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Статті в журналах з теми "Apolipoprotien C III"

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Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 29 січня 2023

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1

Puchois, P., C. Luley, and P. Alaupovic. "Comparison of four procedures for separating apolipoprotein A- and apolipoprotein B-containing lipoproteins in plasma." Clinical Chemistry 33, no. 9 (September 1, 1987): 1597–602. http://dx.doi.org/10.1093/clinchem/33.9.1597.

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Abstract Because lipoproteins containing apolipoprotein A (ApoA-I + ApoA-II) or apolipoprotein B (ApoB) seem to exert opposite effects as risk factors for coronary heart disease, we decided to determine the separability of these two major plasma lipoproteins by procedures originally designed to separate high-density from low- and very-low-density lipoproteins. The presumably ApoB-free lipoproteins isolated from normal plasma by (a) ultracentrifugation at d = 1.063; precipitation with (b) heparin-Mn2+ or (c) phosphotungstate-Mg2+; or (d) immunoprecipitation with antibodies to ApoB were characterized by quantifying cholesterol and apolipoproteins A-I, A-II, B, C-II, C-III, D, E, F, and Lp(a). ApoA- and ApoB-containing lipoproteins were completely separated only by immunoprecipitation with antibodies to ApoB. The ApoB-containing lipoproteins isolated by other procedures always contained 4% to 20% of total plasma ApoA-I and differed substantially from one another with respect to the content of some of the minor apolipoproteins. Measuring apolipoproteins was more reliable than measuring cholesterol for monitoring this separation and for expressing the concentrations of ApoA- and ApoB-containing lipoproteins.

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2

März, W., G. Schenk, and W. Gross. "Apolipoproteins C-II and C-III in serum quantified by zone immunoelectrophoresis." Clinical Chemistry 33, no. 5 (May 1, 1987): 664–69. http://dx.doi.org/10.1093/clinchem/33.5.664.

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Abstract Zone immunoelectrophoresis assays specific for apolipoprotein C-II and C-III have been developed. These simple, accurate, reproducible, and sensitive methods present valid alternatives to conventional immunoassays. In fasting normolipidemic men and women the concentrations of apolipoprotein C-II and C-III were 49 (SD 25) mg/L and 124 (SD 60) mg/L, respectively, with no sex-related differences for either apolipoprotein. The frequency distribution of apolipoprotein C-II was skewed to the right, whereas apolipoprotein C-III was bimodally distributed. Concentrations of each apolipoprotein correlated well with one another and with that of serum triglycerides, but there was virtually no correlation between the apolipoprotein C-II to C-III mass ratio and the concentration of triglycerides. Apolipoprotein C-III, but not apolipoprotein C-II, was statistically associated with total cholesterol.

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3

Visvikis, S., M. F. Dumon, J. Steinmetz, T. Manabe, M. M. Galteau, M. Clerc, and G. Siest. "Plasma apolipoproteins in Tangier disease, as studied with two-dimensional electrophoresis." Clinical Chemistry 33, no. 1 (January 1, 1987): 120–22. http://dx.doi.org/10.1093/clinchem/33.1.120.

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Abstract Tangier disease is characterized by a deficiency of high-density lipoproteins and of their major protein constituent, apolipoprotein (apo) A-I. We used high-resolution two-dimensional electrophoresis to examine the principal plasma apolipoproteins (A-I, A-II, A-IV, E, C-II, and C-III) of three persons with Tangier disease, one homozygous patient and his two heterozygous children, comparing the patterns with those for healthy subjects. Characteristic abnormalities were found in the distribution of the isoproteins of apo A-I, there being a normal concentration of pro apo A-I but dramatically decreased concentrations of the other apo A-I isoproteins. We also found hitherto-undescribed polypeptide abnormalities in apo C-III: sialylated and nonsialylated forms of apo C-III appear as double spots having the same isoelectric points but different molecular masses. No other substantial difference was detected in the polypeptide distribution of the other plasma apolipoproteins.

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4

Hata, M., T. Ito, and K. Ohwada. "Kinetic analysis of apolipoproteins in postprandial hypertriglyceridaemia rabbits." Laboratory Animals 43, no. 2 (April 2009): 174–81. http://dx.doi.org/10.1258/la.2008.007004.

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The postprandial hypertriglyceridaemia (PHT) rabbit, developed as a new animal model of metabolic syndrome, is characterized by PHT, central obesity and glucose intolerance. For detailed investigation of lipid metabolism characteristics in PHT rabbit, the plasma levels of apolipoproteins A-I, B, C-II, C-III and E were measured. Movements of apolipoproteins B100 and B48 were investigated using sodium dodecyl sulphate–polyacrylamide gel electrophoresis to determine whether postprandially increased triglyceride is exogenous or endogenous. The level of apolipoproteins A-I, B, C-II and E were increased in PHT rabbit after feeding. Apolipoproteins B100 and B48 were detected in the plasma fraction of d < 1.006 g/mL of the PHT rabbit. The postprandial increase in apolipoprotein B in the PHT rabbit reflects a numerical increase in lipoprotein particles in the blood; the increase in apolipoproteins C-II and E suggests some disturbance in lipoprotein catabolism. Apolipoprotein B48 was detected postprandially in PHT rabbits. These results suggest that delayed catabolism of exogenous lipids caused the retention of chylomicron remnants in the blood. Results also suggest that activities of the lipolytic enzyme lipoprotein lipase and hepatic triglyceride lipase were deficient and that the hepatic uptake of exogenous lipoproteins was delayed in the PHT rabbit. Especially, for examining remnant hyperlipoproteinaemia in humans, PHT rabbit is an excellent animal model for hypertriglyceridaemia research.

