Journal articles: 'High density lipoproteins'

1

Annema, Wijtske, and Arnold von Eckardstein. "High-Density Lipoproteins." Circulation Journal 77, no. 10 (2013): 2432–48. http://dx.doi.org/10.1253/circj.cj-13-1025.

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Sparks, Charles E., James P. Corsetti, and Janet D. Sparks. "High-density lipoproteins." Current Opinion in Lipidology 25, no. 3 (June 2014): 230–32. http://dx.doi.org/10.1097/mol.0000000000000079.

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Haghikia, Arash, and Ulf Landmesser. "High-Density Lipoproteins." Cardiology Clinics 36, no. 2 (May 2018): 317–27. http://dx.doi.org/10.1016/j.ccl.2017.12.013.

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Zheng, Chunyu, and Masanori Aikawa. "High-Density Lipoproteins." Journal of the American College of Cardiology 60, no. 23 (December 2012): 2380–83. http://dx.doi.org/10.1016/j.jacc.2012.08.999.

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Koller, Elisabeth, Ivo Volf, Aner Gurvitz, and Franz Koller. "Modified Low-Density Lipoproteins and High-Density Lipoproteins." Pathophysiology of Haemostasis and Thrombosis 35, no. 3-4 (2006): 322–45. http://dx.doi.org/10.1159/000093225.

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6

Whayne, Thomas F. "High-density Lipoprotein Cholesterol: Current Perspective for Clinicians." Angiology 60, no. 5 (February 23, 2009): 644–49. http://dx.doi.org/10.1177/0003319709331392.

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High-density lipoproteins are regarded as “good guys” but not always. Situations involving high-density lipoproteins are discussed and medication results are considered. Clinicians usually consider high-density lipoprotein cholesterol. Nicotinic acid is the best available medication to elevate high-density lipoprotein cholesterol and this appears beneficial for cardiovascular risk. The major problem with nicotinic acid is that many patients do not tolerate the associated flushing. Laropiprant decreases this flushing and has an approval in Europe but not in the United States. The most potent medications for increasing high-density lipoprotein cholesterol are cholesteryl ester transfer protein inhibitors. The initial drug in this class, torcetrapib, was eliminated by excess cardiovascular problems. Two newer cholesteryl ester transfer protein inhibitors, R1658 and anacetrapib, initially appear promising. High-density lipoprotein cholesterol may play an important role in improving cardiovascular risk in the 60% of patients who do not receive cardiovascular mortality/morbidity benefit from low-density lipoproteins reduction by statins.

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Carcelain, G., F. David, S. Lepage, D. Bonnefont-Rousselot, J. Delattre, A. Legrand, J. Peynet, and S. Troupel. "Simple Method for Quantifying Alpha-Tocopherol in Low-Density+Very-Low-Density Lipoproteins and in High-Density Lipoproteins." Clinical Chemistry 38, no. 9 (September 1, 1992): 1792–95. http://dx.doi.org/10.1093/clinchem/38.9.1792.

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Abstract We assessed the distribution of alpha-tocopherol in serum lipoprotein samples after separating the lipoprotein fractions by either sequential ultracentrifugation or selective precipitation with sodium phosphotungstate-magnesium chloride reagent. alpha-Tocopherol concentrations were determined by reversed-phase high-performance liquid chromatography. After ultracentrifugation, we found that in men, low- and very-low-density serum lipoproteins (LDL-VLDL) contained 53.6% of alpha-tocopherol vs 46.4% in high-density lipoproteins (HDL). In women, serum LDL-VLDL contained 45.6% alpha-tocopherol after ultracentrifugation vs 54.4% in HDL. After selective precipitation, the proportions of alpha-tocopherol in men were 56.1% in LDL-VLDL vs 43.9% in HDL, and in women, 45.4% in LDL-VLDL vs 54.6% in HDL. After selective precipitation, alpha-tocopherol recovery from whole lipoprotein fractions was 97% to 100% vs 80% after ultracentrifugation, thus allowing more accurate alpha-tocopherol quantification than after separation by ultracentrifugation.

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Murzakhanova, Adela F., Vladimir N. Oslopov, Konstantin S. Sergienko, Elena V. Khazova, and Julia V. Oslopova. "High-density lipoprotein cholesterol — friend or enemy?" Kazan medical journal 103, no. 1 (February 7, 2022): 79–88. http://dx.doi.org/10.17816/kmj2022-79.

