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1

Ozsavci, Derya, A. Nazli, O. Bingol Ozakpinar, G. Yanikkaya Demirel, B. Vanizor Kural, and A. Sener. "Native High-Density Lipoprotein and Melatonin Improve Platelet Response Induced by Glycated Lipoproteins." Folia Biologica 64, no. 4 (2018): 144–52. http://dx.doi.org/10.14712/fb2018064040144.

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Activated platelets and glycated lipoproteins are responsible for atherothrombosis in diabetics. Melatonin and native high-density lipoproteins are crucial in the preservation of pro/oxidant-antioxidant balance. The aim of the present study was to investigate the in vitro effects of native high-density lipoproteins and melatonin on altering the platelet response induced by glycated lipoproteins. Low-density lipoproteins and high-density lipoproteins were purified from plasma by ultracentrifugation and were glycated with glucose for three weeks. After incubation with or without melatonin/or nat
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2

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 (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-lymph
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3

Myers, D. E., W. N. Huang, and R. G. Larkins. "Lipoprotein-induced prostacyclin production in endothelial cells and effects of lipoprotein modification." American Journal of Physiology-Cell Physiology 271, no. 5 (1996): C1504—C1511. http://dx.doi.org/10.1152/ajpcell.1996.271.5.c1504.

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Although lipoprotein modification has been implicated in atherogenesis, the effect of modified forms of lipoproteins on vascular cell function has not been fully resolved. We have investigated lipoprotein-induced prostaglandin production by macrovascular endothelial cells. This study delineates early responses of endothelial cells after exposure to native and modified forms of the lipoproteins. Modification of lipoproteins by oxidation or glycation significantly affected the capacity of lipoproteins to induce prostacyclin (PGI2) production by bovine aortic endothelial cells (BAEC). Modified lo
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4

Yasmin, Raheela, Aashi Ahmed, Ambreen Javed, et al. "The Effect of Blood Sugar Fasting Levels on Diabetic Dyslipidemia." Pakistan Journal of Medical and Health Sciences 16, no. 4 (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 lipopro
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5

Huang, Haibin, Mingqun Lin, Xueqi Wang, et al. "Proteomic Analysis of and Immune Responses to Ehrlichia chaffeensis Lipoproteins." Infection and Immunity 76, no. 8 (2008): 3405–14. http://dx.doi.org/10.1128/iai.00056-08.

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ABSTRACT Ehrlichia chaffeensis is an obligately intracellular gram-negative bacterium and is the etiologic agent of human monocytic ehrlichiosis (HME). Although E. chaffeensis induces the generation of several cytokines and chemokines by leukocytes, E. chaffeensis lacks lipopolysaccharide and peptidoglycan. Bioinfomatic analysis of the E. chaffeensis genome, however, predicted genes encoding 15 lipoproteins and 3 posttranslational lipoprotein-processing enzymes. The present study showed that by use of multidimensional liquid chromatography followed by tandem mass spectrometry, all predicted li
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6

Dodds, P. F., A. Lopez-Johnston, V. A. Welch, and M. I. Gurr. "The effects of chemically modifying serum apolipoproteins on their ability to activate lipoprotein lipase." Biochemical Journal 242, no. 2 (1987): 471–78. http://dx.doi.org/10.1042/bj2420471.

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Lipoprotein lipase activity was measured in an acetone-dried-powder preparation from rat epididymal adipose tissue using pig serum or pig serum lipoprotein, which had been chemically modified, as activator. Modification of acidic amino acids of lipoproteins with NN-dimethyl-1,3-diamine resulted in a complete loss of ability to activate lipoprotein lipase. Modification of 34% of lipoprotein arginine groups with cyclohexanedione resulted in the loss of 75% of the activation of lipoprotein lipase; approx. 42% of the original activity was recovered after reversal of the modification. This effect w
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7

Giesecke, Yvonne, Samuel Soete, Katarzyna MacKinnon, et al. "Developing Electron Microscopy Tools for Profiling Plasma Lipoproteins Using Methyl Cellulose Embedment, Machine Learning and Immunodetection of Apolipoprotein B and Apolipoprotein(a)." International Journal of Molecular Sciences 21, no. 17 (2020): 6373. http://dx.doi.org/10.3390/ijms21176373.