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5

Miller, Michael. "Apolipoprotein C-III." Arteriosclerosis, Thrombosis, and Vascular Biology 37, no. 6 (June 2017): 1013–14. http://dx.doi.org/10.1161/atvbaha.117.309493.

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6

Huff, Murray W., and Robert A. Hegele. "Apolipoprotein C-III." Circulation Research 112, no. 11 (May 24, 2013): 1405–8. http://dx.doi.org/10.1161/circresaha.113.301464.

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7

Kohan, Alison B. "Apolipoprotein C-III." Current Opinion in Endocrinology & Diabetes and Obesity 22, no. 2 (April 2015): 119–25. http://dx.doi.org/10.1097/med.0000000000000136.

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8

Wang, Wenyu, Piers Blackett, Sohail Khan, and Elisa Lee. "Apolipoproteins A-I, B, and C-III and Obesity in Young Adult Cherokee." Journal of Lipids 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/8236325.

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Since young adult Cherokee are at increased risk for both diabetes and cardiovascular disease, we assessed association of apolipoproteins (A-I, B, and C-III in non-HDL and HDL) with obesity and related risk factors. Obese participants (BMI ≥ 30) aged 20–40 years (n=476) were studied. Metabolically healthy obese (MHO) individuals were defined as not having any of four components of the ATP-III metabolic syndrome after exclusion of waist circumference, and obese participants not being MHO were defined as metabolically abnormal obese (MAO). Associations were evaluated by correlation and regression modeling. Obesity measures, blood pressure, insulin resistance, lipids, and apolipoproteins were significantly different between groups except for total cholesterol, LDL-C, and HDL-apoC-III. Apolipoproteins were not correlated with obesity measures with the exception of apoA-I with waist and the waist : height ratio. In a logistic regression model apoA-I and the apoB : apoA-I ratio were significantly selected for identifying those being MHO, and the result (C-statistic = 0.902) indicated that apoA-I and the apoB : apoA-I ratio can be used to identify a subgroup of obese individuals with a significantly less atherogenic lipid and apolipoprotein profile, particularly in obese Cherokee men in whom MHO is more likely.

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9

Huet, G., M. C. Dieu, A. Martin, G. Grard, J. M. Bard, P. Fossati, and P. Degand. "Heterozygous hypobetalipoproteinemia with fasting chylomicronemia." Clinical Chemistry 37, no. 2 (February 1, 1991): 296–300. http://dx.doi.org/10.1093/clinchem/37.2.0296.

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Abstract We describe a disorder in which low-density lipoprotein (LDL)-cholesterol and apolipoprotein B are in low concentration (0.47 mmol/L and 0.28 g/L, respectively) and chylomicrons are still present in plasma after an 18-h fast. The d less than 1.006 fraction was isolated by flotation ultracentrifugation and the apolipoproteins were analyzed by electrophoresis, immunoblotting with anti-apolipoprotein B-100 antiserum, and isoelectric focusing. In the d less than 1.006 fraction of the fasting serum, we found an apolipoprotein B form with the same apparent molecular mass as apolipoprotein B-48 and similar in amount to apolipoprotein B-100 (respective percentages, 46% and 54%). The monosialylated form of the apolipoprotein C-III was severely decreased. After an oral fat load, the repartition of the two species of apolipoprotein B did not change greatly (respective percentages, 60% and 40%), and the concentration of serum triglyceride increased only from 1.20 to 1.65 mmol/L.

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10

Wang, C. S., W. J. McConathy, H. U. Kloer, and P. Alaupovic. "Modulation of lipoprotein lipase activity by apolipoproteins. Effect of apolipoprotein C-III." Journal of Clinical Investigation 75, no. 2 (February 1, 1985): 384–90. http://dx.doi.org/10.1172/jci111711.

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11

Muhtaseb, Najah Al, Abdul Razak Al Yousuf, and J. S. Bajaj. "Apolipoprotein A-I, A-II, B, C-II, and C-III in Children with Insulin-dependent Diabetes Mellitus." Pediatrics 89, no. 5 (May 1, 1992): 936–41. http://dx.doi.org/10.1542/peds.89.5.936.

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This study was conducted to determine whether changes in the levels of plasma apolipoproteins (apo) A-I, A-II, B, C-II, and C-III, along with cholesterol and triglycerides, could provide additional information on these parameters in relation to the control of glycemia. Plasma and lipoprotein lipids and apolipoprotein levels were measured in 123 insulin-dependent diabetic childern (4- to 12-years-old), classified into good, fair, and poor diabetic control based on HbAlc and fructosamine levels, and in 62 comparable healthy controls. Total cholesterol, very low density lipoprotein cholesterol, and low density lipoprotein cholesterol, as well as total triglycenides, very low density lipoprotein, low density lipoprotein, and high density lipoprotein (HDL) triglycerides, and apo B and apo C-III were increased significantly in children with fair and poor diabetic control. While in diabetic children with good control, only very low density lipoprotein cholesterol was elevated significantly compared with healthy control subjects. Conversely, the levels of cholesterol in HDL, HDL2, HDL3, and apo A-I were decreased significantly in the three diabetic groups, but apo A-II and apo C-II did not change. We conclude that in children with insulin-dependent diabetes mellitus, abnormalities in plasma lipid, lipoprotein, and apolipoprotein levels occur, the extent of which depends on the degree (extent) of glycemic control (the poorer the control the more substantial the abnormality). We suggest that measurement of apo C-III level along with apo B and apo A-I in these patients may be a sensitive indicator to alterations in glycemic control.

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12

Blanchard, Valentin, Damien Garçon, Catherine Jaunet, Kevin Chemello, Stéphanie Billon-Crossouard, Audrey Aguesse, Aya Garfa, et al. "A high-throughput mass spectrometry-based assay for large-scale profiling of circulating human apolipoproteins." Journal of Lipid Research 61, no. 7 (May 13, 2020): 1128–39. http://dx.doi.org/10.1194/jlr.d120000835.