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The article provides a review of the literature on the effect of excess and deficiency of high-density lipoprotein cholesterol on the prevention and treatment of cardiovascular pathology. Information about high-density lipoproteins structure, function, antiatherogenic role and the prospect of using various high-density lipoproteins subclasses in the pharmacotherapy of dyslipidemic conditions are also described. It is proven that a lowered level of such cholesterol is a predictor of cardiovascular disease. At the same time, many observations confirm the correlation between elevated high-density lipoprotein levels and mortality from myocardial infarction and other acute cardiovascular conditions. In large studies, the use of cholesterol ester transfer protein inhibitors and other drugs increased the level of high-density lipoprotein, but the unreduced risk of cardiovascular disease confirms the lack of positive results from the use as a therapeutic target. In addition, it was found that the composition of high-density lipoprotein cholesterol protein differs in healthy and diseased people: it becomes dysfunctional, losing its antioxidant and anti-inflammatory properties in diseased individuals. The atheroprotective activity of properly functioning high-density lipoprotein cholesterol is often impaired in clinical situations associated with oxidative stress. In these cases, high-density lipoproteins can have some changes, and even if the quantity is within the normal range, the quality is no longer the same. Thus, it is necessary to identify a better therapeutic target than high-density lipoprotein cholesterol levels, as there is currently insufficient clinical trial data to recommend targeted high-density lipoprotein therapy.

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Sviridov, Dmitri, and Alan T. Remaley. "High-density lipoprotein mimetics: promises and challenges." Biochemical Journal 472, no. 3 (November 27, 2015): 249–59. http://dx.doi.org/10.1042/bj20150832.

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Lipoprotein mimetics were designed to recreate one or several functions of lipoproteins in context of cardiovascular disease; however, the current applications are much broader. Here we discuss the design principles, mechanisms of action, indications and efficacy of lipoprotein mimetics.

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Faria, Eliana Cotta de, Adriana Celeste Gebrin, Wilson Nadruz Júnior, and Lucia Nassi Castilho. "Phospholipid transfer protein activity in two cholestatic patients." Sao Paulo Medical Journal 122, no. 4 (2004): 175–77. http://dx.doi.org/10.1590/s1516-31802004000400009.

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CONTEXT: Plasma phospholipid transfer protein mediates the transfer of phospholipids from triglyceride-rich lipoproteins, very low density lipoproteins and low density lipoproteins to high density lipoproteins, a process that is also efficient between high density lipoprotein particles. It promotes a net movement of phospholipids, thereby generating small lipid-poor apolipoprotein AI that contains particles and subfractions that are good acceptors for cell cholesterol efflux. CASE REPORT: We measured the activity of plasma phospholipid transfer protein in two cholestatic patients, assuming that changes in activity would occur in serum that was positive for lipoprotein X. Both patients presented severe hypercholesterolemia, high levels of low density lipoprotein cholesterol and, in one case, low levels of high density lipoprotein cholesterol and high levels of phospholipid serum. The phospholipid transfer activity was close to the lower limit of the reference interval. To our knowledge, this is the first time such results have been presented. We propose that phospholipid transfer protein activity becomes reduced under cholestasis conditions because of changes in the chemical composition of high density lipoproteins, such as an increase in phospholipids content. Also, lipoprotein X, which is rich in phospholipids, could compete with high density lipoproteins as a substrate for phospholipid transfer protein.

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Biggerstaff, Kyle D., and Joshua S. Wooten. "Understanding lipoproteins as transporters of cholesterol and other lipids." Advances in Physiology Education 28, no. 3 (September 2004): 105–6. http://dx.doi.org/10.1152/advan.00048.2003.

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A clear picture of lipoprotein metabolism is essential for understanding the pathophysiology of atherosclerosis. Many students are taught that low-density lipoprotein-cholesterol is “bad” and high-density lipoprotein-cholesterol is “good.” This misconception leads to students thinking that lipoproteins are types of cholesterol rather than transporters of lipid. Describing lipoproteins as particles that are composed of lipid and protein and illustrating the variation in particle density that is determined by the constantly changing lipid and protein composition clarifies the metabolic pathway and physiological function of lipoproteins as lipid transporters. Such a description will also suggest the critical role played by apolipoproteins in lipid transport. The clarification of lipoproteins as particles that change density will help students understand the nomenclature used to classify lipoproteins as well.

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12

Cochran, Blake J., Kwok-Leung Ong, Bikash Manandhar, and Kerry-Anne Rye. "High Density Lipoproteins and Diabetes." Cells 10, no. 4 (April 9, 2021): 850. http://dx.doi.org/10.3390/cells10040850.

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Epidemiological studies have established that a high plasma high density lipoprotein cholesterol (HDL-C) level is associated with reduced cardiovascular risk. However, recent randomised clinical trials of interventions that increase HDL-C levels have failed to establish a causal basis for this relationship. This has led to a shift in HDL research efforts towards developing strategies that improve the cardioprotective functions of HDLs, rather than simply increasing HDL-C levels. These efforts are also leading to the discovery of novel HDL functions that are unrelated to cardiovascular disease. One of the most recently identified functions of HDLs is their potent antidiabetic properties. The antidiabetic functions of HDLs, and recent key advances in this area are the subject of this review. Given that all forms of diabetes are increasing at an alarming rate globally, there is a clear unmet need to identify and develop new approaches that will complement existing therapies and reduce disease progression as well as reverse established disease. Exploration of a potential role for HDLs and their constituent lipids and apolipoproteins in this area is clearly warranted. This review highlights focus areas that have yet to be investigated and potential strategies for exploiting the antidiabetic functions of HDLs.

