. The findings are presented separately as a series of original publications. Study 1 Twelve men with the metabolic syndrome and ten lean men were studied in a case-control setting. ... These findings explain the HDL raising effects of rosuvastatin in the metabolic syndrome. Collectively, these studies suggest that the dyslipidemia of the metabolic syndrome results from increased production rates of VLDL and LDL particles, reduced fractional catabolic rates of these lipoproteins, together with accelerated catabolism of HDL particles. Treatment with rosuvastatin increases the catabolic rates of all apoB-containing lipoproteins and at a higher dose, decreases LDL apoB production. These effects are consistent with inhibition of cholesterol synthesis leading to an upregulation of LDL receptors. Rosuvastatin decreases the fractional catabolism of HDL particles. The effects of rosuvastatin on HDL kinetics may be related to a reduction in triglyceride concentration and cholesterol ester transfer protein activity. These findings are consistent with the general hypothesis that apolipoprotein kinetics are altered in the metabolic syndrome, and that statin therapy improves these kinetic abnormalities.
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Sun, Feifei. "Measurement of Endogenous and Exogenous Triacylglycerol Kinetics in the fed and fasted state using stable isotopes." Thesis, University of Surrey, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492925.
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Emerging evidence has shown that an abnormal postprandial accumulation of dietary tat IS atherogenic. The aim of this study is to measure triacylglycerol (TAG) kinetics in endogenous and exogenous lipoproteins in both fed and fasted states using stable isotopes.
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Alshayji, Iqbal. "Development and application of a novel method to determine large very low density lipoprotein (VLDL1) kinetics." Thesis, University of Glasgow, 2008. http://theses.gla.ac.uk/253/.
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High concentrations of large very low density lipoproteins (VLDL1) give rise to atherogenic dyslipidaemia, which is usually associated with insulin resistant conditions (e.g. obesity) and increases the risk for cardiovascular disease (CVD). Isotopic tracer methods for determining VLDL1 kinetics are costly, time-consuming, labour intensive and need experience and skill to calculate the kinetic parameters. The aim of this thesis was to develop a simpler and cost-effective method of obtaining triglyceride-rich lipoproteins (TRL) kinetic data, based on the fact that chylomicrons (CM) or CM-like particles (e.g. Intralipid) compete with large VLDL1 for the same lipoprotein lipase (LPL)-mediated catalytic pathway. From this method, it was possible to determine VLDL1-triglyceride (TG) and -apolipoprotein (apo) B production rates and the Intralipid-TG clearance rate (as a surrogate measure of CM clearance). Kinetic data obtained from this method agreed with values and relationships obtained from stable isotope methods. The protocol is relatively quick, inexpensive, and transferable to non-specialist laboratories. As a first application, the ‘Intralipid method’ was used to investigate the effects of hyperinsulinaemia and hyperglycaemia due to glucose ingestion on VLDL1-TG and -apoB production rates and Intralipid-TG clearance rate. This showed that hepatic VLDL1 production is suppressed in response to hyperinsulinaemia and that the change in Intralipid-TG clearance rate with hyperinsulinaemia correlated significantly with HOMA-estimated insulin resistance (HOMA-IR). In addition, alanine aminotranferase (ALT) concentrations (a marker for liver fat), within normal range, predicted the extent of hepatic VLDL1 suppression. Secondly, the Intralipid method was used to investigate the mechanisms responsible for the hypotriglyceridaemic effect of a moderate exercise session (120 min walking at 50% VO2max) in overweight/obese middle-aged men; the section of the population at high risk of CVD in whom exercise-for-health guidelines are targeted. This showed that the exercise-induced reduction in plasma TG was due to increased VLDL1-TG and -apoB clearance, rather than decreased hepatic production. Exercise also increased Intralipid-TG clearance rate, but to a lesser extent than VLDL1, suggesting an increased affinity of VLDL1 for LPL-mediated lipolysis post-exercise. Taken together, the Intralipid method is a relatively simple, safe and cost-effective method to determine in VLDL1-TG and -apoB production rates and Intralipid-TG clearance rates. It is also sensitive enough to detect physiological changes in TRL kinetics.
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Hirata, Rosario Dominguez Crespo. "Efeito da apolipoproteína B no metabolismo de emulsões semelhantes à fase lipídica da LDL, em ratos." Universidade de São Paulo, 1991. http://www.teses.usp.br/teses/disponiveis/9/9132/tde-13052008-155801/.