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Apolipoproteins govern lipoprotein metabolism and are promising biomarkers of metabolic and cardiovascular diseases. Unlike immunoassays, MS enables the quantification and phenotyping of multiple apolipoproteins. Hence, here, we aimed to develop a LC-MS/MS assay that can simultaneously quantitate 18 human apolipoproteins [A-I, A-II, A-IV, A-V, B48, B100, C-I, C-II, C-III, C-IV, D, E, F, H, J, L1, M, and (a)] and determined apoE, apoL1, and apo(a) phenotypes in human plasma and serum samples. The plasma and serum apolipoproteins were trypsin digested through an optimized procedure and peptides were extracted and analyzed by LC-MS/MS. The method was validated according to standard guidelines in samples spiked with known peptide amounts. The LC-MS/MS results were compared with those obtained with other techniques, and reproducibility, dilution effects, and stabilities were also assessed. Peptide markers were successfully selected for targeted apolipoprotein quantification and phenotyping. After optimization, the assay was validated for linearity, lower limits of quantification, accuracy (biases: –14.8% to 12.1%), intra-assay variability [coefficients of variation (CVs): 1.5–14.2%], and inter-assay repeatability (CVs: 4.1–14.3%). Bland-Altman plots indicated no major statistically significant differences between LC-MS/MS and other techniques. The LC-MS/MS results were reproducible over five repeated experiments (CVs: 1.8–13.7%), and we identified marked differences among the plasma and serum samples. The LC-MS/MS assay developed here is rapid, requires only small sampling volumes, and incurs reasonable costs, thus making it amenable for a wide range of studies of apolipoprotein metabolism. We also highlight how this assay can be implemented in laboratories.

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13

Parsy, D., V. Clavey, C. Fievet, I. Kora, P. Duriez, and J. C. Fruchart. "Quantification of apolipoprotein C-III in serum by a noncompetitive immunoenzymometric assay." Clinical Chemistry 31, no. 10 (October 1, 1985): 1632–35. http://dx.doi.org/10.1093/clinchem/31.10.1632.

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Abstract We used a noncompetitive immunoenzymometric assay to measure the concentration of total apolipoprotein C-III in human sera. Affinity-purified antibodies to apolipoprotein C-III were adsorbed to the surface of microtiter plates. After washing, this solid-phase antibody was incubated with antigen (serum from fasting subjects), washed, and then incubated with peroxidase-labeled purified antibodies to apolipoprotein C-III. After a last washing, the bound label was assayed, providing a direct measurement of the antigen. Optimized technical conditions for the assay yielded assay CVs of 3.5 and 5.6% for within- and between-run precision, respectively. Analytical recovery of apolipoprotein C-III added to a serum was quantitative (97%). This noncompetitive assay can be used to measure apolipoprotein C-III in different lipoprotein fractions (very-low or high-density fractions) and yields values that compare favorably with those obtained by electroimmunoassay (r = 0.94). The assay offers several advantages over existing techniques--sensitivity, specificity, simplicity, and no use of radioisotopes--and hyperlipemic samples can be used.

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14

Zielińska, A., E. Zielinska, J. Wroński, J. Natorska, A. Paradowska-Gorycka, and P. Głuszko. "AB0083 RELATIONSHIP BETWEEN APOLIPOPROTEIN C-III AND ACTIVATED FACTOR VII-ANTITHROMBIN COMPLEXES IN PATIENTS WITH RHEUMATOID ARTHRITIS AND PSORIATIC ARTHRITIS." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 1173.2–1173. http://dx.doi.org/10.1136/annrheumdis-2022-eular.3547.

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BackgroundBoth rheumatoid arthritis (RA) and psoriatic arthritis (PsA) are associated with increased cardiovascular risk and thrombosis. Alterations in plasma lipids levels, including apolipoproteins are recognized as the important risk factors of cardiovascular disorders. Activated Factor VII -anti- Thrombin complex (FVIIa-AT) is a marker of the extrinsic coagulation cascade activation, the pathway accelerated by interaction with plasma apolipoprotein C-III (Apo-CIII) (1).ObjectivesTo investigate the associations between plasma FVIIa-AT concentration, lipid profile including apolipoprotein CIII, and markers of disease activity in patients with RA and PsA.Methods41 patients with RA, 38 with PsA, and 22 healthy controls, all not taking anticoagulant drugs were selected for the study. The lipid profile comprised triglycerides (TG), total cholesterol (TCh), low (LDL), and high-density lipoprotein (HDL). Serum levels of Apo C-III were measured using a Human ApoCIII ELISA kit CellBiolabs Inc.Austria. FVIIa–AT plasma concentrations were determined using ELISA test. C-reactive protein (CRP) level was measured using the immunoturbidimetric assay. All measurements were performed by a technician blinded to sample origin. The Mann-Whitney test and Kruskal Wallis tests were applied for intergroup comparisons, and correlations were assessed using Spearman’s rank tests, due to data non-normal distribution.ResultsThe highest serum levels of Apo C-III were found in RA patients (median: 99.9μg/ml, min.-max. 8.7–199) compared to PsA (30.86μg/ml, 12.4–125.8) and controls (9.5 μg/ml, 3.7–29.2), p<0.001. RA and PsA patients revealed higher FVIIa-AT plasma levels than controls (RA median 153.8 pM, min.—max. 57.0–397.8, PsA 157.6 pM, 64.9– 323.8 vs controls 104.5 pM, 68.9–150.9, p<0.001). In RA and PsA patients ApoCIII correlated positively with TG levels (r=0.35, p=0.027 and r=0.38, p=0.018 respectively). In all patients and controls, Apo C-III levels correlated positively with FVIIa-AT concentrations (r=0.45 p<0.001). No significant differences were found in the serum concentrations of TCh, LDL, HDL, TG, and CRP, between the groups of RA and PsA patients.ConclusionElevated concentrations of both, apolipoprotein CIII and activated FVII-AT complexes in rheumatic patients suggest associations between plasma lipoproteins and activation of coagulation cascade leading to a pro-thrombotic state in patients with RA and PsA. Further studies on these relationships are necessary taking into account various clinical conditions of patients and treatment.References[1]Martinelli N et al. Apolipoprotein C-III Strongly Correlates with Activated Factor VII-Anti-Thrombin Complex: An Additional Link between Plasma Lipids and Coagulation. Thromb Haemost. 2019; 119: 192-202.Disclosure of InterestsNone declared