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13

Shih, Amy Y., Stephen G. Sligar, and Klaus Schulten. "Maturation of high-density lipoproteins." Journal of The Royal Society Interface 6, no. 39 (July 2009): 863–71. http://dx.doi.org/10.1098/rsif.2009.0173.

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Human high-density lipoproteins (HDLs) are involved in the transport of cholesterol. The mechanism by which HDL assembles and functions is not well understood owing to a lack of structural information on circulating spherical HDL. Here, we report a series of molecular dynamics simulations that describe the maturation of discoidal HDL into spherical HDL upon incorporation of cholesterol ester as well as the resulting atomic level structure of a mature circulating spherical HDL particle. Sixty cholesterol ester molecules were added in a stepwise fashion to a discoidal HDL particle containing two apolipoproteins wrapped around a 160 dipalmitoylphosphatidylcholine lipid bilayer. The resulting matured particle, captured in a coarse-grained description, was then described in a consistent all-atom representation and analysed in chemical detail. The simulations show that maturation results from the formation of a highly dynamic hydrophobic core comprised of cholesterol ester surrounded by phospholipid and protein; the two apolipoprotein strands remain in a belt-like conformation as seen in the discoidal HDL particle, but with flexible N- and C-terminal helices and a central region stabilized by salt bridges. In the otherwise flexible lipoproteins, a less mobile central region provides an ideal location to bind lecithin cholesterol acyltransferase, the key enzyme that converts cholesterol to cholesterol ester during HDL maturation.

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14

Dastani, Zari, James C. Engert, Jacques Genest, and Michel Marcil. "Genetics of high-density lipoproteins." Current Opinion in Cardiology 21, no. 4 (July 2006): 329–35. http://dx.doi.org/10.1097/01.hco.0000231403.94856.cd.

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15

Dayspring, Thomas. "High-Density Lipoproteins: Emerging Knowledge." Journal of the CardioMetabolic Syndrome 2, no. 1 (January 2007): 59–62. http://dx.doi.org/10.1111/j.1559-4564.2007.06008.x.

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16

Gordon, David J. "FACTORS AFFECTING HIGH-DENSITY LIPOPROTEINS." Endocrinology and Metabolism Clinics of North America 27, no. 3 (September 1998): 699–709. http://dx.doi.org/10.1016/s0889-8529(05)70034-7.

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17

Garner, Brett, Paul K. Witting, A. Reginald Waldeck, Julie K. Christison, Mark Raftery, and Roland Stocker. "Oxidation of High Density Lipoproteins." Journal of Biological Chemistry 273, no. 11 (March 13, 1998): 6080–87. http://dx.doi.org/10.1074/jbc.273.11.6080.

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Garner, Brett, A. Reginald Waldeck, Paul K. Witting, Kerry-Anne Rye, and Roland Stocker. "Oxidation of High Density Lipoproteins." Journal of Biological Chemistry 273, no. 11 (March 13, 1998): 6088–95. http://dx.doi.org/10.1074/jbc.273.11.6088.

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19

Das, Dipak K. "Cardioprotection With High-Density Lipoproteins." Circulation Research 92, no. 3 (February 21, 2003): 258–60. http://dx.doi.org/10.1161/01.res.0000058881.44913.7b.

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20

Rader, Daniel J. "High-density lipoproteins and atherosclerosis." American Journal of Cardiology 90, no. 8 (October 2002): 62–70. http://dx.doi.org/10.1016/s0002-9149(02)02635-8.

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21

Barter, Philip. "Metabolic abnormalities: high-density lipoproteins." Endocrinology and Metabolism Clinics of North America 33, no. 2 (June 2004): 393–403. http://dx.doi.org/10.1016/j.ecl.2004.03.006.

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22

Schmitz, Gerd, and Karl J. Lackner. "High-density lipoproteins and atherosclerosis." Current Opinion in Lipidology 4, no. 5 (October 1993): 392–400. http://dx.doi.org/10.1097/00041433-199310000-00008.

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23

von Eckardstein, Arnold, Jerzy-Roch Nofer, and Gerd Assmann. "High Density Lipoproteins and Arteriosclerosis." Arteriosclerosis, Thrombosis, and Vascular Biology 21, no. 1 (January 2001): 13–27. http://dx.doi.org/10.1161/01.atv.21.1.13.

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24

Cushman, Paul, Joseph Barboriak, and John Kalbfleisch. "Alcohol: High Density Lipoproteins, Apolipoproteins." Alcoholism: Clinical and Experimental Research 10, no. 2 (March 1986): 154–57. http://dx.doi.org/10.1111/j.1530-0277.1986.tb05063.x.

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25

Fontanals-Ferrer, N., J. Serrat-Serrat, A. Sorribas-Vivas, C. Gonzalez-Garcia, F. Gonzalez-Sastre, and J. Gomez-Gerique. "Quick method of determining lipoproteins, including those of intermediate density, in serum." Clinical Chemistry 34, no. 9 (September 1, 1988): 1753–57. http://dx.doi.org/10.1093/clinchem/34.9.1749.