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Plasma lipoproteins are important carriers of cholesterol and have been linked strongly to cardiovascular disease (CVD). Our study aimed to achieve fine-grained measurements of lipoprotein subpopulations such as low-density lipoprotein (LDL), lipoprotein(a) (Lp(a), or remnant lipoproteins (RLP) using electron microscopy combined with machine learning tools from microliter samples of human plasma. In the reported method, lipoproteins were absorbed onto electron microscopy (EM) support films from diluted plasma and embedded in thin films of methyl cellulose (MC) containing mixed metal stains, pr
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8

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 tha
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9

Renee Ruhaak, L., Arnoud van der Laarse, and Christa M. Cobbaert. "Apolipoprotein profiling as a personalized approach to the diagnosis and treatment of dyslipidaemia." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 56, no. 3 (2019): 338–56. http://dx.doi.org/10.1177/0004563219827620.

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An elevated low-density lipoprotein cholesterol concentration is a classical risk factor for cardiovascular disease. This has led to pharmacotherapy in patients with atherosclerotic heart disease or high heart disease risk with statins to reduce serum low-density lipoprotein cholesterol. Even in patients in whom the target levels of low-density lipoprotein cholesterol are reached, there remains a significant residual cardiovascular risk; this is due, in part, to a focus on low-density lipoprotein cholesterol alone and neglect of other important aspects of lipoprotein metabolism. A more refined
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10

Öörni, Katariina, Satu Lehti, Peter Sjövall, and Petri T. Kovanen. "Triglyceride-Rich Lipoproteins as a Source of Proinflammatory Lipids in the Arterial Wall." Current Medicinal Chemistry 26, no. 9 (2019): 1701–10. http://dx.doi.org/10.2174/0929867325666180530094819.

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Apolipoprotein B –containing lipoproteins include triglyceride-rich lipoproteins (chylomicrons and their remnants, and very low-density lipoproteins and their remnants) and cholesterol-rich low-density lipoprotein particles. Of these, lipoproteins having sizes below 70-80 nm may enter the arterial wall, where they accumulate and induce the formation of atherosclerotic lesions. The processes that lead to accumulation of lipoprotein-derived lipids in the arterial wall have been largely studied with a focus on the low-density lipoprotein particles. However, recent observational and genetic studie
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11

Niu, You-Guo, and Rhys D. Evans. "Metabolism of very-low-density lipoprotein and chylomicrons by streptozotocin-induced diabetic rat heart: effects of diabetes and lipoprotein preference." American Journal of Physiology-Endocrinology and Metabolism 295, no. 5 (2008): E1106—E1116. http://dx.doi.org/10.1152/ajpendo.90260.2008.

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Very-low-density lipoprotein (VLDL) and chylomicrons (CM) are major sources of fatty acid supply to the heart, but little is known about their metabolism in diabetic myocardium. To investigate this, working hearts isolated from control rats and diabetic rats 2 wk following streptozotocin (STZ) injection were perfused with control and diabetic lipoproteins. Analysis of the diabetic lipoproteins showed that both VLDL and CM were altered compared with control lipoproteins; both were smaller and had different apolipoprotein composition. Heparin-releasable lipoprotein lipase (HR-LPL) activity was i
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12

Neufeld, Edward B., Masaki Sato, Scott M. Gordon, et al. "ApoA-I-Mediated Lipoprotein Remodeling Monitored with a Fluorescent Phospholipid." Biology 8, no. 3 (2019): 53. http://dx.doi.org/10.3390/biology8030053.

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We describe simple, sensitive and robust methods to monitor lipoprotein remodeling and cholesterol and apolipoprotein exchange, using fluorescent Lissamine Rhodamine B head-group tagged phosphatidylethanolamine (*PE) as a lipoprotein reference marker. Fluorescent Bodipy cholesterol (*Chol) and *PE directly incorporated into whole plasma lipoproteins in proportion to lipoprotein cholesterol and phospholipid mass, respectively. *Chol, but not *PE, passively exchanged between isolated plasma lipoproteins. Fluorescent apoA-I (*apoA-I) specifically bound to high-density lipoprotein (HDL) and remode
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13

Biggerstaff, Kyle D., and Joshua S. Wooten. "Understanding lipoproteins as transporters of cholesterol and other lipids." Advances in Physiology Education 28, no. 3 (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 a
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14

Adam, Leonie, and Thomas Bobbert. "Non-HDL-Cholesterin." Diabetes aktuell 18, no. 06 (2020): 242–46. http://dx.doi.org/10.1055/a-1237-6894.

