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Journal articles on the topic 'Lipoprotein kinetics'

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Published: 4 June 2021

Last updated: 1 February 2022

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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 &lt; .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 &lt; .0001) and VLDL-LPS (P = .033); free LPS was associated with HDL-LPS (P &lt; .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 &lt; 0.01), and LDL production was increased in heterozygous FH patients (18.9 ± 7.0 vs. 9.9 ± 4.2 mg/kg·day; P&lt; 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.

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Tremblay, André J., Benoît Lamarche, Jean-Charles Hogue, and Patrick Couture. "n-3 Polyunsaturated Fatty Acid Supplementation Has No Effect on Postprandial Triglyceride-Rich Lipoprotein Kinetics in Men with Type 2 Diabetes." Journal of Diabetes Research 2016 (2016): 1–5. http://dx.doi.org/10.1155/2016/2909210.

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Dietary n-3 polyunsaturated fatty acids (PUFAs) have been proposed to modulate plasma lipids, lipoprotein metabolism, and inflammatory state and to reduce triglyceride (TG) concentrations. The present double-blind, randomized, placebo-controlled, crossover study investigated the effects of n-3 PUFA supplementation at 3 g/d for 8 weeks on the intravascular kinetics of intestinally derived apolipoprotein (apo) B-48-containing lipoproteins in 10 men with type 2 diabetes.In vivokinetics of the TG-rich lipoprotein (TRL) apoB-48 and VLDL apoB-100 were assessed using a primed-constant infusion of L-[5,5,5-D3] leucine for 12 hours in a fed state. Compared with the placebo, n-3 PUFA supplementation significantly reduced fasting TG concentrations by −9.7% (P=0.05) but also significantly increased plasma levels of cholesterol (C) (+6.0%,P=0.05), LDL-C (+12.2%,P=0.04), and HDL-C (+8.4,P=0.007). n-3 PUFA supplementation had no significant impact on postprandial TRL apoB-48 and VLDL apoB-100 levels or on the production or catabolic rates of these lipoproteins. These data indicate that 8-week supplementation with n-3 PUFAs in men with type 2 diabetes has no beneficial effect on TRL apoB-48 and VLDL apoB-100 levels or kinetics.

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Edelberg, J. M., та S. V. Pizzo. "Lipoprotein (a) promotes plasmin inhibition by α2-antiplasmin". Biochemical Journal 286, № 1 (1992): 79–84. http://dx.doi.org/10.1042/bj2860079.

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Plasmin inhibition by alpha 2-antiplasmin (alpha 2AP) is regulated by the vascular components fibrin(ogen) fragments, plasminogen and lipoprotein (a). Kinetic analysis demonstrates that CNBr-derived fibrinogen fragments completely protect plasmin from alpha 2AP. Plasminogen and 6-aminohexanoic acid decrease the rate of inhibition by 5- and 10-fold respectively. These studies show that CNBr-derived fibrinogen fragments and 6-aminohexanoic acid bind plasmin kringle(s) with binding constants of 2 micrograms/ml and 120 microM respectively, and that plasminogen binds to alpha 2AP with an affinity of 0.5 nM. The unmodulated inhibition is not effected by the presence of lipoprotein (a), but in the presence of protective CNBr-derived fibrinogen fragments the rate of inhibition is increased by the presence of the lipoprotein. The kinetics demonstrate that lipoprotein (a) binds to CNBr-derived fibrinogen fragments with an affinity of 4 nM, displacing plasmin from the protective surface. In addition, tissue-type plasminogen activator and trypsin inhibition by alpha 2AP is not slowed by the presence of CNBr-derived fibrinogen fragments or plasminogen (Pg), respectively. These kinetics suggest that the initial reversible interaction between plasmin and alpha 2AP is mediated by binding of the inhibitor to the kringle 1 domain of plasmin, with a reversible inhibition constant (Ki) of 5.0 x 10(-10) M. Under conditions where this kringle-inhibitor interaction is blocked, the reversible inhibition still occurs between the plasmin and alpha 2AP, but the initial Ki is increased to 5.0 x 10(-9) M. These data suggest that, in the circulation, plasmin inhibition by alpha 2AP may be down-regulated by fibrin, fibrin(ogen) fragments and Pg, but up-regulated by lipoprotein (a) in the presence of fibrin or fibrin(ogen) fragments. The lipoprotein (a)-mediated promotion of plasmin inhibition may provide an additional mechanism by which the lipoprotein impairs fibrinolysis and promotes atherosclerosis.

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Kroon, Abraham A., Martin A. van't Hof, Pierre N. M. Demacker, and Anton F. H. Stalenhoef. "The rebound of lipoproteins after LDL-apheresis. Kinetics and estimation of mean lipoprotein levels." Atherosclerosis 152, no. 2 (2000): 519–26. http://dx.doi.org/10.1016/s0021-9150(00)00371-3.

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HOLDSWORTH, G., J. G. NOEL, M. L. KASHYAP, and R. L. JACKSON. "Kinetics of lipoprotein lipase interaction with triacylglycerol-rich lipoproteins carrying excess apolipoprotein C-III2." Biochemical Society Transactions 13, no. 1 (1985): 131–32. http://dx.doi.org/10.1042/bst0130131.

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Vergès, Bruno. "Abnormalities in lipoprotein kinetics in Type 2 diabetes." Clinical Lipidology 5, no. 2 (2010): 277–89. http://dx.doi.org/10.2217/clp.10.2.

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Foster, D. M., R. C. Boston, and L. A. Zech. "Kinetics of Lipoprotein Metabolism: Special Considerations In Modeling." IFAC Proceedings Volumes 21, no. 1 (1988): 327–32. http://dx.doi.org/10.1016/s1474-6670(17)57575-8.

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Morales, Noppawan Phumala, Pacharaporn Chunephisal, Jindaporn Janprasit, Yuma Ishida, Rataya Luechapudiporn, and Ken-Ichi Yamada. "Kinetics and localisation of haemin-induced lipoprotein oxidation." Free Radical Research 53, no. 9-10 (2019): 968–78. http://dx.doi.org/10.1080/10715762.2019.1660323.