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Abstract We describe an ultracentrifugation method for isolating the different lipoprotein classes relatively quickly. In this method the very-low-density lipoproteins are first separated by non-density-adjusted ultracentrifugation. The resulting infranatant material is then stained with Coomassie Brilliant Blue R-250 and ultracentrifuged in a density gradient. The intermediate-density lipoproteins (IDL), low-density lipoproteins, and high-density lipoproteins fractions are separated by aspiration from the top of the tube. This method can be used to separate, analyze, and quantify lipoproteins, including anomalous lipoproteins such as the IDL. The CVs for the present method never exceeded 15%.

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26

Poteryaeva, O. N., and I. F. Usynin. "Antidiabetic role of high density lipoproteins." Biomeditsinskaya Khimiya 64, no. 6 (2018): 463–71. http://dx.doi.org/10.18097/pbmc20186406463.

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Disturbance in lipid metabolism can be both a cause and a consequence of the development of diabetes mellitus (DM). One of the most informative indicator of lipid metabolism is the ratio of atherogenic and antiatherogenic fractions of lipoproteins and their protein components. The review summarizes literature data and own results indicating the important role of high-density lipoprotein (HDL) and their main protein component, apolipoprotein A-I (apoA-I), in the pathogenesis of type 2 DM. On the one hand, HDL are involved in the regulation of insulin secretion by b-cells and insulin-independent absorption of glucose. On the other hand, insulin resistance and hyperglycemia lead to a decrease in HDL levels and cause modification of their protein component. In addition, HDL, possessing anti-inflammatory and mitogenic properties, provide anti-diabetic protection through systemic mechanisms. Thus, maintaining a high concentration of HDL and apoA-I in blood plasma and preventing their modification are important issues in the context of prevention and treatment of diabetes.

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27

Rosales, Corina, Baiba K. Gillard, Antonio M. Gotto, and Henry J. Pownall. "The Alcohol–High-Density Lipoprotein Athero-Protective Axis." Biomolecules 10, no. 7 (July 1, 2020): 987. http://dx.doi.org/10.3390/biom10070987.

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Ingestion of alcohol is associated with numerous changes in human energy metabolism, especially that of plasma lipids and lipoproteins. Regular moderate alcohol consumption is associated with reduced atherosclerotic cardiovascular disease (ASCVD), an effect that has been attributed to the concurrent elevations of plasma high-density lipoprotein-cholesterol (HDL-C) concentrations. More recent evidence has accrued against the hypothesis that raising plasma HDL concentrations prevents ASCVD so that other metabolic processes associated with alcohol consumption have been considered. This review explored the roles of other metabolites induced by alcohol consumption—triglyceride-rich lipoproteins, non-esterified free fatty acids, and acetate, the terminal alcohol metabolite in athero-protection: Current evidence suggests that acetate has a key role in athero-protection but additional studies are needed.

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Sparks, D. L., J. Frohlich, P. Cullis, and P. H. Pritchard. "Cholesteryl ester transfer activity in plasma measured by using solid-phase-bound high-density lipoprotein." Clinical Chemistry 33, no. 3 (March 1, 1987): 390–93. http://dx.doi.org/10.1093/clinchem/33.3.390.

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Abstract We studied the ability of lipid-transfer factors in plasma to promote transfer, to endogenous lipoproteins, of [3H]cholesteryl ester from high-density lipoprotein (HDL) covalently bound to Sepharose 4B beads. After incubation for 2 h at 37 degrees C, 12 to 14% of the [3H]cholesteryl ester had been transferred to the lipoproteins of the plasma, in the proportions 57% to HDL and 43% to low- and very-low-density lipoproteins. This process was a function of the amount of plasma present and was stimulated by addition of partly purified lipid-transfer protein. Transfer also depended on the concentration of donor HDL but was independent of the amount of acceptor lipoprotein. This simple evaluation of cholesteryl ester transfer does not require removal of lipoproteins from the plasma before incubation.

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Rip, J. W., M. M. Blais, and L. W. Jiang. "Low-density lipoprotein as a transporter of dolichol intermediates in the mammalian circulation." Biochemical Journal 297, no. 2 (January 15, 1994): 321–25. http://dx.doi.org/10.1042/bj2970321.

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The cholesteryl esters which make up the bulk of the core of the human low-density lipoprotein particle were removed by extraction into heptane and replaced with the fluorescent anthroyl or N-(7-nitrobenzyl-2-oxa-1,3-diazol-4-yl)aminohexanoyl esters of dolichol. The reconstituted low-density lipoproteins were efficiently internalized by normocholesterolaemic human fibroblasts but not by fibroblasts from patients lacking the low-density-lipoprotein receptor, or lacking the ability to internalize the receptor-lipoprotein complex. In normal fibroblasts, the reconstituted low-density lipoproteins were delivered to lysosomes after internalization. The results suggest that (i) dolichol intermediates in the human circulation are normally carried on low-density lipoproteins and (ii) that low-density lipoproteins are involved in the accumulation of dolichol intermediates in lysosomes during normal human aging and in certain diseases involving the lysosome. In addition, by incorporating these very hydrophobic probes into low-density lipoprotein, they can be presented to cells in culture at high concentration in a water-soluble form.