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15

von Eckardstein, A., H. Holz, M. Sandkamp, W. Weng, H. Funke, and G. Assmann. "Apolipoprotein C-III(Lys58----Glu). Identification of an apolipoprotein C-III variant in a family with hyperalphalipoproteinemia." Journal of Clinical Investigation 87, no. 5 (May 1, 1991): 1724–31. http://dx.doi.org/10.1172/jci115190.

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16

Nicolay, Alain, Elise Lombard, Emmanuelle Arlotto, Vincent Saunier, Anne-Marie Lorec-Penet, Denis Lairon, and Henri Portugal. "Evaluation of new apolipoprotein C-II and apolipoprotein C-III automatized immunoturbidimetric kits." Clinical Biochemistry 39, no. 9 (September 2006): 935–41. http://dx.doi.org/10.1016/j.clinbiochem.2006.04.021.

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17

Dallinga-Thie, G. M., X. D. Bu, M. van Linde-Sibenius Trip, J. I. Rotter, A. J. Lusis, and T. W. de Bruin. "Apolipoprotein A-I/C-III/A-IV gene cluster in familial combined hyperlipidemia: effects on LDL-cholesterol and apolipoproteins B and C-III." Journal of Lipid Research 37, no. 1 (January 1996): 136–47. http://dx.doi.org/10.1016/s0022-2275(20)37642-2.

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18

TAKAMATSU, Shigeru, Yoko KAWAMURA, Ikuko OSANAI, Kei SATOH, Seitoku MIZUNO, and Bunichiro SHOJI. "Serum Apolipoprotein C-III in Cerebrovascular Disorders." Journal of Japan Atherosclerosis Society 13, no. 4 (1985): 923–29. http://dx.doi.org/10.5551/jat1973.13.4_923.

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19

van den Broek, Irene, Fred P. H. T. M. Romijn, Jan Nouta, Arnoud van der Laarse, Jan W. Drijfhout, Nico P. M. Smit, Yuri E. M. van der Burgt, and Christa M. Cobbaert. "Automated Multiplex LC-MS/MS Assay for Quantifying Serum Apolipoproteins A-I, B, C-I, C-II, C-III, and E with Qualitative Apolipoprotein E Phenotyping." Clinical Chemistry 62, no. 1 (January 1, 2016): 188–97. http://dx.doi.org/10.1373/clinchem.2015.246702.

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Abstract BACKGROUND Direct and calculated measures of lipoprotein fractions for cardiovascular risk assessment suffer from analytical inaccuracy in certain dyslipidemic and pathological states, most commonly hypertriglyceridemia. LC-MS/MS has proven suitable for multiplexed quantification and phenotyping of apolipoproteins. We developed and provisionally validated an automated assay for quantification of apolipoprotein (apo) A-I, B, C-I, C-II, C-III, and E and simultaneous qualitative assessment of apoE phenotypes. METHODS We used 5 value-assigned human serum pools for external calibration. Serum proteins were denatured, reduced, and alkylated according to standard mass spectrometry–based proteomics procedures. After trypsin digestion, peptides were analyzed by LC-MS/MS. For each peptide, we measured 2 transitions. We compared LC-MS/MS results to those obtained by an immunoturbidimetric assay or ELISA. RESULTS Intraassay CVs were 2.3%–5.5%, and total CVs were 2.5%–5.9%. The LC-MS/MS assay correlated (R = 0.975–0.995) with immunoturbidimetric assays with Conformité Européenne marking for apoA-I, apoB, apoC-II, apoC-III, and apoE in normotriglyceridemic (n = 54) and hypertriglyceridemic (n = 46) sera. Results were interchangeable for apoA-I ≤3.0 g/L (Deming slope 1.014) and for apoB-100 ≤1.8 g/L (Deming slope 1.016) and were traceable to higher-order standards. CONCLUSIONS The multiplex format provides an opportunity for new diagnostic and pathophysiologic insights into types of dyslipidemia and allows a more personalized approach for diagnosis and treatment of lipid abnormalities.

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20

Wolska, Anna, Larry Lo, Denis O. Sviridov, Mohsen Pourmousa, Milton Pryor, Soumitra S. Ghosh, Rahul Kakkar, et al. "A dual apolipoprotein C-II mimetic–apolipoprotein C-III antagonist peptide lowers plasma triglycerides." Science Translational Medicine 12, no. 528 (January 29, 2020): eaaw7905. http://dx.doi.org/10.1126/scitranslmed.aaw7905.