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A LDL contitui-se de uma fase lipídica, uma esfera composta principalmente de um núcleo de colesterol esterificado envolto por uma camada de fosfolipídeos. A fase lipídica junta-se uma única molécula protéica, a polipoproteina B (apo B). A LDL é removida da circulação por mediação de receptores específicos, os receptores B. E, que reconhecem não só a apo B da LDL mas também a apo E, que está presente em outras lipoproteínas. Estudou-se neste trabalho a influencia da apo B no metabolismo da LDL, através de um modelo de emulsões semelhantes à fase lipídica da LDL, constituídas de oleato de colesterol (29%), fosfatidilcolina (69%) e trioleina (2%), preparadas por sonicação, seguida de ultracentrifugação. As emulsões, com seus componentes lipídicos marcados isotopicamente, foram associadas à apo B e injetadas no rato, determinando-se sua remoção plasmática e captação pelos diversos órgãos do animal. Os resultados foram comparados com o metabolismo da emulsão sem associação da apo B a sua estrutura e com o da LDL natural. Verificou-se que a presença de apo B retardou a remoção plasmática das partículas da emulsão. Por outro lado, o oleato de colesterol da emulsão com apo B foi removido do compartimento plasmático numa taxa semelhante à da LDL natural, o que demonstra a adequação do modelo utilizado à situação fisiológica. Tanto as emulsões quanto a LDL natural foram captadas principalmente pelo fígado. Entretanto, a captação hepática da emulsão sem apo B foi maior a da emulsão com apo B e a da LDL. A incubação das emulsões com HDL do plasma de rato mostrou que a emulsão sem apo B adquiriu mais apo E que a emulsão com apo B. Portanto, essas diferenças de comportamento metabólico provavelmente se devem à maior afinidade dos receptores B, E hepáticos por partículas que contem mais apo E, em comparação às que contêm a apo B. O aumento da atividade dos receptores B, E, induzido pelo tratamento com 17 α-etinil estradiol, resultou no aumento da cinética plasmática das duas emulsões. Porém, à taxa de remoção plasmática da emulsão sem apo B também foi maior no grupo tratado com o estrógeno. Esses dados indicam que as emulsões com apo B associada a sua estrutura apresentam comportamento metabólico muito semelhante ao da LDL. Portanto, o modelo das emulsões análogas à LDL parece ser um instrumento eficiente no estudo do metabolismo daquela lipoproteína.<br>The effects of apolipoprotein B (apo B) on the metabolism of emulsions constituted of cholesteryl oleate (29%), phosphatidycholine (69%) and triolein (2%) were studied in rats. After intra-arterial injection of the radiolabelled emulsions, plasma removal of the emulsions was reduced in presence of apo B. On the other hand, the cholesteryl ester moiety of the apob B emulsion was removed at the same rate as native LDL. Emulsions and LDL were taken up mainly by the liver 24 h after the injection. However, the hepatic uptake of the apo B emulsion was similar to LDL and lower than that of the apo B-free emulsion. These differences in metabolic behaviour were probably due to the lower hepatic B, E, receptor affinity to apo B contained in the emulsions associated to apo B and in LDL, compared to the apo B-free emulsions. The latter, as confirmed in the in vitro experiments, is capable of adsorbing more apo E, and this apolipoprotein has higher affinity for the receptor. Enhanced receptor activity induced by pre-treatment of the rats with 17 α-ehymylestradiol resulted in augmented plasma removal of both emulsions but nonetheless the cholesteryl ester plasma removal of the apo B-containing particles was still lower, compared to that of the apo B-free emulsion. These data indicate that apo B-containing emulsion exhibits metabolic behaviour similar to that of LDL, and this emulsion can be an adequate tool to test LDL metabolism.
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Mason, Susan Leigh. "Metabolism of triacylglycerol-rich lipoproteins in sheep." Lincoln University, 1991. http://hdl.handle.net/10182/1756.
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This thesis describes two approaches for studying of lipoprotein metabolism in sheep. The first approach involves the assay of lipoprotein lipase (LPL) activity to determine the role of lipoprotein-triacylglycerol fatty acids in fat deposition in sheep. This enzyme is the rate limiting enzyme in the hydrolysis of fatty acids from lipoprotein-triacylglycerol. The second approach was to characterize and quantify in vivo lipoprotein metabolism using iodinated very low density lipoprotein (¹²⁵I-VLDL) and low density lipoprotein (¹³¹I-LDL). Cross-bred lambs were divided into two treatment groups and either weaned early at 5 weeks of age or remained suckling. Lambs were slaughtered at 12 or 23 weeks at which time the body composition and adipose tissue LPL activity were determined. The differences in rearing led to differences in body composition. The suckled lambs were larger and fatter than weaned lambs. The increased fatness in the suckled lambs was associated with increased LPL activity (U/mg protein) in subcutaneous adipose tissue and was reflected in higher LPL activity in post-heparin plasma (PHP) taken 2 days prior to slaughter. The role of insulin in the regulation of LPL activity was investigated by either infusing a subset of the weaned and suckled lambs with insulin for 7 or 18 weeks or using the euglycemic clamp technique to study the effect of short insulin infusions. The long term infusion of insulin had no significant effect on PHP LPL or on adipose tissue LPL (U/g tissue). However, after infusing insulin for 6h at 6.3 mU.kg⁻·⁷⁵.h⁻¹ during the euglycemic clamps, a two fold increase in LPL activity in biopsied subcutaneous adipose tissue was observed. In the second approach, in vivo lipoprotein metabolism was investigated in 4 lambs using apolipoprotein B as a marker. Following the simultaneous injection of ¹²⁵I VLDL and ¹³¹I VLDL, the specific activities of apoB in VLDL, IDL and LDL fractions were determined. ApoB specific activity curves demonstrated that VLDL is metabolised to IDL and subsequently to LDL. The turnover of VLDL-B (3.45mg.d⁻¹.kg⁻¹) and LDL-B (4.8mg.d⁻¹.kg⁻¹) was calculated by fitting the VLDL-¹²⁵I-B and LDL-¹³¹I-B specific activity data to a mono-exponential equation. The metabolism of lipoproteins, inferred from the study of apoB, was shown to be similar in sheep to that reported in other animals although the amount of lipoprotein synthesised was low. A model to describe the kinetics of apoB metabolism in sheep was developed using SAAM. The proposed model features a three pool delipidation chain for VLDL, and subsystems containing two pools for IDL and LDL. IDL may be catabolised to LDL or cleared directly from the plasma. The developed model can now be used to compare the metabolism of lipoproteins in different physiological states and to design new experiments to study lipoprotein metabolism further.