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Ranganathan, Subramanian, John D. Gasman, Hideo Matsuura, and Bruce A. Kottke. "Lipoprotein-mediated efflux of radiolabeled cholesterol from cells does not indicate net removal of cellular cholesterol mass." Biochemistry and Cell Biology 67, no. 10 (October 1, 1989): 719–23. http://dx.doi.org/10.1139/o89-107.

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The efflux of cholesterol from human skin fibroblasts was determined using radioisotope techniques and mass measurements. When the cells were labeled with [14C]- or [3H]-cholesterol and then incubated with very low density, low density, or high density lipoproteins or with serum, 20 to 30% of the label was released into the medium in 20 h. However, when the cellular cholesterol content was determined after incubation with various lipoproteins under identical conditions, only the heavier subfraction of high density lipoproteins (HDL3) caused a significant decrease in cellular cholesterol. This net removal of cholesterol can be observed in the cells without overloading them with cholesterol, by incubation with low density lipoproteins. Time studies indicated that at least 24 h of incubation is required to detect significant removal of cellular cholesterol. These experiments show that methods using the release of labeled cholesterol from cultured cells to determine net cholesterol removal mediated by high density lipoprotein, although currently used by many investigators, can lead to erroneous conclusions when employed without the measurement of cholesterol mass.Key words: low-density lipoproteins, high-density lipoproteins, fibroblasts, cholesterol, bidirectional flux.

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31

Roche, D., V. Atger, N. T. Le Quang, A. Girard, and O. G. Ekindjian. "Polyacrylamide gel electrophoresis in quantification of high-density lipoprotein cholesterol." Clinical Chemistry 31, no. 11 (November 1, 1985): 1893–95. http://dx.doi.org/10.1093/clinchem/31.11.1893.

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Abstract We evaluated a method for quantifying high-density lipoprotein cholesterol in plasma, based on electrophoretic migration of the prestained (with Sudan Black III) sample through a discontinuous polyacrylamide++ gel and densitometric integration of the stain associated with each class of lipoprotein. With this method, operations can be carried out on all types of lipoproteins over a broad range of concentrations. Overloading with very-low and low-density lipoproteins did not affect reliability within a wide range of HDL concentrations (0.45 to 16.60 mmol/L). Results for 22 individual plasma samples from normal and dyslipemic subjects correlated well with those by ultracentrifugal analysis (r=0.96; Student's t= 0.90, p > 0.30). We conclude that this method is reliable, sensitive, and accurate, It may be used for simultaneously typing dyslipoproteinemias and assaying HDL cholesterol.

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Yasmin, Raheela, Aashi Ahmed, Ambreen Javed, Maleha Asim, Rabbia Shabbir, Shahida Mushtaq, and Faiza Irshad. "The Effect of Blood Sugar Fasting Levels on Diabetic Dyslipidemia." Pakistan Journal of Medical and Health Sciences 16, no. 4 (April 26, 2022): 360–61. http://dx.doi.org/10.53350/pjmhs22164360.

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Background: Diabetic dyslipidemia is a group of lipoprotein defects described by raised triglycerides, elevated low density lipoprotein and reduced levels of high density lipoprotein. Objective: To assess the effect of blood sugar fasting levels on individual lipoproteins. Study design: Cross-sectional study Place and duration of study: Fauji Foundation Hospital Rawalpindi & POF Hospital Wah Cantt from 1st February 2014 to 31st July 2014. Methodology: Fifty patients with age from 30 to 70 years were enrolled. Patients' body mass index was calculated. Serum cholesterol, high density lipoprotein and triglyceride levels were estimated by enzymatic colorimetric kit. Low density lipoprotein was calculated by Friedewald equation. Results: The mean blood sugar fasting level was 204.050±87.0755. The P-value of low density lipoproteins to blood sugar fasting and cholesterol to high density lipoprotein ratio blood sugar fasting were significant i.e. 0.03 and<0.001 respectively. Conclusion: Dyslipidemia worsened with uncontrolled blood sugar fasting. Elevated low density lipoprotein and cholesterol to high density lipoprotein ratio was observed. Keywords: Blood sugar fasting, Type 2 diabetes mellitus (T2DM), Cardiovascular system (CVS), Dyslipidemia, high density lipoprotein (HDL)

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Klimov, A. N., L. A. Kozhemyakin, V. M. Pleskov, and L. I. Andreeva. "Antioxidant effect of high-density lipoproteins in peroxidation of low-density lipoproteins." Bulletin of Experimental Biology and Medicine 103, no. 5 (May 1987): 622–25. http://dx.doi.org/10.1007/bf00841817.

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Maran, Logeswaran, Auni Hamid, and Shahrul Bariyah Sahul Hamid. "Lipoproteins as Markers for Monitoring Cancer Progression." Journal of Lipids 2021 (September 13, 2021): 1–17. http://dx.doi.org/10.1155/2021/8180424.