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Parhofer, Klaus G., Thomas Demant, Michael M. Ritter, H. Christian Geiss, Markus Donner, and Peter Schwandt. "Lipoprotein (a) metabolism estimated by nonsteady-state kinetics." Lipids 34, no. 4 (1999): 325–35. http://dx.doi.org/10.1007/s11745-999-0370-z.

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Tselmin, S., G. Müller, U. Schatz, U. Julius, S. R. Bornstein, and B. Hohenstein. "Kinetics of Lipoprotein(a) in patients undergoing weekly lipoprotein apheresis for Lp(a) hyperlipoproteinemia." Atherosclerosis Supplements 30 (November 2017): 209–16. http://dx.doi.org/10.1016/j.atherosclerosissup.2017.05.033.

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Steenson, Simon, Fariba Shojaee-Moradie, Martin B. Whyte, et al. "The Effect of Fructose Feeding on Intestinal Triacylglycerol Production and De Novo Fatty Acid Synthesis in Humans." Nutrients 12, no. 6 (2020): 1781. http://dx.doi.org/10.3390/nu12061781.

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A high fructose intake exacerbates postprandial plasma triacylglycerol (TAG) concentration, an independent risk factor for cardiovascular disease, although it is unclear whether this is due to increased production or impaired clearance of triacylglycerol (TAG)-rich lipoproteins. We determined the in vivo acute effect of fructose on postprandial intestinal and hepatic lipoprotein TAG kinetics and de novo lipogenesis (DNL). Five overweight men were studied twice, 4 weeks apart. They consumed hourly mixed-nutrient drinks that were high-fructose (30% energy) or low-fructose (<2% energy) for 11 h. Oral 2H2O was administered to measure fasting and postprandial DNL. Postprandial chylomicron (CM)-TAG and very low-density lipoprotein (VLDL)-TAG kinetics were measured with an intravenous bolus of [2H5]-glycerol. CM and VLDL were separated by their apolipoprotein B content using antibodies. Plasma TAG (p < 0.005) and VLDL-TAG (p = 0.003) were greater, and CM-TAG production rate (PR, p = 0.046) and CM-TAG fractional catabolic rate (FCR, p = 0.073) lower when high-fructose was consumed, with no differences in VLDL-TAG kinetics. Insulin was lower (p = 0.005) and apoB48 (p = 0.039), apoB100 (p = 0.013) and non-esterified fatty acids (NEFA) (p = 0.013) were higher after high-fructose. Postprandial hepatic fractional DNL was higher than intestinal fractional DNL with high-fructose (p = 0.043) and low-fructose (p = 0.043). Fructose consumption had no effect on the rate of intestinal or hepatic DNL. We provide the first measurement of the rate of intestinal DNL in humans. Lower CM-TAG PR and CM-TAG FCR with high-fructose consumption suggests lower clearance of CM, rather than elevated production, may contribute to elevated plasma TAG, possibly due to lower insulin-mediated stimulation of lipoprotein lipase.

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Schwaiger, Johannes P., Yoshinobu Nakada, Ramona Berberich, et al. "Lipoprotein Kinetics in Male Hemodialysis Patients Treated with Atorvastatin." Clinical Journal of the American Society of Nephrology 8, no. 8 (2013): 1319–26. http://dx.doi.org/10.2215/cjn.10881012.

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Ooi, Esther M. M., Gerald F. Watts, Maryam S. Farvid, et al. "High-density Lipoprotein Apolipoprotein A-I Kinetics in Obesity." Obesity Research 13, no. 6 (2005): 1008–16. http://dx.doi.org/10.1038/oby.2005.118.

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Chi-Sun, Wang, Jean A. Hartsuck, and Dieter Weiser. "Kinetics of acylglycerol hydrolysis by human milk lipoprotein lipase." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 837, no. 2 (1985): 111–18. http://dx.doi.org/10.1016/0005-2760(85)90233-4.

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Levels, J. H. M., J. A. Marquart, P. R. Abraham, et al. "Lipopolysaccharide Is Transferred from High-Density to Low-Density Lipoproteins by Lipopolysaccharide-Binding Protein and Phospholipid Transfer Protein." Infection and Immunity 73, no. 4 (2005): 2321–26. http://dx.doi.org/10.1128/iai.73.4.2321-2326.2005.

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ABSTRACT Lipopolysaccharide (LPS), the major outer membrane component of gram-negative bacteria, is a potent endotoxin that triggers cytokine-mediated systemic inflammatory responses in the host. Plasma lipoproteins are capable of LPS sequestration, thereby attenuating the host response to infection, but ensuing dyslipidemia severely compromises this host defense mechanism. We have recently reported that Escherichia coli J5 and Re595 LPS chemotypes that contain relatively short O-antigen polysaccharide side chains are efficiently redistributed from high-density lipoproteins (HDL) to other lipoprotein subclasses in normal human whole blood (ex vivo). In this study, we examined the role of the acute-phase proteins LPS-binding protein (LBP) and phospholipid transfer protein (PLTP) in this process. By the use of isolated HDL containing fluorescent J5 LPS, the redistribution of endotoxin among the major lipoprotein subclasses in a model system was determined by gel permeation chromatography. The kinetics of LPS and lipid particle interactions were determined by using Biacore analysis. LBP and PLTP were found to transfer LPS from HDL predominantly to low-density lipoproteins (LDL), in a time- and dose-dependent manner, to induce remodeling of HDL into two subpopulations as a consequence of the LPS transfer and to enhance the steady-state association of LDL with HDL in a dose-dependent fashion. The presence of LPS on HDL further enhanced LBP-dependent interactions of LDL with HDL and increased the stability of the HDL-LDL complexes. We postulate that HDL remodeling induced by LBP- and PLTP-mediated LPS transfer may contribute to the plasma lipoprotein dyslipidemia characteristic of the acute-phase response to infection.

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Warwick, G. L., C. J. Packard, L. Murray, et al. "Effect of simvastatin on plasma lipid and lipoprotein concentrations and low-density lipoprotein metabolism in the nephrotic syndrome." Clinical Science 82, no. 6 (1992): 701–8. http://dx.doi.org/10.1042/cs0820701.