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Uliaque, Cugat Katia. "Implementation of stable isotopes lipoprotein kinetic studies: effects on HDL metabolism of a Mediterranean type diet rich in MUFAs from virgin olive oil." Doctoral thesis, Universitat Rovira i Virgili, 2007. http://hdl.handle.net/10803/8658.
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The anti-atherogenic effects ascribed to a Mediterranean-type diet rich in monounsaturated<br/>fatty acids (MUFAs) from virgin olive oil are due, partly, to an increase in, or maintenance of,<br/>plasma concentrations of high density lipoprotein (HDL) cholesterol. However, the underlying<br/>mechanisms that may explain these concentrations are not well characterised, to-date.<br/>Apolipoprotein (apo) A-I (apoA-I) is the major HDL apo and its kinetic parameters, such as<br/>production rate and catabolic rate, reflect the kinetics of the HDL particle. Our working<br/>hypothesis is as follows: a Mediterranean-type diet rich in MUFAs from virgin olive oil,<br/>compared to a STEP II diet, increases or preserves HDL cholesterol concentrations due to an<br/>increase in apoA-I production and not to a decrease in apoA-I catabolism. Kinetic studies<br/>using stable isotopes are, perhaps, the best approach in physiologically evaluating apo<br/>production and catabolism in humans. This methodology has not as yet been implemented in<br/>Spain. Objectives: to implement the necessary methodology to perform kinetic studies of apo<br/>B-100 and, especially, of apoA-I and apoA-II in volunteers in vivo using stable isotopes to<br/>label proteins in vivo. Further, we used this methodology to analyse the overall effects of a<br/>Mediterranean-type diet rich in monounsaturated fatty acids from virgin olive oil compared<br/>with a low-fat, STEP II diet, on HDL and low density lipoprotein (LDL) metabolism. Design:<br/>we conducted a crossover, randomised study with dietary intervention periods of 4 weeks,<br/>interspersed with a washout period between diets. A total of 10 healthy, moderately<br/>hypercholesterolaemic, male volunteers consumed the two diets. The project was approved<br/>by the Clinical Research Ethical Committee of the Hospital Universitari de Sant Joan, Reus.<br/>Instrumentation: kinetic studies were performed at the end of each diet using a 16h primed<br/>constant infusion of stable isotope<br/>2<br/>H3-L-leucine. Lipoprotein fractions were separated using<br/>ultracentrifugation technique. Stable isotope incorporated into proteins was measured using<br/>GC-MS. The data obtained were analysed applying multi-compartmental modelling technique<br/>with the SAAM II program. ApoA-I and A-II kinetic studies were conducted in our Research<br/>Unit in Reus. Apo B-100 kinetic studies and kinetic parameter modelling were performed in<br/>collaboration with Dr. Caslake and Professor Packard of the Vascular Biochemistry Section,<br/>Division of Cardiovascular & Medical Sciences, Royal Infirmary, University of Glasgow,<br/>Glasgow, Scotland. Results: the Mediterranean diet, compared to the STEP II diet,<br/>significantly increases apoA-I plasma concentrations. A total of 17 kinetic studies have been<br/>performed but, due to methodological complexity, only the results of 7 kinetic studies (4<br/>following a Mediterranean diet and 3 following a STEP II diet) that have been analysed in a<br/>GC-MS to-date, are presented in this thesis. Despite the limitation of the low number of<br/>kinetic studies analysed, we are able to document that the Mediterranean diet induces a high<br/>apoA-I HDL production rate compared to the STEP II diet. Also, the Mediterranean diet<br/>induces a high apo B-100 LDL production rate and fractional catabolic rate compared to the<br/>STEP II diet. Conclusions: we have, for the first time in Spain, implemented the necessary<br/>methodology to perform apo B-100, apoA-I and A-II kinetic studies in vivo using stable<br/>isotopes in human subjects. A high apoA-I production rate is the main determinant of high<br/>plasma concentrations of apoA-I, and not variations in its catabolism. Lipoprotein kinetic<br/>studies enable the monitoring of lipoprotein metabolic parameters and the investigation of<br/>nutritional and pharmacologic interventions in the primary and secondary prevention of<br/>cardiovascular disease targets.