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Lipoproteins are among the contributors of energy for the survival of cancer cells. Studies indicate there are complex functions and metabolism of lipoproteins in cancer. The current review is aimed at providing updates from studies related to the monitoring of lipoproteins in different types of cancer. This had led to numerous clinical and experimental studies. The review covers the major lipoproteins such as LDL cholesterol (LDL-C), oxidized low-density lipoprotein cholesterol (oxLDL-C), very low-density lipoprotein cholesterol (VLDL-C), and high-density lipoprotein cholesterol (HDL-C). This is mainly due to increasing evidence from clinical and experimental studies that relate association of lipoproteins with cancer. Generally, a significant association exists between LDL-C with carcinogenesis and high oxLDL with metastasis. This warrants further investigations to include Mendelian randomization design and to be conducted in a larger population to confirm the significance of LDL-C and its oxidized form as prognostic markers of cancer.

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De Sanctis, Juan B., Isaac Blanca, and Nicholas E. Bianco. "Effects of Different Lipoproteins on the Proliferative Response of Interleukin-2-Activated T Lymphocytes and Large Granular Lymphocytes." Clinical Science 89, no. 5 (November 1, 1995): 511–19. http://dx.doi.org/10.1042/cs0890511.

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1. T lymphocytes and large granular lymphocytes internalized chylomicrons, very low-density lipoprotein, low-density lipoprotein, high-density lipoprotein and acetyl modified low-density lipoprotein through different receptors as assessed by flow cytometry. The observed internalization ranged from 8% to 20%. 2. All lipoproteins induced proliferative responses in T lymphocytes and large granular lymphocytes at optimum concentrations (40 μg of protein/ml for all lipoproteins except high-density lipoprotein). Chylomicrons, very low-density lipoprotein and low-density lipoprotein increased T-lymphocyte proliferative response by fourfold while inducing respectively a seven-, nine- and sevenfold increment in large granular lymphocytes. Similarly, high-density lipoprotein and acetyl modified low-density lipoprotein respectively induced a nine- and sevenfold increment in T cells and a 17- and eightfold increment in large granular lymphocyte proliferative response. 3. Both cell types internalized more lipoprotein when they were stimulated with interleukin 2. Chylomicrons and low-density lipoprotein internalization was increased threefold and very low-density lipoprotein internalization twofold, while high-density lipoprotein internalization was unchanged in both cell types. Acetyl modified low-density lipoprotein internalization was fourfold higher in large granular lymphocytes only. 4. The proliferative response of interleukin-2 stimulated cells was different from that of unstimulated cells. Chylomicrons and very low-density lipoprotein induced a sixfold increment in T-cell proliferative response but only a fourfold increment in large granular lymphocytes. Low-density lipoprotein and acetyl modified low-density lipoprotein induced respectively a sevenfold and eightfold increment in T cells and a eightfold and threefold increment in large granular lymphocyte proliferative response. Highdensity lipoprotein did not affect T-lymphocyte proliferative response while inducing a twofold increase in large granular lymphocytes. 5. Lipoproteins are important in the proliferative response of unstimulated and interleukin-2-stimulated cells.

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Gotto, Antonio M. "Interrelationship of triglycerides with lipoproteins and high-density lipoproteins." American Journal of Cardiology 66, no. 6 (September 1990): A20—A23. http://dx.doi.org/10.1016/0002-9149(90)90565-i.

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37

Barbagallo, Carlo M., Maurizio R. Averna, Giovanni Fradà, Davide Noto, Giovanni Cavera, and Alberto Notarbartolo. "Lipoprotein Profile and High-Density Lipoproteins: Subfractions Distribution in Centenarians." Gerontology 44, no. 2 (1998): 106–10. http://dx.doi.org/10.1159/000021992.

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38

Hojnacki, Jerome L., Joanne E. Cluette-Brown, John J. Mulligan, Stephanie M. Hagan, Kathleen E. Mahony, Susan K. Witzgall, Thaddeus V. Osmolski, and Joseph J. Barboriak. "Effect of Ethanol Dose on Low density Lipoproteins and High Density Lipoprotein Subfractions." Alcoholism: Clinical and Experimental Research 12, no. 1 (February 1988): 149–54. http://dx.doi.org/10.1111/j.1530-0277.1988.tb00150.x.

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39

Sparks, D. L., J. Frohlich, and P. H. Pritchard. "Cholesteryl ester transfer activity in plasma of patients with familial high-density lipoprotein deficiency." Clinical Chemistry 34, no. 9 (September 1, 1988): 1812–15. http://dx.doi.org/10.1093/clinchem/34.9.1805.

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Abstract We determined cholesteryl ester transfer activity in whole plasma and in lipoprotein-depleted plasma of normolipidemic subjects and of patients with severe high-density lipoprotein (HDL) deficiency: Tangier disease, lecithin:cholesterol acyltransferase (LCAT) deficiency, and "fish-eye" disease. Transfer rates in plasma were positively correlated (r = 0.950) with rates measured in the absence of the endogenous lipoproteins. This suggests that lipoprotein composition and content may not affect total cholesteryl ester transfer activity in normolipidemic and the HDL-deficient subjects. Cholesteryl ester transfer from solid-phase-bound HDL to plasma lipoproteins was decreased by 39% in fish-eye disease and 33% in LCAT deficiency but increased by 57% in Tangier disease, as compared with normal values. Changes were similar for lipoprotein-depleted plasma from the same individuals. Transfer to plasma HDL was significantly decreased in all HDL-deficient patients, whereas transfer to very-low- and low-density lipoproteins was increased only in Tangier disease. Differences in transfer rates between the patients studied appeared to reflect the LCAT activity and the need to transport cholesteryl ester rather than the HDL cholesterol concentration. Thus, the concentration of HDL in plasma does not directly affect total cholesteryl ester transfer activity in HDL deficiency.