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ZUSAMMENFASSUNGDie diabetische Stoffwechsellage korreliert häufig mit einer Dyslipidämie, die sich typischerweise durch erhöhte Triglyzeride, niedriges HDL-Cholesterin und eine hohe Konzentration an small dense LDL-Cholesterin (LDL: low-density lipoprotein) auszeichnet. Zur kardiovaskulären Risikostratifizierung bei Diabetes mellitus Typ 2 eignet sich die Verwendung von Non-HDL-Cholesterin (HDL: high-density lipoprotein), um sämtliche potenziell atherogene Lipoproteine – VLDL (very-low-density lipoprotein), IDL (intermediate-density lipoprotein), LDL, Lipoprotein(a), Chylomikronen, Remnants –
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15

Rota, Simin, Nicola A. McWilliam, Trevor P. Baglin, and Christopher D. Byrne. "Atherogenic Lipoproteins Support Assembly of the Prothrombinase Complex and Thrombin Generation: Modulation by Oxidation and Vitamin E." Blood 91, no. 2 (1998): 508–15. http://dx.doi.org/10.1182/blood.v91.2.508.

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AbstractThe importance of lipoproteins in the etiology of atherosclerosis is well established. Evidence is now accumulating to implicate thrombin in the pathogenesis of atherosclerosis. We have investigated whether atherogenic lipoproteins can support thrombin generation. In the absence of platelets or endothelial cells, both very low-density lipoprotein (VLDL) and oxidized low-density lipoprotein (LDL) support assembly of the prothrombinase complex and generation of thrombin. Thrombin generation (per μg of apolipoprotein) supported by VLDL was 19.4-fold greater than that supported by high-den
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16

Rota, Simin, Nicola A. McWilliam, Trevor P. Baglin, and Christopher D. Byrne. "Atherogenic Lipoproteins Support Assembly of the Prothrombinase Complex and Thrombin Generation: Modulation by Oxidation and Vitamin E." Blood 91, no. 2 (1998): 508–15. http://dx.doi.org/10.1182/blood.v91.2.508.508_508_515.

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The importance of lipoproteins in the etiology of atherosclerosis is well established. Evidence is now accumulating to implicate thrombin in the pathogenesis of atherosclerosis. We have investigated whether atherogenic lipoproteins can support thrombin generation. In the absence of platelets or endothelial cells, both very low-density lipoprotein (VLDL) and oxidized low-density lipoprotein (LDL) support assembly of the prothrombinase complex and generation of thrombin. Thrombin generation (per μg of apolipoprotein) supported by VLDL was 19.4-fold greater than that supported by high-density lip
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17

Karpe, F., A. S. Bickerton, L. Hodson, B. A. Fielding, G. D. Tan, and K. N. Frayn. "Removal of triacylglycerols from chylomicrons and VLDL by capillary beds: the basis of lipoprotein remnant formation." Biochemical Society Transactions 35, no. 3 (2007): 472–76. http://dx.doi.org/10.1042/bst0350472.

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The triacylglycerol content of chylomicrons and VLDL (very-low-density lipoprotein) compete for the same lipolytic pathway in the capillary beds. Although chylomicron triacylglycerols appear to be the favoured substrate for lipoprotein lipase, VLDL particles compete in numbers. Methods to quantify the specific triacylglycerol removal from VLDL and chylomicrons may involve endogenous labelling of the triacylglycerol substrate with stable isotopes in combination with arteriovenous blood sampling in humans. Arteriovenous quantification of remnant lipoproteins suggests that adipose tissue with its
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18

Basile-Borgia, Annette, and John H. Abel. "Lipoproteins in heart disease." Perfusion 11, no. 4 (1996): 338–45. http://dx.doi.org/10.1177/026765919601100407.

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Most lipids are carried in the circulation by lipoproteins. Liproproteins and their associated proteins, called apolipoproteins, are currently being studied in an effort to further our understanding of atherosclerotic cardiovascular disease. Lipoprotein assembly, secretion, transportation, modification and clearance are essential elements of healthy lipid metabolism. When one or more of these key steps becomes altered, various disease states are induced. Current data suggest that lipoprotein(a), a low density lipoprotein (LDL)-like particle, is an acute phase reactant that plays a critical rol
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19

Ruiz-Albusac, J. M., E. Velázquez, and A. Montes. "Differential precipitation of isolated human plasma lipoproteins with heparin and manganese chloride." Clinical Chemistry 34, no. 2 (1988): 240–43. http://dx.doi.org/10.1093/clinchem/34.2.235.