<br>Els efectes antiaterogènics atribuïts a una dieta de tipus mediterrani, rica en àcids grassos<br/>monoinsaturats (AGM), aportats per oli d'oliva verge, són deguts, en part, a l'augment o al<br/>manteniment de les concentracions plasmàtiques de colesterol de les lipoproteïnes d'alta<br/>densitat (HDL). No obstant i fins al moment, no es coneixen del tot els mecanismes que<br/>expliquen aquestes concentracions. L'apolipoproteïna (apo) A-I (apoA-I) és l'apolipoproteïna<br/>majoritària de les HDL i els seus paràmetres cinètics, com ara la taxa de producció i la taxa<br/>de catabolisme, reflexen la cinètica de les partícules d'HDL. La nostra hipòtesi de treball és la<br/>següent: una dieta Mediterrània rica en AGM aportats per oli d'oliva verge, comparada amb<br/>una dieta STEP II, incrementa o manté els nivells de colesterol de les HDL degut a un<br/>augment de la producció i no a una disminució de la degradació d'apoA-I. Possiblement, la<br/>realització d'estudis de cinètiques utilitzant isòtops estables és la forma més fisiològica<br/>d'avaluar la producció i la degradació d'apolipoproteïnes en l'home. Objectiu: Implementar la<br/>metodologia necessària per realitzar cinètiques d'apo B-100 i, especialment, d'apoA-I i<br/>d'apoA-II en voluntaris in vivo utilitzant isòtops estables com a marcatge de les proteïnes.<br/>Aplicar aquesta metodologia per comparar els efectes d'una dieta Mediterrània rica en oli<br/>d'oliva verge amb una dieta pobra en greixos STEP II sobre el metabolisme de les HDL i de<br/>les lipoproteïnes de baixa densitat (LDL). Disseny: Estudi creuat randomitzat de 4 setmanes<br/>d'intervenció dietètica, amb un període de rentat entre elles. 10 voluntaris, homes sans,<br/>moderadament hipercolesterolèmics van seguir ambdues dietes. Aquest estudi va ser<br/>aprovat pel Comitè d'Ètica i d'Investigació Clínica de l'Hospital Universitari de Sant Joan de<br/>Reus. Instrumentalització: Estudi cinètic mitjançant la injecció i perfusió d'isòtop estable 2H3-<br/>L-leucina en forma d'un bolus inicial i de perfusió durant 16h al final de cada dieta. Les<br/>diferents fraccions lipoproteïques es van separar per ultracentrifugació. La detecció d'isòtop<br/>incorporat va ser mitjançant GC-MS. Les dades obtingudes es van analitzar amb models<br/>multicompartimentals i el programa SAAM II. Els estudis cinètics d'apoA-I i d'apoA-II es van<br/>posat a punt i realitzat a la nostra Unitat de Recerca a Reus. Els estudis d'apo B-100 i la<br/>modelització de les dades cinètiques es van realitzar en colClaboració amb el grup de recerca<br/>de la Vascular Biochemistry Section, Division of Cardiovascular & Medical Sciences, Royal<br/>Infirmary, University of Glasgow, Glasgow). Resultats: La dieta Mediterrània, comparada<br/>amb la dieta STEP II, incrementa significativament la concentració plasmàtica d'apoA-I.<br/>S'han realizat 17 cinètiques però, degut a la complexitat de la metodologia, en aquesta tesis<br/>es presenten els resultats de les 7 cinètiques (4 després de la dieta Mediterrània i 3 després<br/>de la dieta STEP II) analitzades per GC-MS fins ara. A pesar de l'escàs nombre de cinètiques,<br/>s'observen certes tendències. La dieta Mediterrània, comparada amb la dieta STEP II,<br/>presenta una major taxa de producció d'apoA-I de les HDL, així com una major taxa de<br/>producció i de catabolisme de l'apo B-100 de les LDL. Conclusions: S'ha implementat la<br/>metodologia dels estudis de cinètiques amb isòtops estables de l'apoA-I i l'apoA-II de les<br/>HDL i de l'apo B-100 de les VLDL1, VLDL2, IDL i LDL. El determinant de les concentracions<br/>més elevades d'apoA-I en plasma és una major taxa de producció d'aquesta apo i no<br/>diferències en el seu catabolisme. Les aportacions de las cinètiques de les lipoproteïnes<br/>permetran avançar en els mecanismes lipídics involucrats en les malalties vasculars i aportar<br/>nous aspectes sobre les dianes nutricionals i farmacològiques.
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Barrett, P. Hugh R. "The kinetic analysis and computer modelling of lipoprotein metabolism in man." Title page, table of contents and abstract only, 1989. http://web4.library.adelaide.edu.au/theses/09PH/09phb274.pdf.
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Bertato, Marina da Paz. "Cinética plasmática do colesterol livre e do colesterol esterificado e transferência in vitro de lípides para a HDL, utilizando uma nanoemulsão lipídica artificial, em indivíduos com intolerância à glicose." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-24062010-142720/.