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Hughes, Thomas A., A. Osama Gaber, and Charles E. Montgomery. "Plasma Distribution of Cyclosporine Within Lipoproteins and “In Vitro” Transfer Between Very-Low-Density Lipoproteins, Low-Density Lipoproteins, and High-Density Lipoproteins." Therapeutic Drug Monitoring 13, no. 4 (July 1991): 289–95. http://dx.doi.org/10.1097/00007691-199107000-00002.

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Nauck, M., W. März, B. Haas, and H. Wieland. "Homogeneous assay for direct determination of high-density lipoprotein cholesterol evaluated." Clinical Chemistry 42, no. 3 (March 1, 1996): 424–29. http://dx.doi.org/10.1093/clinchem/42.3.424.

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Abstract We evaluated a new homogeneous assay for quantifying high-density lipoprotein cholesterol (HDL-C). The assay included four reagents: polyethylene glycol for "wrapping" chylomicrons, very-low-density lipoproteins (VLDL), and low-density lipoproteins (LDL); antibodies specific for apolipoprotein (apo) B and apo C-III to produce aggregates of chylomicrons, VLDL, and LDL; enzymes for the enzymatic cholesterol determination of the noncomplexed lipoproteins with 4-aminoantipyrine as the color reagent; and guanidine salt to stop the enzymatic reaction and to solubilize the complexes of apo B-containing lipoproteins, which would otherwise interfere with the reading of absorbance. The total CVs of the new method ranged between 2.4% and 8.4%. The HDL-C values (y) were in good agreement with those by a comparison phosphotungstic acid/MgCl2 method (x): y= 0.987x + 17.2 mg/L (68th percentile of the residuals on the regression line= 21.49, r= 0.970). At triglyceride concentrations of 20 g/L (Intralipid) the homogeneous HDL-C concentrations increased by 2%. Hemoglobin markedly increased the results, whereas bilirubin reduced them. The homogeneous HDL-C assay was easy to handle and allows full automation. This test should considerably facilitate the screening of individuals at an increased risk of cardiovascular disease.

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Levels, J. H. M., J. A. Marquart, P. R. Abraham, A. E. van den Ende, H. O. F. Molhuizen, S. J. H. van Deventer, and J. C. M. Meijers. "Lipopolysaccharide Is Transferred from High-Density to Low-Density Lipoproteins by Lipopolysaccharide-Binding Protein and Phospholipid Transfer Protein." Infection and Immunity 73, no. 4 (April 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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Peynet, J., A. Legrand, B. Messing, F. Thuillier, and F. Rousselet. "An alpha slow-moving high-density-lipoprotein subfraction in serum of a patient with radiation enteritis and peritoneal carcinosis." Clinical Chemistry 35, no. 4 (April 1, 1989): 674–78. http://dx.doi.org/10.1093/clinchem/35.4.674.

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Abstract An alpha slow-moving high-density-lipoprotein (HDL) subfraction was seen in a patient presenting with radiation enteritis and peritoneal carcinosis, who was given long-term cyclic parenteral nutrition. This subfraction, observed in addition to normal HDL, was precipitated with low-density lipoproteins (LDL) and very-low-density lipoproteins (VLDL) by sodium phosphotungstate-magnesium chloride. The patient's serum lipoproteins were analyzed after fractionation by density gradient ultracentrifugation. The alpha slow-moving HDL floated in the ultracentrifugation subfractions with densities ranging from 1.028 to 1.084 kg/L, and their main apolipoproteins included apolipoprotein E in addition to apolipoprotein A-I. These HDL were larger than HDL2. The pathogenesis of this unusual HDL subfraction is hypothesized.

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Et al., Alkhafajy. "A Molecular and Biochemical Study for Cholesteryl Ester Transfer Protein (CETP) Taq1B in Iraqi Patients with Hyperlipidemia." Baghdad Science Journal 16, no. 3(Suppl.) (September 22, 2019): 0747. http://dx.doi.org/10.21123/bsj.2019.16.3(suppl.).0747.