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Recent genetic studies have established that hypertriglyceridemia (HTG) is causally related to cardiovascular disease, making it an active area for drug development. We describe a strategy for lowering triglycerides (TGs) with an apolipoprotein C-II (apoC-II) mimetic peptide called D6PV that activates lipoprotein lipase (LPL), the main plasma TG-hydrolyzing enzyme, and antagonizes the TG-raising effect of apoC-III. The design of D6PV was motivated by a combination of all-atom molecular dynamics simulation of apoC-II on the Anton 2 supercomputer, structural prediction programs, and biophysical techniques. Efficacy of D6PV was assessed ex vivo in human HTG plasma and was found to be more potent than full-length apoC-II in activating LPL. D6PV markedly lowered TG by more than 80% within a few hours in both apoC-II–deficient mice and hAPOC3-transgenic (Tg) mice. In hAPOC3-Tg mice, D6PV treatment reduced plasma apoC-III by 80% and apoB by 65%. Furthermore, low-density lipoprotein (LDL) cholesterol did not accumulate but rather was decreased by 10% when hAPOC3-Tg mice lacking the LDL-receptor (hAPOC3-Tg × Ldlr−/−) were treated with the peptide. D6PV lowered TG by 50% in whole-body inducible Lpl knockout (iLpl−/−) mice, confirming that it can also act independently of LPL. D6PV displayed good subcutaneous bioavailability of about 80% in nonhuman primates. Because it binds to high-density lipoproteins, which serve as a long-term reservoir, it also has an extended terminal half-life (42 to 50 hours) in nonhuman primates. In summary, D6PV decreases plasma TG by acting as a dual apoC-II mimetic and apoC-III antagonist, thereby demonstrating its potential as a treatment for HTG.

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21

Norata, Giuseppe Danilo, Sotirios Tsimikas, Angela Pirillo, and Alberico L. Catapano. "Apolipoprotein C-III: From Pathophysiology to Pharmacology." Trends in Pharmacological Sciences 36, no. 10 (October 2015): 675–87. http://dx.doi.org/10.1016/j.tips.2015.07.001.

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22

Aroner, Sarah A., Ming Yang, Junlong Li, Jeremy D. Furtado, Frank M. Sacks, Anne Tjønneland, Kim Overvad, Tianxi Cai, and Majken K. Jensen. "Apolipoprotein C-III and High-Density Lipoprotein Subspecies Defined by Apolipoprotein C-III in Relation to Diabetes Risk." American Journal of Epidemiology 186, no. 6 (August 4, 2017): 736–44. http://dx.doi.org/10.1093/aje/kwx143.

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23

Riesen, Walter F., and Erich Sturzenegger. "Quantitation of Apolipoprotein C-III in Normal and in Hyperlipaemic Serum Samples by Enzyme-Linked Immunosorbent Assay." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 24, no. 1 (January 1987): 66–72. http://dx.doi.org/10.1177/000456328702400110.

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A specific and sensitive Sandwich enzyme-linked immunosorbent assay (ELISA) for the quantitative determination of apolipoprotein C-III, a major apolipoprotein of human very low density lipoproteins is described. The assay is non-competitive and it uses the same affinity isolated sheep antibody both for coating the wells and as conjugate with alkaline phosphatase. Total serum apo C-III was determined in a normal population of 24 men and 21 women. The difference was not statistically significant. In both sexes apo C-III concentration correlated positively with the serum triglyceride levels. In patients with hyperlipoproteinemia, apo C-III levels were increased.

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24

Sniderman, Allan D., Jean-Charles Hogue, Jean Bergeron, Claude Gagné, and Patrick Couture. "Non-HDL cholesterol and apoB in dyslipidaemia." Clinical Science 114, no. 2 (December 11, 2007): 149–55. http://dx.doi.org/10.1042/cs20070265.

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On the basis of a high correlation, non-HDL-C (non-high-density lipoprotein cholesterol) and apoB (apolipoprotein B) have been suggested to be of equivalent value for clinical practice; however, the strength of this relationship has not been examined in detail in patients with dyslipidaemia. The present study examines the variance of non-HDL-C compared with apoB in 1771 consecutive patients evaluated in a lipid clinic. These patients were divided into normolipidaemic subjects (n=407), type I hyperlipoproteinaemia (n=16), type IIa (n=736) and IIb (n=231) hyperlipoproteinaemia, type III hyperlipoproteinaemia (n=38), type IV hyperlipoproteinaemia (n=509) and type V hyperlipoproteinaemia (n=101). The relationship between non-HDL-C and apoB was examined both in terms of correlation and concordance. Correlation was high, but concordance was only moderate in the normolipidaemic subjects and in those with type IIa and type IIb hyperlipoproteinaemia. Correlation and concordance were both low in the subgroups with type III and type V hyperlipoproteinaemia. In those with type IV hyper-lipoproteinaemia, correlation was moderately high (r=0.74), but concordance was only fair. In conclusion, our results indicate that there is substantial variance of apoB for given values of non-HDL-C in many dyslipidaemic subjects. It follows that correlation is not adequate as a sole judge of equivalence of laboratory parameters.

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25

Lee, Chih-Kuo, Che-Wei Liao, Shih-Wei Meng, Wei-Kai Wu, Jiun-Yang Chiang, and Ming-Shiang Wu. "Lipids and Lipoproteins in Health and Disease: Focus on Targeting Atherosclerosis." Biomedicines 9, no. 8 (August 9, 2021): 985. http://dx.doi.org/10.3390/biomedicines9080985.

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Despite advances in pharmacotherapy, intervention devices and techniques, residual cardiovascular risks still cause a large burden on public health. Whilst most guidelines encourage achieving target levels of specific lipids and lipoproteins to reduce these risks, increasing evidence has shown that molecular modification of these lipoproteins also has a critical impact on their atherogenicity. Modification of low-density lipoprotein (LDL) by oxidation, glycation, peroxidation, apolipoprotein C-III adhesion, and the small dense subtype largely augment its atherogenicity. Post-translational modification by oxidation, carbamylation, glycation, and imbalance of molecular components can reduce the capacity of high-density lipoprotein (HDL) for reverse cholesterol transport. Elevated levels of triglycerides (TGs), apolipoprotein C-III and lipoprotein(a), and a decreased level of apolipoprotein A-I are closely associated with atherosclerotic cardiovascular disease. Pharmacotherapies aimed at reducing TGs, lipoprotein(a), and apolipoprotein C-III, and enhancing apolipoprotein A-1 are undergoing trials, and promising preliminary results have been reported. In this review, we aim to update the evidence on modifications of major lipid and lipoprotein components, including LDL, HDL, TG, apolipoprotein, and lipoprotein(a). We also discuss examples of translating findings from basic research to potential therapeutic targets for drug development.