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O indivíduo com diabetes mellitus tipo 2 apresenta um risco de 2 a 4 vezes maior de desenvolver doença cardiovascular (DCV) quando comparado ao não-diabético, sendo que este aumento do risco para o desenvolvimento da DCV também é observado quando na intolerância à glicose (IG) que ocorre em fases mais precoces da história natural do diabetes. Atribui-se ser a presença da síndrome metabólica (SM), que ocorre na maioria dos pacientes com DM2 e IG, um fator importante para o desenvolvimento da DCV nestes indivíduos. Dos componentes da SM, inúmeros estudos destacam a dislipidemia como um dos principais fatores para este risco. A dislipidemia comumente encontrada na IG é caracterizada por hipertrigliceridemia, baixo HDL-C e presença de LDL pequena e densa. Entretanto, como a elevação dos níveis séricos do LDL-C associada ao surgimento de aterosclerose prematura em indivíduos não diabéticos na maioria das vezes não é observada em pacientes com IG, questiona-se se outras alterações do metabolismo lipídico, tais como alterações da cinética do colesterol ou a transferência de lípides das lipoproteínas para a HDL, poderiam estar relacionadas ao maior risco cardiovascular nestes pacientes. Estudo prévio, utilizando uma nanoemulsão lipídica artificial de LDL, verificou uma remoção mais rápida do colesterol na forma livre em pacientes normolipidêmicos com doença arterial coronária (DAC) quando comparada com controles. No presente estudo, utilizou-se a nanoemulsão lipídica artificial para avaliar se esses dois processos envolvidos no metabolismo da LDL e da HDL estão alterados em pacientes com intolerância à glicose que os predispõem à DAC, relacionando estes resultados com fatores de risco cardiovasculares, tais como a resistência à insulina, a obesidade e a dislipidemia. Para tanto, foram estudados 14 pacientes com IG e 15 controles, sem manifestação clínica de DCV, que não utilizam antidiabéticos orais e hipolipemiantes, comparados com controles pareados para idade, sexo, raça, IMC, tabagismo, consumo de álcool, prática de atividade física e doenças associadas. Para o estudo cinético, a nanoemulsão marcada foi injetada endovenosamente e amostras de sangue coletadas ao longo de 24h para a determinação da radioatividade, das curvas de decaimento plasmático e da taxa fracional de remoção (TFR) dos lípides marcados a partir de um modelo de análise compartimental. Foi medida a taxa de esterificação do 3Hcolesterol livre da nanoemulsão no plasma e avaliada a transferência in vitro de lípides da nanoemulsão para a fração HDL. A resistência à insulina foi estimada pelo modelo matemático de homeostase glicêmica (HOMA) e a adiposidade abdominal por tomografia computadorizada de abdômen. A concentração plasmática de colesterol total, LDL-C, HDL-C, triglicérides e de apolipoproteínas não diferiu entre os grupos. O perfil antropométrico relacionado ao peso, IMC e circunferência abdominal foi semelhante entre os grupos. O grupo IG apresentou maior concentração de insulina de jejum (p=0,01), menor sensibilidade à insulina (p<0,01) e maior índice de resistência à insulina (p<0,01). A TFR 14C-EC foi similar nos dois grupos, porém a TFR 3H-CL foi mais rápida no grupo IG comparado com controle (p=0,04). A porcentagem de esterificação do 3H-colesterol da nanoemulsão bem como a transferência de lípides da nanoemulsão para a fração HDL foram semelhantes entre os grupos. A remoção mais rápida do 3H-colesterol livre mostra que ocorreu uma dissociação das partículas de colesterol da nanoemulsão lipídica nos pacientes com intolerância à glicose. Essa dissociação do colesterol pode refletir alterações no metabolismo intravascular da lipoproteína LDL, as quais podem favorecer a aterogênese nesses pacientes<br>Individuals with diabetes mellitus type 2 are 2 to 4 times more susceptible to cardiovascular disease (CVD) than non-diabetic individuals. This increased risk is also observed for glucose intolerance (GI) which appears in the initial stages of diabetes. The presence of the metabolic syndrome (MS), present in most DM2 and GI patients, is also an important factor contributing to the development of CVD in these individuals. Various MS component studies emphasize dyslipidemia as one of the main contributors for this risk factor. The dyslipidemia commonly associated to GI is characterized by hypertriglyciridemia, low HDL-C and the presence of a small and dense LDL. However, since associated LDL-C levels with the development of premature atherosclerosis in non diabetic individuals is for the most part not observed in GI patients, it is questioned whether other lipid metabolism alterations such as cholesterol kinetics or the lipid transfer to HDL could be related to a greater CVD risk in these individuals. A previous study using an artificial LDL nanoemulsion showed a faster removal rate of the free cholesterol in normolipidemic with coronary artery disease (CAD) patients when compared to control individuals. In this study an artificial lipid nanoemulsion was used to evaluate both these processes involved in the metabolism of LDL and HDL which are both altered in patients with GI that expose them to CAD, and relating the results to CVD factors such as insulin resistance, obesity and dyslipidemia. 14 GI and 15 control individuals participated in this study. All without manifestations of CVD, none using any oral antidiabetic medication or hypolipimeants, paired for age, sex, race, BMI, smoking, alcoholic consumption, physical activity and comorbidities. For the kinetic study, a labeled nanoemulsion was interveneously injected and blood samples collected at determined intervals over a 24 hour period to determine the radiactive plasma decay curves and fractional clearance rate (FCR) of the labeled nanoemulsion lipids through a compartmental analysis model. Plasma esterification rate of the 3H-free cholesterol of the nanoemulsion was measured as was the in vitro transfer from the nanoemulsion to HDL fraction. Insulin resistance was obtained by the glycemic homeostasis mathematical model (HOMA) and abdominal adipose by a computerized tomography of the abdomen. No differences were observed for total cholesterol plasmatic concentrations, LDL-C, HDL-C, triglycerides or apolipoproteins between the two groups. The anthropometric profile related to weight, BMI and abdominal circumference was similar for both groups. The GI group presented higher fasting insulin concentration (p=0.01), less insulin sensitivity (p=0.01) and a greater insulin resistance (p=0.01). The TFR 14C-CE was similar in both groups, although the TFR 3H-CL was faster in the GI group compared to the control group (p=0.04). The esterification percentage of the nanoemulsions 3H-colesterol, as well as the lipid transfer from the nanoemulsion to HDL fraction were similar for both groups. The faster 3H-free cholesterol removal shows that a dissociation of the cholesterol particles of the lipidic nanoemulsion occurred in those patients with GI. This dissociation could possibly reflect alterations in the intravascular LDL lipoprotein metabolism which in turn, may favor atherogenesis in these patients
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Padoveze, Amanda Felippe. "Cinética plasmática e biodistribuição de colesterol livre e colesterol esterificado de uma nanoemulsão (LDE) que se liga aos receptores de LDL em animais controle e com indução de aterosclerose." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-25062009-120520/.