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Abstract We studied the precipitation of isolated lipoproteins with heparin and MnCl2. Lipoproteins were isolated from human plasma by preparative ultracentrifugation and their free cholesterol was labeled. Each lipoprotein fraction was then precipitated at various pHs, with or without bovine serum albumin (60 g/L) present. Under no set of conditions was one class of lipoproteins completely separated from the other two. Specifically, under standard conditions for precipitation of serum lipoproteins (pH 7.4 and protein 60 g/L), 12% of the very-low-density lipoprotein (VLDL) and 8% of the low-de
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20

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 (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
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21

Jameel, Ali H., Maeda M. T. Al-Sulaivany, Saad D. Oleiwi, and Mohammed J. Mohammed. "Physiological Effects of Nano-Magnesium Against Bisphenol A-induced Toxicity in Male Albino Rats." IOP Conference Series: Earth and Environmental Science 1262, no. 6 (2023): 062004. http://dx.doi.org/10.1088/1755-1315/1262/6/062004.

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Abstract This study was conducted to determine the effect of oral administration with two concentrations of 30% and 40% of nano-magnesium on Bisphenol-A in liver enzyme parameters (ALT, AST, ALP), kidney function and lipid profile of male white rats Bisphenol-The concentrations of triglycerides (TG), cholesterol (TC), low-density lipoproteins (LDL), and very low-density lipoproteins (vLDL) were all increased by A, whereas the concentration of high-density lipoproteins (HDL) was decreased. while liver enzyme parameters decreased noticeably. Nano-magnesium treatment led to decreases in levels of
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22

Trentalance, A., G. Bruscalupi, L. Conti Devirgiliis, et al. "Changes in lipoprotein binding and uptake by hepatocytes during rat liver regeneration." Bioscience Reports 9, no. 2 (1989): 231–41. http://dx.doi.org/10.1007/bf01116000.

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The binding and uptake of cholesterol enriched lipoproteins by isolated hepatocytes was decreased at 16 hours after partial hepatectomy, with a tendency to return to control values as the regeneration proceeds. The number of lipoprotein binding sites of total cellular membranes remained similar to control at 16 and 24 hours. The plasma lipoprotein pattern, determined by electrophoretic analysis, showed a lower per cent of very low density lipoproteins (VLDL) and a higher per cent of low density lipoproteins (LDL) at 16 and 24 hours post-partial hepatectomy. At these times, plasma lecithin: cho
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23

Dubrey, Simon W., David A. Reaveley, David G. Leslie, Martina O'Donnell, Bernadette M. O'Connor, and Mary Seed. "Effect of Insulin-Dependent Diabetes Mellitus on Lipids and Lipoproteins: A Study of Identical Twins." Clinical Science 84, no. 5 (1993): 537–42. http://dx.doi.org/10.1042/cs0840537.

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1. Forty-five identical twin pairs, discordant for insulin-dependent diabetes mellitus, were studied with respect to their serum lipid (high-density lipoprotein, low-density lipoprotein, total cholesterol and triacylglycerol) and apoprotein [apoprotein A-I, apoprotein B and lipoprotein (a)] concentrations and apoprotein (a) phenotypes. The twins were compared with an age- and sex-matched non-diabetic control group. 2. A significantly higher value was found only for high-density lipoprotein cholesterol in the diabetic twins of the female twin pairs. 3. Highly significant correlations existed be
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24

Brämswig, Susanne, Anja Kerksiek, Thomas Sudhop, Claus Luers, Klaus Von Bergmann, and Heiner K. Berthold. "Carbamazepine increases atherogenic lipoproteins: mechanism of action in male adults." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 2 (2002): H704—H716. http://dx.doi.org/10.1152/ajpheart.00580.2001.