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26

Alexander, Vickie, Trish Novak, Nicholas Viney, John Su, Jennifer Burkey, Walter Singleton, Richard Geary, and Isis Pharmaceuticals. "AN ANTISENSE INHIBITOR OF APOLIPOPROTEIN C-III LOWERS FASTING PLASMA APOLIPOPROTEIN C-III AND TRIGLYCERIDE CONCENTRATIONS IN HEALTHY VOLUNTEERS." Journal of the American College of Cardiology 59, no. 13 (March 2012): E1685. http://dx.doi.org/10.1016/s0735-1097(12)61686-6.

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27

Gaudet, Daniel, Veronica J. Alexander, Brisson Diane, Karine Tremblay, JoAnn Flaim, Steve Hughes, Walter Singleton, and Richard S. Geary. "An Antisense Inhibitor of Apolipoprotein C-III Substantially Decreases Fasting Apolipoprotein C-III and Triglyceride Levels in LPL Deficiency." Journal of Clinical Lipidology 8, no. 3 (May 2014): 353–54. http://dx.doi.org/10.1016/j.jacl.2014.02.090.

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28

Ooi, Esther M. M., P. Hugh R. Barrett, Dick C. Chan, and Gerald F. Watts. "Apolipoprotein C-III: understanding an emerging cardiovascular risk factor." Clinical Science 114, no. 10 (April 14, 2008): 611–24. http://dx.doi.org/10.1042/cs20070308.

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The concurrence of visceral obesity, insulin resistance and dyslipidaemia comprises the concept of the metabolic syndrome. The metabolic syndrome is an escalating problem in developed and developing societies that tracks with the obesity epidemic. Dyslipidaemia in the metabolic syndrome is potently atherogenic and, hence, is a major risk factor for CVD (cardiovascular disease) in these subjects. It is globally characterized by hypertriglyceridaemia, near normal LDL (low-density lipoprotein)-cholesterol and low plasma HDL (high-density lipoprotein)-cholesterol. ApoC-III (apolipoprotein C-III), an important regulator of lipoprotein metabolism, is strongly associated with hypertriglyceridaemia and the progression of CVD. ApoC-III impairs the lipolysis of TRLs [triacylglycerol (triglyceride)-rich lipoproteins] by inhibiting lipoprotein lipase and the hepatic uptake of TRLs by remnant receptors. In the circulation, apoC-III is associated with TRLs and HDL, and freely exchanges among these lipoprotein particle systems. However, to fully understand the complex physiology and pathophysiology requires the application of tracer methodology and mathematical modelling. In addition, experimental evidence shows that apoC-III may also have a direct role in atherosclerosis. In the metabolic syndrome, increased apoC-III concentration, resulting from hepatic overproduction of VLDL (very-LDL) apoC-III, is strongly associated with delayed catabolism of triacylglycerols and TRLs. Several therapies pertinent to the metabolic syndrome, such as PPAR (peroxisome-proliferator-activated receptor) agonists and statins, can regulate apoC-III transport in the metabolic syndrome. Regulating apoC-III metabolism may be an important new therapeutic approach to managing dyslipidaemia and CVD risk in the metabolic syndrome.

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29

Blackett, Piers R., Robin Germany, Boureima Sambo, and Petar Alaupovic. "Apolipoprotein C-III Bound to Apolipoprotein B-containing Lipoproteins in Obese Girls." Clinical Chemistry 49, no. 2 (February 1, 2003): 303–6. http://dx.doi.org/10.1373/49.2.303.

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30

Beck, L. S., and H. Fromm. "A role for apolipoprotein C-III in hypertriglyceridemia?" Gastroenterology 89, no. 5 (November 1985): 1203–4. http://dx.doi.org/10.1016/0016-5085(85)90232-x.

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31

Ramms, Bastian, and Philip L. S. M. Gordts. "Apolipoprotein C-III in triglyceride-rich lipoprotein metabolism." Current Opinion in Lipidology 29, no. 3 (June 2018): 171–79. http://dx.doi.org/10.1097/mol.0000000000000502.

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32

Wang, Heng, Felicia Hunter, and Dennis D. Black. "Effect of feeding diets of varying fatty acid composition on apolipoprotein expression in newborn swine." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 4 (October 1, 1998): G645—G651. http://dx.doi.org/10.1152/ajpgi.1998.275.4.g645.