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Estudos anteriores em nosso laboratório demonstraram que pacientes portadores de DAC apresentam diferenças no metabolismo do CL e CE de uma nanoemulsão artificial rica em colesterol (LDE), nos quais o CL apresentou maior remoção plasmática e depósito arterial. Dando continuidade a esta linha de pesquisa, neste trabalho foram avaliadas a cinética plasmática, representada pela taxa fracional de remoção (TFR), e a captação do 3H-colesterol livre (3H - CL) e 14C - colesterol esterificado (14C - CE) da LDE por segmentos arteriais e por órgãos de coelhos normais (n=17) e coelhos submetidos à indução de aterosclerose por dieta rica em colesterol (1%) (n=13). Além disso, avaliou-se a captação in vitro do 3H CL e do 14C CE da LDE por células endoteliais aórticas de coelhos. Por último, foi avaliada a influência da inibição da enzima lecitina-colesterol aciltransferase (LCAT), e indiretamente, a esterificação do CL em ratos normais (n=9) e tratados com diazepam (n=9). Em coelhos que receberam dieta normal, não houve diferença entre a remoção plasmática do 3H - CL e do 14C - CE. Em coelhos que desenvolveram hiperlipidemia e aterosclerose através de dieta rica em colesterol, o 3H - CL foi removido mais rapidamente da circulação do que o 14C - CE (p<0,05), entretanto houve maior captação de 14C - CE do que de 3H - CL no arco aórtico (p<0,05). Em ambos os grupos, os principais órgãos captadores de colesterol da LDE foram fígado, pulmão, adrenais e baço (p<0,05). Tanto a TRF quanto a captação hepática de 3H - CL e 14C - CE foram menores no grupo que recebeu a dieta rica em colesterol. Em células endoteliais aórticas de coelhos, a captação de 3H - CL foi maior que a de 14C CE independente da massa de LDE incubada (p<0,01). Em ratos, não houve diferença entre a captação das duas formas de colesterol da LDE pela aorta no grupo controle, entretanto, quando a atividade da LCAT foi diminuída pelo tratamento com diazepam, a captação arterial de 3H - CL foi maior do que a de 14C - CE (p< 0,01). A hiperlipidemia e distúrbios no processo de estabilização do colesterol, favorecem a dissociação entre o CL e o CE das lipoproteínas, e podem elevar o risco de desenvolvimento da aterosclerose, assim como agravar o processo de aterogênese.<br>I n previously studies, it was shown that free cholesterol (FC) and cholesterol ester (CE) of a cholesterol-rich nanoemulsion (LDE) behaves differently in patients with coronary artery disease (CAD). The FC plasma clearance and arterial deposition is greater than CE. In the present study we evaluate the plasma kinetics, estimated by the fractional clearance rate (FCR), and the tissue uptake of 3H-free cholesterol (3H FC) and of 14C cholesterol ester (14C - CE) of LDE by arterial segments and organs of rabbits with (n=13) and without atherosclerosis (n=17). Furthermore, it was evaluated the in vitro uptake of 3H FC and 14C - CE by rabbit aortic endothelial cells. Finally, it was evaluated the inhibition of the enzyme lecithin-cholesterol acyltransferase (LCAT), and indirectly, the FC esterification in rats non-treated (n=9) and treated with diazepam (n=9). In rabbits without atherosclerosis that received an standard diet there was no difference between the plasma clearance of 3H FC and 14C CE. In rabbits with hyperlipidemia and atherosclerosis induced by the cholesterol-rich diet the 3H - FC was removed faster than 14C - CE (p<0.05), however the arch aortic uptake of 14C CE was greater than of 3H - FC (0p<0.05). In both groups, liver, lungs, adrenals and spleen were the principal sites of LDE cholesterol uptake. The FCR and tissue uptake were smaller in rabbits with than those without atherosclerosis. In rabbit aortic endothelial cells the 3H - FC uptake was greater than 14C CE independently of incubated LDE mass (p<0.01). In control rats there was no difference on the arterial uptake of both cholesterol forms of LDE, but when the LCAT activity was diminished by the diazepam treatment, the arterial uptake of 3H FC were greater than 14C CE (p< 0.01). The hyperlipidemia and cholesterol stability alterations may lead to dissociation between lipoproteins FC and CE. This dissociation may increase the risk for atherosclerosis and likewise enhance the severity of atherosclerosis.