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1. The effect of inhibiting the rate-limiting enzyme (3-hydroxy-3-methylglutaryl-CoA reductase, EC 1.1.1.88) in cholesterol synthesis on plasma lipid and lipoprotein concentrations was investigated in 16 patients with primary glomerular disease, heavy proteinuria, well-preserved renal function and hypercholesterolaemia. 2. Detailed studies of low-density lipoprotein metabolism were performed on eight patients before and after 12 weeks of simvastatin therapy. Radioiodinated tracers were used to quantify the fractional catabolic rate of low-density lipoprotein by apolipoprotein B/E receptors and alternative pathways. 3. Simvastatin produced consistent reductions in total plasma cholesterol concentration (median 36.9%), plasma low-density lipoprotein-cholesterol concentration (43.6%) and apolipoprotein B pool size (29.9%). 4. In contrast, the changes in kinetic parameters of low-density lipoprotein metabolism showed no clear pattern. Although an increase in the receptor-mediated catabolism of low-density lipoprotein was demonstrated in five patients, no change or a slight decrease was seen in three patients. Production rates were not significantly altered, although there was a slight decrease in the median value (from 12.4 to 9.7 mg day−1 kg−1). Plasma lathosterol concentration was reduced in all eight patients (range 34–71%), indirectly confirming significant inhibition of cholesterol synthesis. 5. These results suggest that, as in patients with primary moderate hyperlipidaemia, the significant cholesterol-lowering effect of 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors in the nephrotic syndrome is accompanied by variable changes in lipoprotein metabolism. The reasons for this heterogeneous response are unclear. This reflects our limited understanding of the metabolic basis of nephrotic hyperlipidaemia and the relationship between hepatic sterol synthesis and plasma lipoprotein kinetics.

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Ma, Louis, Dick C. Chan, Esther M. M. Ooi, Santica M. Marcovina, P. Hugh R. Barrett, and Gerald F. Watts. "Apolipoprotein(a) Kinetics in Statin-Treated Patients With Elevated Plasma Lipoprotein(a) Concentration." Journal of Clinical Endocrinology & Metabolism 104, no. 12 (2019): 6247–55. http://dx.doi.org/10.1210/jc.2019-01382.

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Abstract Background Lipoprotein(a) [Lp(a)] is a low-density lipoprotein‒like particle containing apolipoprotein(a) [apo(a)]. Patients with elevated Lp(a), even when treated with statins, are at increased risk of cardiovascular disease. We investigated the kinetic basis for elevated Lp(a) in these patients. Objectives Apo(a) production rate (PR) and fractional catabolic rate (FCR) were compared between statin-treated patients with and without elevated Lp(a). Methods The kinetics of apo(a) were investigated in 14 patients with elevated Lp(a) and 15 patients with normal Lp(a) levels matched for age, sex, and body mass index using stable isotope techniques and compartmental modeling. All 29 patients were on background statin treatment. Plasma apo(a) concentration was measured using liquid chromatography–mass spectrometry. Results The plasma concentration and PR of apo(a) were significantly higher in patients with elevated Lp(a) than in patients with normal Lp(a) concentration (all P < 0.01). The FCR of apo(a) was not significantly different between the groups. In univariate analysis, plasma concentration of apo(a) was significantly associated with apo(a) PR in both patient groups (r = 0.699 and r = 0.949, respectively; all P < 0.01). There was no significant association between plasma apo(a) concentration and FCR in either of the groups (r = 0.160 and r = −0.137, respectively). Conclusion Elevated plasma Lp(a) concentration is a consequence of increased hepatic production of Lp(a) particles in these patients. Our findings provide a kinetic rationale for the use of therapies that target the synthesis of apo(a) and production of Lp(a) particles in patients with elevated Lp(a).

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Chrisoulidou, Alexandra, Eleni Kousta, Soundararajan Venkatesan, et al. "Very—low-density lipoprotein apolipoprotein B100 kinetics in adult hypopituitarism." Metabolism 48, no. 8 (1999): 1057–62. http://dx.doi.org/10.1016/s0026-0495(99)90206-8.

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Berglund, Martin, Martin Adiels, Marja-Riitta Taskinen, Jan Borén, and Bernt Wennberg. "Improved Estimation of Human Lipoprotein Kinetics with Mixed Effects Models." PLOS ONE 10, no. 9 (2015): e0138538. http://dx.doi.org/10.1371/journal.pone.0138538.

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Fuh, Martin M. T., C.-Ming Lee, Chii-Y. Jeng, et al. "Effect of chronic renal failure on high-density lipoprotein kinetics." Kidney International 37, no. 5 (1990): 1295–300. http://dx.doi.org/10.1038/ki.1990.114.

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Bagby, G. J., C. B. Corll, and R. R. Martinez. "Triacylglycerol kinetics in endotoxic rats with suppressed lipoprotein lipase activity." American Journal of Physiology-Endocrinology and Metabolism 253, no. 1 (1987): E59—E64. http://dx.doi.org/10.1152/ajpendo.1987.253.1.e59.

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Hypertriglyceridemia observed in animals after bacterial endotoxin administration and some forms of sepsis can result from increased hepatic triacylglycerol (TG) output or decreased TG clearance by extrahepatic tissues. To differentiate between these two possibilities, TG and free fatty acid (FFA) kinetics were determined in control and endotoxin-injected (0.1–0.5 mg/100 g) rats 18 h after treatment. Plasma TG and FFA kinetics were assessed by a constant intravenous infusion with [9,10-3H]palmitate-labeled very low-density lipoprotein and [1–14C]palmitate bound to albumin, respectively. In addition, lipoprotein lipase (LPL) activity was determined in heart, skeletal muscle, and adipose tissue as well as in postheparin plasma of functionally hepatectomized, adrenalectomized, and gonadectomized rats. Plasma FFA acid concentrations were slightly increased in endotoxin-treated rats but their turnover did not differ from control. Endotoxin-treated rats had a threefold increase in plasma TG concentrations and decreased heart, skeletal muscle, and post-heparin plasma LPL activity. Plasma TG turnover was decreased, indicating that hypertriglyceridemia was not due to an increased TG output by the liver. Instead, the endotoxin-induced increase in plasma TG concentration was a consequence of the 80% reduction in TG metabolic clearance rate. Thus, suppression of LPL activity in endotoxic animals impairs TG clearance resulting in hypertriglyceridemia. Furthermore, endotoxin administration reduced the delivery of TG-FFA to extrahepatic tissues because hepatic synthesis and secretion of TG from plasma FFA was decreased and LPL activity was suppressed.