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Treatment with carbamazepine (CBZ) affects cholesterol concentrations, but little is known about the precise nature and underlying mechanisms of changes in lipoprotein metabolism. We investigated prospectively the effects of CBZ on lipid metabolism in normolipemic adults. In 21 healthy males, lipoprotein and noncholesterol sterol concentrations were measured before and during treatment with CBZ for 70 ± 18 days. Thirteen subjects underwent kinetic studies of apolipoprotein-B (ApoB) metabolism with the use of endogenous stable isotope labeling. Lipoprotein kinetic parameters were calculated by
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25

Rüfer, Corinna E., Sabine E. Kulling, Jutta Möseneder, Peter Winterhalter та Achim Bub. "Role of plasma lipoproteins in the transport of the soyabean isoflavones daidzein and daidzein-7-O-β-d-glucoside". British Journal of Nutrition 102, № 6 (2009): 793–96. http://dx.doi.org/10.1017/s0007114509297224.

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Isoflavone intake is associated with various properties beneficial to human health which are related to their antioxidant activity, for example, to their ability to increase LDL oxidation resistance. However, the distribution of isoflavones among plasma lipoproteins has not yet been elucidated in vivo. Therefore, the objective of the present study was to investigate the association between daidzein (DAI) and lipoproteins in human plasma upon administration of the aglycone and glucoside form. Five men aged 22–30 years participated in a randomised, double-blind study in cross-over design. After
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26

Wade, D. P., B. L. Knight, and A. K. Soutar. "Detection of the low-density-lipoprotein receptor with biotin-low-density lipoprotein. A rapid new method for ligand blotting." Biochemical Journal 229, no. 3 (1985): 785–90. http://dx.doi.org/10.1042/bj2290785.

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A new technique has been developed to identify low-density-lipoprotein (LDL) receptors on nitrocellulose membranes, after transfer from SDS/polyacrylamide gels, by ligand blotting with biotin-modified LDL. Modification with biotin hydrazide of periodate-oxidized lipoprotein sugar residues does not affect the ability of the lipoprotein to bind to the LDL receptor. Bound lipoprotein is detected with high sensitivity by a streptavidin-biotin-peroxidase complex, and thus this method eliminates the need for specific antibodies directed against the ligand. The density of the bands obtained is propor
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27

Baumgärtner, Maja, Uwe Kärst, Birgit Gerstel, Martin Loessner, Jürgen Wehland, and Lothar Jänsch. "Inactivation of Lgt Allows Systematic Characterization of Lipoproteins from Listeria monocytogenes." Journal of Bacteriology 189, no. 2 (2006): 313–24. http://dx.doi.org/10.1128/jb.00976-06.

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ABSTRACT Lipoprotein anchoring in bacteria is mediated by the prolipoprotein diacylglyceryl transferase (Lgt), which catalyzes the transfer of a diacylglyceryl moiety to the prospective N-terminal cysteine of the mature lipoprotein. Deletion of the lgt gene in the gram-positive pathogen Listeria monocytogenes (i) impairs intracellular growth of the bacterium in different eukaryotic cell lines and (ii) leads to increased release of lipoproteins into the culture supernatant. Comparative extracellular proteome analyses of the EGDe wild-type strain and the Δlgt mutant provided systematic insight i
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Whayne, Thomas F. "High-density Lipoprotein Cholesterol: Current Perspective for Clinicians." Angiology 60, no. 5 (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 me
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29

Tanaka, Kimie, Shin-Ichi Matsuyama, and Hajime Tokuda. "Deletion of lolB, Encoding an Outer Membrane Lipoprotein, Is Lethal for Escherichia coli and Causes Accumulation of Lipoprotein Localization Intermediates in the Periplasm." Journal of Bacteriology 183, no. 22 (2001): 6538–42. http://dx.doi.org/10.1128/jb.183.22.6538-6542.2001.

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ABSTRACT Outer membrane lipoproteins of Escherichia coli are released from the inner membrane upon the formation of a complex with a periplasmic chaperone, LolA, followed by localization to the outer membrane. In vitro biochemical analyses revealed that the localization of lipoproteins to the outer membrane generally requires an outer membrane lipoprotein, LolB, and occurs via transient formation of a LolB-lipoprotein complex. On the other hand, a mutant carrying the chromosomal lolB gene under the control of thelac promoter-operator grew normally in the absence of LolB induction if the mutant
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30

Levels, J. H. M., P. R. Abraham, A. van den Ende, and S. J. H. van Deventer. "Distribution and Kinetics of Lipoprotein-Bound Endotoxin." Infection and Immunity 69, no. 5 (2001): 2821–28. http://dx.doi.org/10.1128/iai.69.5.2821-2828.2001.