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Oliveira, Carolina Piras de. "Estudo da cinética plasmática do colesterol livre e esterificado em pacientes diabéticos tipo 2 com ou sem doença coronariana diagnosticada." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-10032010-100945/.
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INTRODUÇÃO:. A dislipidemia diabética é um dos principais fatores de risco para doença arterial coronária (DAC) O uso de uma nanoemulsão LDL-símile para avaliar clearance do éster de colesterol(EC) e colesterol livre(CL) do intravascular mostrou uma remoção acentuada do CL e um maior depósito em vasos sanguíneos de indivíduos com DAC avançada. OBJETIVOS: Identificar em DM2 a cinética plasmática do CL e EC; se há diferença na cinética de CL e EC em DM2 assintomáticos para DAC com e sem aterosclerose subclínica. MÉTODOS: Estudou-se 12 DM2 e 09 controles pareados para idade e sexo. A aterosclerose subclínca foi avaliada pela presença de Calcificação na artéria coronária (CAC). A Nanoemulsão artificial LDLsímile com dupla marcação radioativa 14C-EC, 3H-CL foi utilizada para o estudo cinético do colesterol, sendo injetada nos participantes e amostras de sangue foram coletadas durante 24 horas para mensuração da radioatividade. Remoção dos lípides da circulação foi calculada por análise compartimental. Mediu-se a taxa de esterificação do 3H-CL no plasma e avaliou-se a capacidade in vitro da HDL de receber lípides a partir das LDL-símile. RESULTADOS: Os diabéticos tiveram IMC, CA e CA/CQ maior que os controles, respectivamente: 31,9 ± 4,6 vs. 27,1± 2,4, p<0,05; 104,9 ± 9,8 vs. 94,2 ± 7,3, p<0,05; 0,98 ± 0,09 vs.0,89 ± 0,06, p<0,01. A glicemia de jejum (171 ± 96 vs. 83 ± 7,5 mg/dl, p <0,05) e hemoglobina glicada (8,9 ± 2,1 vs. 5,6 ± 0,4%, p<0,05) também foram maiores no DM2. A concentração de colesterol total, LDL, HDL, Triglicérides e apolipoproteínas A1,B e E não diferiu entre os grupos. A Taxa fracional de remoção (TFR)14C-EC foi 22% maior DM2 que nos controles (0,07 ± 0,02 vs. 0,05 ± 0,01 h-1, p<0.01). A TFR3H- CL foi semelhante entre os dois grupos, bem como a esterificação. A presença de CAC no grupo DM2 não alterou a remoção de EC e CL nesses pacientes. In vitro a capacidade da HDL em receber EC (4,2 ± 0,8vs. 3,5 ± 0,6 %, p=0,03) e TG (6,8 ± 1,6 vs. 5,0 ± 1,1, p=0.03) foi maior nos DM2. CONCLUSÕES: A remoção acelerada do 14C-EC na população DM2 e a remoção semelhante do 3H-CL quando comparado com grupo controle, pode sinalizar alterações na gênese da dislipidemia diabética. O fato dos DM2 com CAC assintomática não apresentam alterações na remoção de colesterol livre sinaliza uma provável relação do CL com a instabilidade da placa aterosclerótica.<br>INTRODUTION: The diabetic dyslipidemia is one of the most important risk factor in the development of coronary artery disease (CAD). The LDL-like nanoemulsion is being used to study the clearance of cholesteryl ester(CE) and free cholesterol(FC) from intravascular in patients with advanced CAD and it was shown a higher removal of FC and higher deposit in vases. OBJECTIVE: The aim of this study is to analyze the plasma kinetics of FC and CE in Type 2 Diabetes Mellitus (T2DM); and identify if there are any differences in the removal of FC in the presence of subclinical atherosclerosis in asymptomatic patients with T2DM. METHODS: It was studied 12 T2DM and 09 controls paired by age and gender. The LDL-like nanoemulsion labeled with radioactive: 14C- cholesterol ester (CE), 3H-cholesterol free (CF) was used on plasma kinetics. The nanoemulsion was injected intravenously in all participants and blood sample was collected over 24 hours for radioactivity measurement. The intravascular lipid removal was calculated through compartmental analysis. The intravascular esterification of FC contained in the nanoemulsion was calculated. The ability of HDL to received lipids from LDL-simile were observed in vitro essays. Coronary Calcium Score was detected to identify subclinical atherosclerosis. RESULTS: T2DM patients had a bigger BMI, waist and waist/hip than control, respectively 31.9 ± 4.6 vs. 27.1± 2.4, p<0.05; 104.9 ± 9.8 vs. 94.2±7.3, p<0.05; 0.98± 0.09 vs. 0.89 ± 0.06,p<0.01. Fasting glycemia (171 ± 96 vs. 83 ± 7.5 mg/dl, p <0.05) and glycated hemoglobin( 8.9 ± 2.1 vs. 5.6 ± 0.4%,p<0.05) was higher in T2DM, and there was no differences in the concentration of Total cholesterol, HDL, LDL, Triglycerides and apolipoproteins A1, B and E concentrations. The Fractional Clearance rate (FCR) 14C CE in T2DM was 22% bigger than control ( 0.07 ± 0.02 vs. 0.05± 0.01 h-1, p<0.01). FCR 3H-CF was similar between the groups. The CAC in T2DM did not show differents TFR in CE and FC in these group. In Both groups there was no statistical difference in FC esterification rate. The HDL ability to received CE (4.2 ± 0,8vs. 3.5 ± 0,6 %, p=0,03) and TG (6.8 ± 1.6 vs. 5.0 ± 1.1, p=0.03) from LDL-like nanoemulsion was higher in T2DM. CONCLUSIONS: The higher removal of 14C-CE and similar removal of FC in T2DM can be related to the genese of the diabetic dyslipidemia. The similar removal of FC between the control group and T2DM asymptomatic CAD, with and without subclinical atherosclerosis, could possibly signalize to the relation of FC and the atherosclerotic plaque stability.