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Cholesteryl ester transfer protein gene contains some single nucleotide polymorphisms, which have been associated with serum high-density lipoprotein concentration and other lipoproteins. This study is done for determining of cholesteryl ester transfer protein polymorphism and evaluate its effect on serum lipid profile concentrations in some hyperlipidemic patients compared with healthy subjects in Salah Al-din governorate-Iraq. Blood samples were taken from (90) patients suffering from hyperlipidemia, and (70) samples that were apparently healthy controls. Serum lipid concentrations were measured by enzymatic assays. The polymorphism was genotyped using polymerase chain reaction restriction fragment length polymorphism analysis. The results showed that there was a significant decrease (P<0.05) in the frequency B2 allele, and B1B2, B2B2 genotype, and a significant increase (P<0.05) in the frequency B1 allele, and B1B1 genotype between patients and controls groups. There was a non-significant decrease in the levels of high density lipoproteins, total cholesterol, low density lipoproteins, and very low density lipoproteins levels, and non-significant increase in levels of triglycerides in individuals with the B1B1 genotype than in the B1B2 and B2B2 genotype. However, high density lipoproteins showed a significant decrease (P<0.001) between individuals with the B1B1 genotype and B2B2 genotype. Also, there was a non-significant difference in the levels of high density lipoproteins, total cholesterol, low density lipoproteins, and very low density lipoproteins levels, in individuals with the B1B2 genotype when compared with that of the B2B2 genotype.

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Strazzella, Arianna, Alice Ossoli, and Laura Calabresi. "High-Density Lipoproteins and the Kidney." Cells 10, no. 4 (March 31, 2021): 764. http://dx.doi.org/10.3390/cells10040764.

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Dyslipidemia is a typical trait of patients with chronic kidney disease (CKD) and it is typically characterized by reduced high-density lipoprotein (HDL)-cholesterol(c) levels. The low HDL-c concentration is the only lipid alteration associated with the progression of renal disease in mild-to-moderate CKD patients. Plasma HDL levels are not only reduced but also characterized by alterations in composition and structure, which are responsible for the loss of atheroprotective functions, like the ability to promote cholesterol efflux from peripheral cells and antioxidant and anti-inflammatory proprieties. The interconnection between HDL and renal function is confirmed by the fact that genetic HDL defects can lead to kidney disease; in fact, mutations in apoA-I, apoE, apoL, and lecithin–cholesterol acyltransferase (LCAT) are associated with the development of renal damage. Genetic LCAT deficiency is the most emblematic case and represents a unique tool to evaluate the impact of alterations in the HDL system on the progression of renal disease. Lipid abnormalities detected in LCAT-deficient carriers mirror the ones observed in CKD patients, which indeed present an acquired LCAT deficiency. In this context, circulating LCAT levels predict CKD progression in individuals at early stages of renal dysfunction and in the general population. This review summarizes the main alterations of HDL in CKD, focusing on the latest update of acquired and genetic LCAT defects associated with the progression of renal disease.

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Tang, Xinyu, Maurice Wong, Jennyfer Tena, Chenghao Zhu, Christopher Rhodes, Qingwen Zhou, Anita Vinjamuri, et al. "Quantitative glycoproteomics of high-density lipoproteins." RSC Advances 12, no. 29 (2022): 18450–56. http://dx.doi.org/10.1039/d2ra02294j.

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Kon, Valentina, Hai-Chun Yang, Loren E. Smith, Kasey C. Vickers, and MacRae F. Linton. "High-Density Lipoproteins in Kidney Disease." International Journal of Molecular Sciences 22, no. 15 (July 30, 2021): 8201. http://dx.doi.org/10.3390/ijms22158201.

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Decades of epidemiological studies have established the strong inverse relationship between high-density lipoprotein (HDL)-cholesterol concentration and cardiovascular disease. Recent evidence suggests that HDL particle functions, including anti-inflammatory and antioxidant functions, and cholesterol efflux capacity may be more strongly associated with cardiovascular disease protection than HDL cholesterol concentration. These HDL functions are also relevant in non-cardiovascular diseases, including acute and chronic kidney disease. This review examines our current understanding of the kidneys’ role in HDL metabolism and homeostasis, and the effect of kidney disease on HDL composition and functionality. Additionally, the roles of HDL particles, proteins, and small RNA cargo on kidney cell function and on the development and progression of both acute and chronic kidney disease are examined. The effect of HDL protein modification by reactive dicarbonyls, including malondialdehyde and isolevuglandin, which form adducts with apolipoprotein A-I and impair proper HDL function in kidney disease, is also explored. Finally, the potential to develop targeted therapies that increase HDL concentration or functionality to improve acute or chronic kidney disease outcomes is discussed.

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Lee, Justin MS, and Robin P. Choudhury. "Atherosclerosis regression and high-density lipoproteins." Expert Review of Cardiovascular Therapy 8, no. 9 (September 2010): 1325–34. http://dx.doi.org/10.1586/erc.10.108.

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Ochoa, Maria C., Ignacio Melero, and Pedro Berraondo. "High-density lipoproteins delivering interleukin-15." OncoImmunology 2, no. 4 (April 2013): e23410. http://dx.doi.org/10.4161/onci.23410.

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Assmann, Gerd, and Jerzy-Roch Nofer. "Atheroprotective Effects of High-Density Lipoproteins." Annual Review of Medicine 54, no. 1 (February 2003): 321–41. http://dx.doi.org/10.1146/annurev.med.54.101601.152409.

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Journal articles on the topic 'High density lipoproteins'

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