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Schaefer, Juergen R., Daniel J. Rader, and H. Bryan Brewer. "Investigation of lipoprotein kinetics using endogenous labeling with stable isotopes." Current Opinion in Lipidology 3, no. 3 (1992): 227–32. http://dx.doi.org/10.1097/00041433-199206000-00011.

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Tselmin, Sergey, Gabriele Mueller, Ulrich Julius, and Bernd Hohenstein. "Kinetics of lipoprotein(a) (Lp(a)) under lipoprotein apheresis (La) in patients with severe hyperlp(a)emia." Atherosclerosis 263 (August 2017): e209. http://dx.doi.org/10.1016/j.atherosclerosis.2017.06.676.

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Melville, David, Amita Gorur, and Randy Schekman. "Fatty-acid binding protein 5 modulates the SAR1 GTPase cycle and enhances budding of large COPII cargoes." Molecular Biology of the Cell 30, no. 3 (2019): 387–99. http://dx.doi.org/10.1091/mbc.e18-09-0548.

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COPII-coated vesicles are the primary mediators of ER-to-Golgi trafficking. Sar1, one of the five core COPII components, is a highly conserved small GTPase, which, upon GTP binding, recruits the other COPII proteins to the ER membrane. It has been hypothesized that the changes in the kinetics of SAR1 GTPase may allow for the secretion of large cargoes. Here we developed a cell-free assay to recapitulate COPII-dependent budding of large lipoprotein cargoes from the ER. We identified fatty-acid binding protein 5 (FABP5) as an enhancer of this budding process. We found that FABP5 promotes the budding of particles ∼150 nm in diameter and modulates the kinetics of the SAR1 GTPase cycle. We further found that FABP5 enhances the trafficking of lipoproteins and of other cargoes, including collagen. These data identify a novel regulator of SAR1 GTPase activity and highlight the importance of this activity for trafficking of large cargoes.

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Hooper, Amanda J., Liesl Heeks, Ken Robertson, et al. "Lipoprotein Metabolism in APOB L343V Familial Hypobetalipoproteinemia." Journal of Clinical Endocrinology & Metabolism 100, no. 11 (2015): E1484—E1490. http://dx.doi.org/10.1210/jc.2015-2731.

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Context: Familial hypobetalipoproteinemia (FHBL) is a codominant disorder of lipoprotein metabolism characterized by decreased plasma concentrations of low-density lipoprotein (LDL)-cholesterol and apolipoprotein B (apoB). Objective: The objective was to examine the effect of heterozygous APOB L343V FHBL on postprandial triglyceride-rich lipoprotein (TRL) and fasting lipoprotein metabolism. Methods: Plasma incremental area under the curve apoB-48 and apoB-48 kinetics were determined after ingestion of a standardized oral fat load using compartmental modeling. Very low-density lipoprotein (VLDL)-, intermediate-density lipoprotein (IDL)-, and LDL-apoB kinetics were determined in the fasting state using stable isotope methods and compartmental modeling. Results: The postprandial incremental area under the curve (0–10 h) in FHBL subjects (n = 3) was lower for large TRL-triglyceride (−77%; P &lt; .0001), small TRL-cholesterol (−83%; P &lt; .001), small TRL-triglyceride (−88%; P &lt; .001), and for plasma triglyceride (−70%; P &lt; .01) and apoB (−63%; P &lt; .0001) compared with controls. Compartmental analysis showed that apoB-48 production was lower (−91%; P &lt; .05) compared with controls. VLDL-apoB concentrations in FHBL subjects (n = 2) were lower by more than 75% compared with healthy, normolipidemic control subjects (P &lt; .01). The VLDL-apoB fractional catabolic rate (FCR) was more than 5-fold higher in the FHBL subjects (P = .07). ApoB production rates and IDL- and LDL-apoB FCRs were not different between FHBL subjects and controls. Conclusions: We conclude that when compared to controls, APOB L343V FHBL heterozygotes show lower TRL production with normal postprandial TRL particle clearance. In contrast, VLDL-apoB production was normal, whereas the FCR was higher in heterozygotes compared with lean control subjects. These mechanisms account for the marked hypolipidemic state observed in these FHBL subjects.

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BEAUDEUX, Jean-Louis, Monique GARDES-ALBERT, Jacques DELATTRE, Alain LEGRAND, François ROUSSELET та Jacqueline PEYNET. "Resistance of lipoprotein(a) to lipid peroxidation induced by oxygenated free radicals produced by γ radiolysis: a comparison with low-density lipoprotein". Biochemical Journal 314, № 1 (1996): 277–84. http://dx.doi.org/10.1042/bj3140277.

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Lipid peroxidation of lipoprotein(a) [Lp(a)] by defined oxygen-centred free radicals (O2-· /OH·, O2-·, O2-· /HO2·) produced by γ radiolysis was compared with that of paired samples of low-density lipoprotein (LDL). Lp(a) appeared to be more resistant to oxidation than LDL, as indicated by the kinetic study of four markers of lipid peroxidation: decrease in vitamin E, formation of conjugated dienes and aldehydic products, and modification of electrophoretic mobility. In contrast, similar kinetics of lipid peroxidation were obtained for LDL and Lp(a-), which is the lipoparticle issued following the reductive cleavage of apolipoprotein(a) from Lp(a), thus suggesting that the greater resistance of Lp(a) to lipid peroxidation was due to the presence of apolipoprotein(a). Lipid peroxidation of Lp(a) and LDL induced by peroxyl radicals, which were produced by an azo compound [2,2′-azobis-(2-amidinopropane)dihydrochloride], confirmed both the resistance of Lp(a) to lipid peroxidation and the propensity of Lp(a-) to exhibit a greater susceptibility to oxidation than intact Lp(a). Our findings also indicated that the high content of apolipoprotein(a) in N-acetylneuraminic acid residues was only partly responsible for the resistance of Lp(a) to oxidation.