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ABSTRACT Lipopolysaccharide (LPS), the major glycolipid component of gram-negative bacterial outer membranes, is a potent endotoxin responsible for pathophysiological symptoms characteristic of infection. The observation that the majority of LPS is found in association with plasma lipoproteins has prompted the suggestion that sequestering of LPS by lipid particles may form an integral part of a humoral detoxification mechanism. Previous studies on the biological properties of isolated lipoproteins used differential ultracentrifugation to separate the major subclasses. To preserve the integrity
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31

Whyte, Martin B. "Is high-density lipoprotein a modifiable treatment target or just a biomarker for cardiovascular disease?" JRSM Cardiovascular Disease 8 (January 2019): 204800401986973. http://dx.doi.org/10.1177/2048004019869736.

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Epidemiological data strongly support the inverse association between high-density lipoprotein cholesterol concentration and cardiovascular risk. Over the last three decades, pharmaceutical strategies have been partially successful in raising high-density lipoprotein cholesterol concentration, but clinical outcomes have been disappointing. A recent therapeutic class is the cholesteryl ester transfer protein inhibitor. These drugs can increase circulating high-density lipoprotein cholesterol levels by inhibiting the exchange of cholesteryl ester from high-density lipoprotein for triacylglycerol
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32

Kurano, Makoto, Kuniyuki Kano, Masumi Hara, Kazuhisa Tsukamoto, Junken Aoki, and Yutaka Yatomi. "Regulation of plasma glycero-lysophospholipid levels by lipoprotein metabolism." Biochemical Journal 476, no. 23 (2019): 3565–81. http://dx.doi.org/10.1042/bcj20190498.

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Glycero-lysophospholipids, such as lysophosphatidic acids and lysophosphatidylserine, are gathering attention, since specific receptors have been identified. Most of these compounds have been proposed to be bound to albumin, while their associations with lipoproteins have not been fully elucidated. Therefore, in this study, we aimed to investigate the contents of glycero-lysophospholipids (lysophosphatidic acids, lysophosphatidylcholine, lysophosphatidylethanolamine, lysophosphatidylglycerol, lysophosphatidylinositol, and lysophosphatidylserine) on lipoproteins and the modulation of their meta
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33

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 (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
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Hultin, M., G. Olivecrona, and T. Olivecrona. "Effect of protamine on lipoprotein lipase and hepatic lipase in rats." Biochemical Journal 304, no. 3 (1994): 959–66. http://dx.doi.org/10.1042/bj3040959.

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The polycation protamine impedes the catabolism of triglyceride-rich lipoproteins and this has been suggested to be due to intravascular inactivation of lipoprotein lipase. We have made intravenous injections of protamine to rats and found that both lipoprotein lipase and hepatic lipase activities were released to plasma. The effect of protamine was more short-lived than that obtained by injection of heparin. The release of hepatic lipase by protamine was as effective as the release by heparin, while the amount of lipoprotein lipase released by protamine was only about one-tenth of that releas
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35

Klobučar, Iva, Lidija Hofmann, Hansjörg Habisch, et al. "Advanced Oxidation Protein Products Are Strongly Associated with the Serum Levels and Lipid Contents of Lipoprotein Subclasses in Healthy Volunteers and Patients with Metabolic Syndrome." Antioxidants 13, no. 3 (2024): 339. http://dx.doi.org/10.3390/antiox13030339.

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The association between advanced oxidation protein products (AOPPs) and lipoprotein subclasses remains unexplored. Therefore, we performed comprehensive lipoprotein profiling of serum using NMR spectroscopy and examined the associations of lipoprotein subclasses with the serum levels of AOPPs in healthy volunteers (HVs) and patients with metabolic syndrome (MS). The serum levels of AOPPs were significantly positively correlated with the serum levels of very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and low-density lipoprotein (LDL); however, they were significantl
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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
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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 (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 modi
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Collins, Lisamarie A., Shama P. Mirza, Ahmed H. Kissebah, and Michael Olivier. "Integrated approach for the comprehensive characterization of lipoproteins from human plasma using FPLC and nano-HPLC-tandem mass spectrometry." Physiological Genomics 40, no. 3 (2010): 208–15. http://dx.doi.org/10.1152/physiolgenomics.00136.2009.