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The purpose of this study was to determine the effect of chronic (1 wk) feeding of dietary triacylglycerol (TG) of varying fatty acid composition on small intestinal and hepatic apolipoprotein expression, as well as serum lipid and apolipoprotein concentrations, in newborn swine. Two-day-old female swine were fed one of three diets by gavage with the following lipid composition: medium-chain TG (MCT; MCT oil), intermediate-chain saturated TG (ICST; coconut oil), and long-chain polyunsaturated TG (LCPUT; safflower oil) at 753 kJ ⋅ kg−1 ⋅ day−1with 51% of energy from fat. After 1 wk, serum lipids and apolipoprotein concentrations were measured, and jejunal apolipoprotein B (apo B) and apo A-I mass and apo B, apo A-I, apo A-IV, and apo C-III synthesis were measured. Liver was processed for determination of apo B and apo A-I mass and apo B, apo A-I, apo C-III, and β-actin mRNA abundance by slot blot hybridization. Compared with the MCT and LCPUT groups, the ICST group had higher total serum cholesterol, TG, high-density lipoprotein (HDL)-cholesterol, and apo A-I concentrations. There were no differences among the three groups for intestinal apolipoprotein mass or synthesis. In liver, apo A-I mass was highest in the ICST group. Liver apo A-I and apo C-III mRNA abundance was highest in the ICST group. Among all three groups, hepatic apo A-I mass correlated significantly with plasma HDL-cholesterol concentrations, and serum TG concentrations correlated with hepatic apo C-III mRNA abundance. In conclusion, we found that in the newborn piglet, chronic feeding of ICST increases serum total cholesterol, TG, HDL-cholesterol, and apo A-I concentrations and hepatic expression of apo A-I and apo C-III mRNA, compared with feeding of MCT or LCPUT. We speculate that increased hepatic apo A-I expression may contribute to the higher serum HDL and apo A-I concentrations in the ICST animals. Increased hepatic expression of apo C-III with ICST feeding may contribute to the higher serum TG concentrations by apo C-III-mediated inhibition of the catabolism of triacylglycerol-rich lipoproteins.

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33

Wopereis, Suzan, Stephanie Grünewald, Éva Morava, Johannes M. Penzien, Paz Briones, M. Teresa Garcı́a-Silva, Pierre N. M. Demacker, Karin M. L. C. Huijben, and Ron A. Wevers. "Apolipoprotein C-III Isofocusing in the Diagnosis of Genetic Defects in O-Glycan Biosynthesis." Clinical Chemistry 49, no. 11 (November 1, 2003): 1839–45. http://dx.doi.org/10.1373/clinchem.2003.022541.

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Abstract Background: Defects in the biosynthesis of N-glycans may be found by isoelectric focusing (IEF) of plasma transferrin. No test is available to demonstrate O-glycan biosynthesis defects. Methods: We used isoforms of apolipoprotein C-III (apoC-III) as a marker for the biosynthesis of core 1 mucin type O-glycans. Plasma samples from patients with primary defects and secondary alterations in N-glycan biosynthesis were studied by apoC-III isofocusing. Results: Age-related reference values for apoC-III were determined. Plasma samples from patients with the primary congenital disorders of glycosylation (CDG) types Ia–Ic, Ie, If, IIa, and IId all showed a normal apoC-III isofocusing profile. Plasma from two patients with CDG type IIx were tested: one showed a normal apoC-III distribution, whereas the other showed a hypoglycosylation profile. In plasma from patients with hemolytic uremic syndrome (HUS), a hypoglycosylation profile was obtained. Conclusions: IEF of apoC-III is a rapid and simple technique that may be used as a screening assay for abnormalities in core 1 mucin type O-glycans. Evidence that a patient in this study has a primary genetic defect affecting both N- and O-glycosylation provides the first example of an inborn error of metabolism affecting the biosynthesis of core 1 mucin type O-glycans. Our data narrow the options for the position of the primary defect in this patient down to a step in the biosynthesis, activation, or transfer of galactose or N-acetylneuraminic acid to both N- and O-glycans. Circulating neuraminidase excreted by Streptococcus pneumoniae caused the high percentage of asialo apoC-III in two HUS patients.

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34

Alessandri, Cesare, Stefania Basili, Marina Maurelli, Paola Andreozzi, Anna Colletta, Michele Paradiso, and Corrado Cordova. "Apolipoproteins C-II and C-III in Peripheral Arterial Disease." Angiology 45, no. 2 (February 1994): 131–36. http://dx.doi.org/10.1177/000331979404500208.

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35

HIBINO, Akira, Susumu YUKAWA, Takao MAEDA, Toshihiko MIYAI, Masahiro KINOSHITA, and Hiroshi NOMOTO. "Very Low Density Lipoprotein-triglyceride Hydrolysis by Lipoprotein Lipase and Apolipoprotein C-II/C-III Ratio in Very Low Density Lipoproteins." Journal of Japan Atherosclerosis Society 15, no. 1 (1987): 255–59. http://dx.doi.org/10.5551/jat1973.15.1_255.

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36

Breyer, Emelita D., Ngoc-Anh Le, Xianzhou Li, Deborah Martinson, and W. Virgil Brown. "Apolipoprotein C-III displacement of apolipoprotein E from VLDL: effect of particle size." Journal of Lipid Research 40, no. 10 (October 1999): 1875–82. http://dx.doi.org/10.1016/s0022-2275(20)34904-x.

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37

Mendivil, Carlos O., Chunyu Zheng, Jeremy Furtado, Julian Lel, and Frank M. Sacks. "Metabolism of Very-Low-Density Lipoprotein and Low-Density Lipoprotein Containing Apolipoprotein C-III and Not Other Small Apolipoproteins." Arteriosclerosis, Thrombosis, and Vascular Biology 30, no. 2 (February 2010): 239–45. http://dx.doi.org/10.1161/atvbaha.109.197830.

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38

Chan, Dick C., Gerald F. Watts, Minh N. Nguyen, and P. Hugh R. Barrett. "Apolipoproteins C-III and A-V as Predictors of Very-Low-Density Lipoprotein Triglyceride and Apolipoprotein B-100 Kinetics." Arteriosclerosis, Thrombosis, and Vascular Biology 26, no. 3 (March 2006): 590–96. http://dx.doi.org/10.1161/01.atv.0000203519.25116.54.

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39

WOO, SANG-KOO, and HYUN-SIK KANG. "Apolipoprotein C-III SstI Genotypes Modulate Exercise-Induced Hypotriglyceridemia." Medicine & Science in Sports & Exercise 36, no. 6 (June 2004): 955–59. http://dx.doi.org/10.1249/01.mss.0000128200.38372.82.