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Magnoni, Leonardo, Eric Vaillancourt, and Jean-Michel Weber. "High resting triacylglycerol turnover of rainbow trout exceeds the energy requirements of endurance swimming." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 1 (2008): R309—R315. http://dx.doi.org/10.1152/ajpregu.00882.2007.

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Fish may use lipoproteins instead of albumin-bound fatty acids to fuel endurance exercise, but lipoprotein kinetics have never been measured in ectotherms. In vivo bolus injections of labeled very-low-density lipoproteins (3H-VLDL labeled in vivo from donor fish) and continuous infusions of Intralipid (3H-labeled artificial emulsion) were used to investigate the effects of prolonged exercise (6 h at 1.5 body length/s) and heparin (600 U/kg) on the turnover rate of circulating triacylglycerol (TAG) in rainbow trout. We hypothesized that swimming would stimulate TAG turnover rate to fuel working muscles and that heparin would reduce flux by releasing lipoprotein lipase (LPL) from endothelial cells. Results from both tracer methods show that the baseline TAG turnover rate of trout ranges from 24 to 49 μmol TAG·kg−1·min−1 and exceeds all values measured to date in endotherms. More important, this high resting turnover rate is not stimulated during swimming, because it can already cover several times the energy requirements of locomotion. The fact that heparin causes a 50% decrease in baseline TAG turnover rate suggests that fish LPL must be bound to the endothelium for normal tissue uptake of fatty acids supplied by lipoproteins, as in mammals. We propose that the high resting TAG turnover rate of rainbow trout could be needed by ectotherms for rapid restructuring of membrane phospholipids. The continuous tracer infusion method implemented here could be a versatile tool to investigate the potential role of lipoproteins in providing fatty acids for rapid homeoviscous adaptation.

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LASS, Achim, Jutta BELKNER, Hermann ESTERBAUER, and Hartmut KÜHN. "Lipoxygenase treatment render low-density lipoprotein susceptible to Cu2+-catalysed oxidation." Biochemical Journal 314, no. 2 (1996): 577–85. http://dx.doi.org/10.1042/bj3140577.

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Oxidative modification of low-density lipoprotein (LDL) has been implicated in foam-cell formation at all stages of atherosclerosis. Since transition metals and mammalian 15-lipoxygenases are capable of oxidizing LDL to its atherogenic form, a concerted action of these two catalysts in atherogenesis has been suggested. Cu2+-catalysed LDL oxidation is characterized by a kinetic lag period in which the lipophilic antioxidants are decomposed and by a complex mixture of unspecific oxidation products. We investigated the kinetics of the 15-lipoxygenase-catalysed oxygenation of LDL and found that the enzyme is capable of oxidizing LDL in the presence of the endogenous lipophilic antioxidants. In contrast with the Cu2+-catalysed reaction, no kinetic lag phase was detected. The pattern of products formed during short-term incubations was highly specific, with cholesterol-esterified (13S)-hydroperoxy-(9Z,11E)-octadecadienoic acid being the major product. However, after long-term incubations the product pattern was less specific. Preincubation with 15-lipoxygenase rendered human LDL more susceptible to Cu2+-catalysed oxidation as indicated by a dramatic shortening of the lag period. Addition of Cu2+ to lipoxygenase-treated LDL led to a steep decline in its antioxidant content and to a greatly reduced lag period. Interestingly, if normalized to a comparable hydroperoxide content, autoxidation and addition of exogenous hydroperoxy fatty acids both failed to overcome the lag period. The local peroxide concentrations in various LDL subcompartments will be discussed as a possible reason for this unexpected behaviour.

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Al-Shayji, Iqbal A. R., Muriel J. Caslake, and Jason M. R. Gill. "Effects of moderate exercise on VLDL1and Intralipid kinetics in overweight/obese middle-aged men." American Journal of Physiology-Endocrinology and Metabolism 302, no. 3 (2012): E349—E355. http://dx.doi.org/10.1152/ajpendo.00498.2011.

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Prior moderate exercise reduces plasma triglyceride (TG)-rich lipoprotein concentrations, mainly in the large very low-density lipoprotein (VLDL1) fraction, but the mechanism responsible is unclear. We investigated the effects of brisk walking on TG-rich lipoprotein kinetics using a novel method. Twelve overweight/obese middle-aged men underwent two kinetic studies, involving infusion of Intralipid to block VLDL1catabolism, in random order. On the afternoon prior to infusion, subjects either walked on a treadmill for 2 h at ∼50% maximal oxygen uptake or performed no exercise. Multiple blood samples were taken during and after infusion for separation of Intralipid (Sf400) and VLDL1(Sf60–400). VLDL1-TG and -apoB production rates were calculated from their linear rises during infusion; fractional catabolic rates (FCR) were calculated by dividing linear rises by fasting concentrations. Intralipid-TG FCR was determined from the postinfusion exponential decay. Exercise reduced fasting VLDL1-TG concentration by 30% ( P = 0.007) and increased TG enrichment of VLDL1particles [30% decrease in cholesteryl ester (CE)/TG ratio ( P = 0.007); 26% increase in TG/apoB ratio ( P = 0.059)]. Exercise also increased VLDL1-TG, VLDL1-apoB, and Intralipid-TG FCRs by 82, 146, and 43%, respectively (all P < 0.05), but had no significant effect on VLDL1-TG or -apoB production rates. The exercise-induced increase in VLDL1-apoB FCR correlated strongly with the exercise-induced changes in VLDL1CE/TG ( r = −0.659, r = 0.020) and TG/apoB ( r = 0.785, P = 0.002) ratios. Thus, exercise-induced reductions in VLDL1concentrations are mediated by increased catabolism, rather than reduced production, which may be facilitated by compositional changes to VLDL1particles that increase their affinity for clearance from the circulation.

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Vega, G. L., H. H. Hobbs, and S. M. Grundy. "Low density lipoprotein kinetics in a family having defective low density lipoprotein receptors in which hypercholesterolemia is suppressed." Arteriosclerosis and Thrombosis: A Journal of Vascular Biology 11, no. 3 (1991): 578–85. http://dx.doi.org/10.1161/01.atv.11.3.578.