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The implication of the various lipoprotein classes in the development of atherosclerotic cardiovascular disease has served to focus a great deal of attention on these particles over the past half-century. Using knowledge gained by the sequencing of the human genome, recent research efforts have been directed toward the elucidation of the proteomes of several lipoprotein subclasses. One of the challenges of such proteomic experimentation is the ability to initially isolate plasma lipoproteins subsequent to their analysis by mass spectrometry. Although several methods for the isolation of plasma
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Das, Sankar, Taisei Kanamoto, Xiuchun Ge, et al. "Contribution of Lipoproteins and Lipoprotein Processing to Endocarditis Virulence in Streptococcus sanguinis." Journal of Bacteriology 191, no. 13 (2009): 4166–79. http://dx.doi.org/10.1128/jb.01739-08.

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ABSTRACT Streptococcus sanguinis is an important cause of infective endocarditis. Previous studies have identified lipoproteins as virulence determinants in other streptococcal species. Using a bioinformatic approach, we identified 52 putative lipoprotein genes in S. sanguinis strain SK36 as well as genes encoding the lipoprotein-processing enzymes prolipoprotein diacylglyceryl transferase (lgt) and signal peptidase II (lspA). We employed a directed signature-tagged mutagenesis approach to systematically disrupt these genes and screen each mutant for the loss of virulence in an animal model of
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Szczepanek, S. M., S. Frasca, V. L. Schumacher, et al. "Identification of Lipoprotein MslA as a Neoteric Virulence Factor of Mycoplasma gallisepticum." Infection and Immunity 78, no. 8 (2010): 3475–83. http://dx.doi.org/10.1128/iai.00154-10.

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ABSTRACT Many lipoproteins are expressed on the surfaces of mycoplasmas, and some have been implicated as playing roles in pathogenesis. Family 2 lipoproteins of Mycoplasma pneumoniae have a conserved “mycoplasma lipoprotein X” central domain and a “mycoplasma lipoprotein 10” C-terminal domain and are differentially expressed in response to environmental conditions. Homologues of family 2 lipoproteins are Mycoplasma specific and include the lipoprotein of Mycoplasma gallisepticum, encoded by the MGA0674 gene. Comparative transcriptomic analysis of the M. gallisepticum live attenuated vaccine s
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Zheng, Chunyu, Allison B. Andraski, Christina Khoo, Jeremy D. Furtado, and Frank M. Sacks. "Food Intake Suppresses ApoB Secretion and Fractional Catabolic Rates in Humans." Arteriosclerosis, Thrombosis, and Vascular Biology 44, no. 2 (2024): 435–51. http://dx.doi.org/10.1161/atvbaha.123.319769.

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BACKGROUND: Humans spend much of the day in the postprandial state. However, most research and clinical guidelines on plasma lipids pertain to blood drawn after a 12-hour fast. We aimed to study the metabolic differences of apoB lipoproteins between the fasting and postprandial states. METHODS: We investigated plasma apoB metabolism using stable isotope tracers in 12 adult volunteers under fasting and continuous postprandial conditions in a randomized crossover study. We determined the metabolism of apoB in multiple lipoprotein subfractions, including light and dense VLDLs (very-low-density li
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Harbaum, Lars, Pavandeep Ghataorhe, John Wharton, et al. "Reduced plasma levels of small HDL particles transporting fibrinolytic proteins in pulmonary arterial hypertension." Thorax 74, no. 4 (2018): 380–89. http://dx.doi.org/10.1136/thoraxjnl-2018-212144.

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BackgroundAberrant lipoprotein metabolism has been implicated in experimental pulmonary hypertension, but the relevance to patients with pulmonary arterial hypertension (PAH) is inconclusive.ObjectiveTo investigate the relationship between circulating lipoprotein subclasses and survival in patients with PAH.MethodsUsing nuclear magnetic resonance spectroscopy, 105 discrete lipoproteins were measured in plasma samples from two cohorts of patients with idiopathic or heritable PAH. Data from 1124 plasma proteins were used to identify proteins linked to lipoprotein subclasses. The physical presenc
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Herdt, Thomas H., and Jennifer C. Smith. "Blood-Lipid and Lactation-Stage Factors Affecting Serum Vitamin E Concentrations and Vitamin E Cholesterol Ratios in Dairy Cattle." Journal of Veterinary Diagnostic Investigation 8, no. 2 (1996): 228–32. http://dx.doi.org/10.1177/104063879600800213.