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40

Adiels, Martin, Marja‐Riitta Taskinen, Elias Björnson, Linda Andersson, Niina Matikainen, Sanni Söderlund, Juhani Kahri, et al. "Role of apolipoprotein C‐III overproduction in diabetic dyslipidaemia." Diabetes, Obesity and Metabolism 21, no. 8 (August 2019): 1861–70. http://dx.doi.org/10.1111/dom.13744.

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41

Sacks, Frank M., Chunyu Zheng, and Jeffrey S. Cohn. "Complexities of plasma apolipoprotein C-III metabolism: Fig. 1." Journal of Lipid Research 52, no. 6 (March 18, 2011): 1067–70. http://dx.doi.org/10.1194/jlr.e015701.

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42

de Messieres, Michel, Rick K. Huang, Yi He, and Jennifer C. Lee. "Amyloid Triangles, Squares, and Loops of Apolipoprotein C-III." Biochemistry 53, no. 20 (May 13, 2014): 3261–63. http://dx.doi.org/10.1021/bi500502d.

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43

Ahmad, Tareq Y., John R. Guyton, James T. Sparrow, and Joel D. Morrisett. "Apolipoprotein C-III/sphingomyelin recombinants: formation, isolation, and characterization." Biochemistry 25, no. 15 (July 1986): 4407–14. http://dx.doi.org/10.1021/bi00363a035.

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44

Malmendier, C. L., J. F. Lontie, G. A. Grutman, and C. Delcroix. "Metabolism of apolipoprotein C-III in normolipemic human subjects." Atherosclerosis 69, no. 1 (January 1988): 51–59. http://dx.doi.org/10.1016/0021-9150(88)90288-2.

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45

Yao, Zemin, and Yuwei Wang. "Apolipoprotein C-III and hepatic triglyceride-rich lipoprotein production." Current Opinion in Lipidology 23, no. 3 (June 2012): 206–12. http://dx.doi.org/10.1097/mol.0b013e328352dc70.

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46

Chan, Dick C., Gerald F. Watts, Trevor G. Redgrave, Trevor A. Mori, and P. Hugh R. Barrett. "Apolipoprotein B-100 kinetics in visceral obesity: Associations with plasma apolipoprotein C-III concentration." Metabolism 51, no. 8 (August 2002): 1041–46. http://dx.doi.org/10.1053/meta.2002.33339.

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47

Schoch, Leonie, Pablo Sutelman, Rosa Suades, Laura Casani, Teresa Padro, Lina Badimon, and Gemma Vilahur. "Hypercholesterolemia-Induced HDL Dysfunction Can Be Reversed: The Impact of Diet and Statin Treatment in a Preclinical Animal Model." International Journal of Molecular Sciences 23, no. 15 (August 2, 2022): 8596. http://dx.doi.org/10.3390/ijms23158596.

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High-density lipoproteins (HDL) undergo adverse remodeling and loss of function in the presence of comorbidities. We assessed the potential of lipid-lowering approaches (diet and rosuvastatin) to rescue hypercholesterolemia-induced HDL dysfunction. Hypercholesterolemia was induced in 32 pigs for 10 days. Then, they randomly received one of the 30-day interventions: (I) hypercholesterolemic (HC) diet; (II) HC diet + rosuvastatin; (III) normocholesterolemic (NC) diet; (IV) NC diet + rosuvastatin. We determined cholesterol efflux capacity (CEC), antioxidant potential, HDL particle number, HDL apolipoprotein content, LDL oxidation, and lipid levels. Hypercholesterolemia time-dependently impaired HDL function (−62% CEC, −11% antioxidant index (AOI); p < 0.01), increased HDL particles numbers 2.8-fold (p < 0.0001), reduced HDL-bound APOM (−23%; p < 0.0001), and increased LDL oxidation 1.7-fold (p < 0.0001). These parameters remained unchanged in animals on HC diet alone up to day 40, while AOI deteriorated up to day 25 (−30%). The switch to NC diet reversed HDL dysfunction, restored apolipoprotein M content and particle numbers, and normalized cholesterol levels at day 40. Rosuvastatin improved HDL, AOI, and apolipoprotein M content. Apolipoprotein A-I and apolipoprotein C-III remained unchanged. Lowering LDL-C levels with a low-fat diet rescues HDL CEC and antioxidant potential, while the addition of rosuvastatin enhances HDL antioxidant capacity in a pig model of hypercholesterolemia. Both strategies restore HDL-bound apolipoprotein M content.

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48

Ondruskova, Nina, Tomas Honzik, Hana Kolarova, Zuzana Pakanova, Jan Mucha, Jiri Zeman, and Hana Hansikova. "Aberrant apolipoprotein C-III glycosylation in glycogen storage disease type III and IX." Metabolism 82 (May 2018): 135–41. http://dx.doi.org/10.1016/j.metabol.2018.01.004.

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49

Aguilar-Recarte, David, Xavier Palomer, and Manuel Vázquez-Carrera. "Uncovering the role of apolipoprotein C-III in insulin resistance." Clínica e Investigación en Arteriosclerosis (English Edition) 33, no. 2 (March 2021): 108–15. http://dx.doi.org/10.1016/j.artere.2021.04.002.

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50

van Capelleveen, Julian C., Sophie J. Bernelot Moens, Xiaohong Yang, John J. P. Kastelein, Nicholas J. Wareham, Aeilko H. Zwinderman, Erik S. G. Stroes, et al. "Apolipoprotein C-III Levels and Incident Coronary Artery Disease Risk." Arteriosclerosis, Thrombosis, and Vascular Biology 37, no. 6 (June 2017): 1206–12. http://dx.doi.org/10.1161/atvbaha.117.309007.

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