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Lanza-Jacoby, S., and A. Tabares. "Triglyceride kinetics, tissue lipoprotein lipase, and liver lipogenesis in septic rats." American Journal of Physiology-Endocrinology and Metabolism 258, no. 4 (1990): E678—E685. http://dx.doi.org/10.1152/ajpendo.1990.258.4.e678.

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The mechanism for the development of hypertriglyceridemia during gram-negative sepsis was studied by examining liver production and clearance of very-low-density lipoprotein (VLDL) triglyceride (TG). To assess liver output and peripheral clearance the kinetics of VLDL-TG were determined by a constant iv infusion of [2-3H]glycerol-labeled VLDL. Clearance of VLDL-TG was also evaluated by measuring activities of lipoprotein lipase (LPL) in heart, soleus muscle, and adipose tissue from fasted control, fasted E. coli-treated, fed control, and fed E. coli-treated rats. Lewis inbred rats, 275-300 g, were made septic with 8 x 10(7) live E. coli colonies per 100 g body wt. Twenty-four hours after E. coli injection, serum TG, free fatty acids (FFA), and cholesterol of fasted E. coli-treated rats were elevated by 170, 76, and 16%, respectively. The elevation of serum TG may be attributed to the 67% decrease in clearance rate of VLDL-TG in fasted E. coli-treated rats compared with their fasted controls. The suppressed activities of LPL in adipose tissue, skeletal muscle, and heart were consistent with reduced clearance of TG. Secretion of VLDL-TG declined by 31% in livers of fasted E. coli-treated rats, which was accompanied by a twofold increase in the composition of liver TG. Rates of in vivo TG synthesis in livers of the fasted E. coli-treated rats were twofold higher than in those of fasted control rats. Decreased rate of TG appearance along with the increase in liver synthesis of TG contributed to the elevation of liver lipids in the fasted E. coli-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

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Gormsen, Lars C., Birgitte Nellemann, Lars P. Sørensen, Michael D. Jensen, Jens S. Christiansen, and Søren Nielsen. "Impact of body composition on very-low-density lipoprotein-triglycerides kinetics." American Journal of Physiology-Endocrinology and Metabolism 296, no. 1 (2009): E165—E173. http://dx.doi.org/10.1152/ajpendo.90675.2008.

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Upper body obese (UBO) subjects have greater cardiovascular disease risk than lower body obese (LBO) or lean subjects. Obesity is also associated with hypertriglyceridemia that may involve greater production and impaired removal of very-low-density lipoprotein (VLDL)-triglycerides (TG). In these studies, we assessed the impact of body composition on basal VLDL-TG production, VLDL-TG oxidation, and VLDL-TG storage. VLDL-TG kinetics were assessed in 10 UBO, 10 LBO, and 10 lean women using a bolus injection of [1-14C]VLDL-TG. VLDL-TG oxidation was measured by 14CO2 production (hyamine trapping) and VLDL-TG adipose tissue storage by fat biopsies. Insulin sensititvity was assessed by the hyperinsulinemic-euglycemic clamp technique and body composition by dual X-ray absorptiometry in combination with computed tomography. Hepatic VLDL-TG production was significantly greater in UBO than in lean women [(μmol/min) UBO: 64.8 (SD 40.0) vs. LBO: 42.5 (SD 25.6) vs. lean: 31.8 (SD 13.3), P = 0.04], whereas VLDL-TG oxidation was similar in the three groups and averaged 20% of resting energy expenditure [(μmol/min) UBO: 38.3 (SD 26.5) vs. LBO: 23.5 (SD 13.5) vs. lean: 21.1 (SD 9.7), P = 0.09]. In UBO women, more VLDL-TG was deposited in upper body subcutaneous fat [VLDL-TG redeposition in abdominal adipose tissue (μmol/min): UBO: 5.0 (SD 2.9) vs. LBO: 4.0 (SD 3.2) vs. lean: 1.3 (SD 1.0), ANOVA P = 0.01]; in LBO women, more VLDL-TG was deposited in femoral fat [VLDL-TG redeposition in femoral adipose tissue (μmol/min): UBO: 5.1 (SD 3.1) vs. LBO: 5.8 (SD 4.3) vs. lean: 2.3 (SD 1.5), ANOVA P = 0.04]. Only a small proportion of VLDL-TG (8–16%) was partitioned into redeposition in either group. We found that elevated VLDL-TG production without concomitant increased clearance via oxidation and adipose tissue redeposition contributes to hypertriglyceridemia in UBO women.

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Kazumi, Tsutomu, Mladen Vranic, Hanoch Bar-On та George Steiner. "Portal ν peripheral hyperinsulinemia and very low density lipoprotein triglyceride kinetics". Metabolism 35, № 11 (1986): 1024–28. http://dx.doi.org/10.1016/0026-0495(86)90038-7.

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Gogonea, Valentin, Judith Peters, Gary S. Gerstenecker, et al. "Protein Backbone and Average Particle Dynamics in Reconstituted Discoidal and Spherical HDL Probed by Hydrogen Deuterium Exchange and Elastic Incoherent Neutron Scattering." Biomolecules 10, no. 1 (2020): 121. http://dx.doi.org/10.3390/biom10010121.

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Lipoproteins are supramolecular assemblies of proteins and lipids with dynamic characteristics critically linked to their biological functions as plasma lipid transporters and lipid exchangers. Among them, spherical high-density lipoproteins are the most abundant forms of high-density lipoprotein (HDL) in human plasma, active participants in reverse cholesterol transport, and associated with reduced development of atherosclerosis. Here, we employed elastic incoherent neutron scattering (EINS) and hydrogen-deuterium exchange mass spectrometry (HDX-MS) to determine the average particle dynamics and protein backbone local mobility of physiologically competent discoidal and spherical HDL particles reconstituted with human apolipoprotein A-I (apoA-I). Our EINS measurements indicated that discoidal HDL was more dynamic than spherical HDL at ambient temperatures, in agreement with their lipid-protein composition. Combining small-angle neutron scattering (SANS) with contrast variation and MS cross-linking, we showed earlier that the most likely organization of the three apolipoprotein A-I (apoA-I) chains in spherical HDL is a combination of a hairpin monomer and a helical antiparallel dimer. Here, we corroborated those findings with kinetic studies, employing hydrogen-deuterium exchange mass spectrometry (HDX-MS). Many overlapping apoA-I digested peptides exhibited bimodal HDX kinetics behavior, suggesting that apoA-I regions with the same amino acid composition located on different apoA-I chains had different conformations and/or interaction environments.