Book chapters on the topic "Lipoprotein kinetics"
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Duverger, Nicolas, Nordine Ghalim, Nathalie Theret, et al. "Lipoprotein A-I Containing Particles." In Hypercholesterolemia, Hypocholesterolemia, Hypertriglyceridemia, in Vivo Kinetics. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5904-3_12.
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Olivecrona, Thomas, Gunilla Bengtsson-Olivecrona, Magnus Hultin, et al. "What Factors Regulate the Action of Lipoprotein Lipase?" In Hypercholesterolemia, Hypocholesterolemia, Hypertriglyceridemia, in Vivo Kinetics. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5904-3_41.
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Brewer, H. B., D. J. Rader, J. M. Hoeg, A. Mann, and G. Tennyson. "Recent Advances in Lipoprotein Metabolism and the Genetic Dyslipoproteinemias." In Hypercholesterolemia, Hypocholesterolemia, Hypertriglyceridemia, in Vivo Kinetics. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5904-3_29.
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Fojo, S. S., J. L. de Gennes, U. Beisiegel, et al. "Molecular Genetics of ApoC-II and Lipoprotein Lipase Deficiency." In Hypercholesterolemia, Hypocholesterolemia, Hypertriglyceridemia, in Vivo Kinetics. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5904-3_40.
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Chamberlain, J. C., J. A. Thorn, R. Morgan, et al. "Genetic Variation at the Lipoprotein Lipase Gene Associates with Coronary Arteriosclerosis." In Hypercholesterolemia, Hypocholesterolemia, Hypertriglyceridemia, in Vivo Kinetics. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5904-3_32.
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Alaupovic, P., D. H. Blackenhorn, C. Knight-Gibson, et al. "ApoB-Containing Lipoprotein Particles as Risk Factors for Coronary Artery Disease." In Hypercholesterolemia, Hypocholesterolemia, Hypertriglyceridemia, in Vivo Kinetics. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5904-3_36.
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Djavaheri, Mojgan, and Lawrence P. Aggerbeck. "Investigation of Structural Domains in Human Serum Low Density Lipoprotein Apolipoprotein B100." In Hypercholesterolemia, Hypocholesterolemia, Hypertriglyceridemia, in Vivo Kinetics. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5904-3_4.
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Marcel, Yves L., Alan R. Tall, Mireille Hogue, Ross W. Milne, and Ruth McPherson. "Plasma Lipoprotein Phenotype in Response to Cholesteryl Ester Transfer Protein Levels in Dyslipoproteinemia." In Hypercholesterolemia, Hypocholesterolemia, Hypertriglyceridemia, in Vivo Kinetics. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5904-3_9.
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Orekhov, Alexander N., and Vladimir V. Tertov. "Antibody-Like Immunoglobulins G Against Low Density Lipoprotein that Stimulate LIPID Accumulation in Cultured Cells." In Hypercholesterolemia, Hypocholesterolemia, Hypertriglyceridemia, in Vivo Kinetics. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5904-3_48.
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Van Tol, A., T. Van Gent, L. M. Scheek, et al. "Lipoprotein Structure and Metabolism During Progression and Regression of Atherosclerosis in Pigs Fed With Fish Oil-Derived Fatty Acids." In Hypercholesterolemia, Hypocholesterolemia, Hypertriglyceridemia, in Vivo Kinetics. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5904-3_50.
Full textConference papers on the topic "Lipoprotein kinetics"
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Babushkina, G. V., and A. V. Kartelishev. "Kinetics of blood lipoprotein spectrum indices in patients with angina pectoris during and after low-intensity laser therapy as a paraclinical criterion for treatment efficiency." In Low-Level Laser Therapy, edited by Tatiana I. Solovieva. SPIE, 2001. http://dx.doi.org/10.1117/12.425514.
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