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Catanese, Maria Teresa, Helenia Ansuini, Rita Graziani, et al. "Role of Scavenger Receptor Class B Type I in Hepatitis C Virus Entry: Kinetics and Molecular Determinants." Journal of Virology 84, no. 1 (2009): 34–43. http://dx.doi.org/10.1128/jvi.02199-08.

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ABSTRACT Scavenger receptor class B type I (SR-BI) is an essential receptor for hepatitis C virus (HCV) and a cell surface high-density-lipoprotein (HDL) receptor. The mechanism of SR-BI-mediated HCV entry, however, is not clearly understood, and the specific protein determinants required for the recognition of the virus envelope are not known. HCV infection is strictly linked to lipoprotein metabolism, and HCV virions may initially interact with SR-BI through associated lipoproteins before subsequent direct interactions of the viral glycoproteins with SR-BI occur. The kinetics of inhibition of cell culture-derived HCV (HCVcc) infection with an anti-SR-BI monoclonal antibody imply that the recognition of SR-BI by HCV is an early event of the infection process. Swapping and single-substitution mutants between mouse and human SR-BI sequences showed reduced binding to the recombinant soluble E2 (sE2) envelope glycoprotein, thus suggesting that the SR-BI interaction with the HCV envelope is likely to involve species-specific protein elements. Most importantly, SR-BI mutants defective for sE2 binding, although retaining wild-type activity for receptor oligomerization and binding to the physiological ligand HDL, were impaired in their ability to fully restore HCVcc infectivity when transduced into an SR-BI-knocked-down Huh-7.5 cell line. These findings suggest a specific and direct role for the identified residues in binding HCV and mediating virus entry. Moreover, the observation that different regions of SR-BI are involved in HCV and HDL binding supports the hypothesis that new therapeutic strategies aimed at interfering with virus/SR-BI recognition are feasible.

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Castro Cabezas, M., C. Verseyden, S. Meijssen, H. Jansen, and D. W. Erkelens. "Effects of Atorvastatin on the Clearance of Triglyceride-Rich Lipoproteins in Familial Combined Hyperlipidemia." Journal of Clinical Endocrinology & Metabolism 89, no. 12 (2004): 5972–80. http://dx.doi.org/10.1210/jc.2003-031329.

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Abstract Familial combined hyperlipidemia (FCHL) patients have an impaired catabolism of postprandial triglyceride (TG)-rich lipoproteins (TRLs). We investigated whether atorvastatin corrects the delayed clearance of large TRLs in FCHL by evaluating the acute clearance of Intralipid (10%) and TRLs after oral fat-loading tests. Sixteen matched controls were included. Atorvastatin reduced fasting plasma TG (from 3.6 ± 0.4 to 2.5 ± 0.3 mm; mean ± sem) without major effects on fasting apolipoprotein B48 (apoB48) and apoB100 in large TRLs. Atorvastatin significantly reduced fasting intermediate density lipoprotein (Svedberg flotation, 12–20)-apoB100 concentrations. After Intralipid, TG in plasma and TRL showed similar kinetics in FCHL before and after atorvastatin treatment, although compared with controls, the clearance of large TRLs was only significantly slower in untreated FCHL, suggesting an improvement by atorvastatin. Investigated with oral fat-loading tests, the clearance of very low density lipoprotein (Sf20–60)-apoB100 improved by 24%, without major changes in the other fractions. The most striking effects of atorvastatin on postprandial lipemia in FCHL were on hepatic TRL, without major improvements on intestinal TRLs. Fasting plasma TG should be reduced more aggressively in FCHL to overcome the lipolytic disturbance causing delayed clearance of postprandial TRLs.

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Magkos, Faidon, Bruce W. Patterson, and Bettina Mittendorfer. "No effect of menstrual cycle phase on basal very-low-density lipoprotein triglyceride and apolipoprotein B-100 kinetics." American Journal of Physiology-Endocrinology and Metabolism 291, no. 6 (2006): E1243—E1249. http://dx.doi.org/10.1152/ajpendo.00246.2006.

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Dyslipidemia, manifested by increased plasma triglyceride (TG), increased total and LDL-cholesterol concentrations and decreased HDL-cholesterol concentration, is an important risk factor for cardiovascular disease. Premenopausal women have a less atherogenic plasma lipid profile and a lower risk of cardiovascular disease than men, but this female advantage disappears after menopause. This suggests that female sex steroids affect lipoprotein metabolism. The impact of variations in the availability of ovarian hormones during the menstrual cycle on lipoprotein metabolism is not known. We therefore investigated whether very-low-density lipoprotein (VLDL)-TG and VLDL-apolipoprotein B-100 (apoB-100) kinetics are different during the follicular (FP) and luteal phases (LP) of the menstrual cycle. We studied seven healthy, premenopausal women (age 27 ± 2 yr, BMI 25 ± 2 kg/m2) once during FP and once during LP. We measured VLDL-TG, VLDL-apoB-100, and plasma free fatty acid (FFA) kinetics by using stable isotope-labeled tracers, VLDL subclass profile by nuclear magnetic resonance spectroscopy, whole body fat oxidation by indirect calorimetry, and the plasma concentrations of lipoprotein lipase (LPL) and hepatic lipase (HL) by ELISA. VLDL-TG and VLDL-apoB-100 concentrations in plasma, VLDL-TG and VLDL-apoB-100 secretion rates and mean residence times, VLDL subclass distribution, FFA concentration and rate of appearance in plasma, whole body substrate oxidation, and LPL and HL concentrations in plasma were not different during the FP and the LP. We conclude that VLDL-TG and VLDL-apoB-100 metabolism is not affected by menstrual cycle phase.

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MACPHEE, Colin H., Kitty E. MOORES, Helen F. BOYD, et al. "Lipoprotein-associated phospholipase A2, platelet-activating factor acetylhydrolase, generates two bioactive products during the oxidation of low-density lipoprotein: use of a novel inhibitor." Biochemical Journal 338, no. 2 (1999): 479–87. http://dx.doi.org/10.1042/bj3380479.

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A novel and potent azetidinone inhibitor of the lipoprotein-associated phospholipase A2 (Lp-PLA2), i.e. platelet-activating factor acetylhydrolase, is described for the first time. This inhibitor, SB-222657 (Ki = 40±3 nM, kobs/[I] = 6.6×105 M-1·s-1), is inactive against paraoxonase, is a poor inhibitor of lecithin:cholesterol acyltransferase and has been used to investigate the role of Lp-PLA2 in the oxidative modification of lipoproteins. Although pretreatment with SB-222657 did not affect the kinetics of low-density lipoprotein (LDL) oxidation by Cu2+ or an azo free-radical generator as determined by assay of lipid hydroperoxides (LOOHs), conjugated dienes and thiobarbituric acid-reacting substances, in both cases it inhibited the elevation in lysophosphatidylcholine content. Moreover, the significantly increased monocyte chemoattractant activity found in a non-esterified fatty acid fraction from LDL oxidized by Cu2+ was also prevented by pretreatment with SB-222657, with an IC50 value of 5.0±0.4 nM. The less potent diastereoisomer of SB-222657, SB-223777 (Ki = 6.3±0.5 µM, kobs/[I] = 1.6×104 M-1·s-1), was found to be significantly less active in both assays. Thus, in addition to generating lysophosphatidylcholine, a known biologically active lipid, these results demonstrate that Lp-PLA2 is capable of generating oxidized non-esterified fatty acid moieties that are also bioactive. These findings are consistent with our proposal that Lp-PLA2 has a predominantly pro-inflammatory role in atherogenesis. Finally, similar studies have demonstrated that a different situation exists during the oxidation of high-density lipoprotein, with enzyme(s) other than Lp-PLA2 apparently being responsible for generating lysophosphatidylcholine.

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Watts, Gerald F., Juying Ji, Dick C. Chan, et al. "Relationships between changes in plasma lipid transfer proteins and apolipoprotein B-100 kinetics during fenofibrate treatment in the metabolic syndrome." Clinical Science 111, no. 3 (2006): 193–99. http://dx.doi.org/10.1042/cs20060072.

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The aim of the present study was to investigate the association between changes in apoB (apolipoprotein B-100) kinetics and plasma PLTP (phospholipid transfer protein) and CETP (cholesteryl ester transfer protein) activities in men with MetS (the metabolic syndrome) treated with fenofibrate. Eleven men with MetS underwent a double-blind cross-over treatment with fenofibrate (200 mg/day) or placebo for 5 weeks. Compared with placebo, fenofibrate significantly increased the FCRs (fractional catabolic rates) of apoB in VLDL (very-low-density lipoprotein), IDL (intermediate-density lipoprotein) and LDL (low-density lipoprotein) (all P<0.01), with no significant reduction (−8%; P=0.131) in VLDL-apoB PR (production rate), but an almost significant increase (+15%, P=0.061) in LDL-apoB PR. Fenofibrate significantly lowered plasma TG [triacylglycerol (triglyceride); P<0.001], the VLDL-TG/apoB ratio (P=0.003) and CETP activity (P=0.004), but increased plasma HDL (high-density lipoprotein)-cholesterol concentration (P<0.001) and PLTP activity (P=0.03). The increase in PLTP activity was positively associated with the increase in both LDL-apoB FCR (r=0.641, P=0.034) and PR (r=0.625, P=0.040), and this was independent of the fall in plasma CETP activity and lathosterol level. The decrease in CETP activity was positively associated with the decrease in VLDL-apoB PR (r=0.615, P=0.044), but this association was not robust and not independent of changes in PLTP activity and lathosterol levels. Hence, in MetS, the effects of fenofibrate on plasma lipid transfer protein activities, especially PLTP activity, may partially explain the associated changes in apoB kinetics.

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Cortes, Charles W., Paul D. Thompson, Niall M. Moyna, et al. "Protein kinetics in stable heart failure patients." Journal of Applied Physiology 94, no. 1 (2003): 295–300. http://dx.doi.org/10.1152/japplphysiol.00654.2001.

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Heart failure (HF) is a slow progressive syndrome characterized by low cardiac output and peripheral metabolic, biochemical, and histological alterations. Protein loss and reduced protein turnover occur with aging, but the consequences of congestive HF (CHF) superimposed on the normal aging response are unknown. This study has two objectives: 1) to determine whether there was a difference between older age-matched controls and those with stable HF (i.e., ischemic pathology) in whole body protein turnover and 2) to determine whether protein metabolism in liver and skeletal muscle protein turnover is impacted by CHF. We measured the whole body protein synthesis rate with a U-15N-labeled algal protein hydrolysate in 10 patients with CHF and in 10 age-matched controls. Muscle fractional synthesis rate of lateral vastus muscle was determined with [U-13C]alanine on muscle biopsies obtained by a standard percutaneous needle biopsy technique. Fractional synthesis rates of five plasma proteins of hepatic origin (fibrinogen, complement C-3, ceruloplasmin, transferrin, and very low-density lipoprotein apoliprotein B-100) were determined by using2H5-labeled l-phenylalanine as tracer. Results showed that whole body protein synthesis rate was reduced in CHF patients (3.09 ± 0.19 vs. 2.25 ± 0.71 g protein · kg−1 · day−1, P < 0.05) as was muscle fractional synthesis rate (3.02 ± 0.58 vs. 1.33 ± 0.71%/day, P < 0.05) and very low-density lipoprotein apoliprotein B-100 (265 ± 25 vs. 197 ± 16%/day, P < 0.05). CHF patients were hyperinsulinemic (9.6 ± 3.1 vs. 47.0 ± 7.8 μU/ml, P < 0.01). The results were compared with those found with bed rest patients. In conclusion, protein turnover is depressed in CHF patients, and both skeletal muscle and liver are impacted. These results are similar to those found with bed rest, which suggests that inactivity is a factor in depressed protein metabolism.

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Lu, James, Norman A. Mazer, and Katrin Hübner. "Mathematical models of lipoprotein metabolism and kinetics: current status and future perspective." Clinical Lipidology 8, no. 5 (2013): 595–604. http://dx.doi.org/10.2217/clp.13.52.

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