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The distribution of cholesterol and vitamin E among the various lipoprotein density fractions in bovine blood was measured. The percentage of total plasma vitamin E and cholesterol in the various lipoprotein fractions was very-low-density lipoprotein, 2% and 2%, respectively; low-density lipoprotein, 17% and 22%, respectively; and high-density lipoprotein, 77% and 72%, respectively. Only 3% of plasma vitamin E was not associated with the lipoproteins. Vitamin E cholesterol ratios were not significantly different among lipoprotein fractions ( P = 0.3). These results indicate that vitamin E and
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Mortensen, Jonas Ellegaard, Trygve Andreassen, Dorte Aalund Olsen, et al. "Serum Lipoprotein Profiling by NMR Spectroscopy Reveals Alterations in HDL-1 and HDL-2 Apo-A2 Subfractions in Alzheimer’s Disease." International Journal of Molecular Sciences 25, no. 21 (2024): 11701. http://dx.doi.org/10.3390/ijms252111701.

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Identifying biomarkers for Alzheimer’s disease (AD) is crucial, due to its complex pathology, which involves dysfunction in lipid transport, contributing to neuroinflammation, synaptic loss, and impaired amyloid-β clearance. Nuclear magnetic resonance (NMR) is able to quantify and stratify lipoproteins. The study investigated lipoproteins in blood from AD patients, aiming to evaluate their diagnostic potential. Serum and plasma were collected from AD patients (n = 25) and healthy individuals (n = 25). We conducted a comprehensive lipoprotein profiling on serum samples using NMR spectroscopy, a
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Takahashi, M., Y. Yui, H. Yasumoto, et al. "Lipoproteins are inhibitors of endothelium-dependent relaxation of rabbit aorta." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 1 (1990): H1—H8. http://dx.doi.org/10.1152/ajpheart.1990.258.1.h1.

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The present study was performed to investigate plasma inhibitors of endothelium-dependent relaxation other than hemoglobin and low-density lipoprotein (LDL). We purified an inhibitor that contained a protein of 28,000 Da from human plasma by ammonium sulfate precipitation and serial chromatography. NH2-terminal sequence analysis revealed the protein to be homologous with human apolipoprotein A-I (Apo A-I), a major apolipoprotein of high-density lipoprotein (HDL). Very low-density lipoprotein (VLDL), LDL, and HDL obtained from rabbit plasma reversed endothelium-dependent relaxation of rabbit ao
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KIBKAŁO, DMYTRO, OLGA TYMOSZENKO, and HALINA WIKULINA. "erum interleukin content and lipid metabolism in cows with subclinical ketosis." Medycyna Weterynaryjna 79, no. 11 (2023): 582–86. http://dx.doi.org/10.21521/mw.6820.

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This paper analyses the diagnostic utility of interleukins (1, 4, 6) and lipid metabolism products (cholesterol, triacylglycerols, lipoprotein fractions) in subclinical ketosis in cows. It was found that serum levels of proinflammatory (IL-1 and IL-6) and anti-inflammatory (IL-4) interleukins in cows with ketosis did not differ from those in clinically healthy animals. This therefore indicates the absence of inflammation in the subclinical form of ketosis. These data were also confirmed by normal α1- and α2-globulin levels. IL-6 is known to increase the synthesis of acute phase inflammatory pr
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47

Denham, E. L., P. N. Ward, and J. A. Leigh. "Lipoprotein Signal Peptides Are Processed by Lsp and Eep of Streptococcus uberis." Journal of Bacteriology 190, no. 13 (2008): 4641–47. http://dx.doi.org/10.1128/jb.00287-08.

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ABSTRACT Lipoprotein signal peptidase (lsp) is responsible for cleaving the signal peptide sequence of lipoproteins in gram-positive bacteria. Investigation of the role of Lsp in Streptococcus uberis, a common cause of bovine mastitis, was undertaken using the lipoprotein MtuA (a protein essential for virulence) as a marker. The S. uberis lsp mutant phenotype displayed novel lipoprotein processing. Not only was full-length (uncleaved) MtuA detected by Western blotting, but during late log phase, a lower-molecular-weight derivative of MtuA was evident. Similar analysis of an S. uberis double mu
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48

Ye, S. Q., V. N. Trieu, D. L. Stiers, and W. J. McConathy. "Interactions of low density lipoprotein2 and other apolipoprotein B-containing lipoproteins with lipoprotein(a)." Journal of Biological Chemistry 263, no. 13 (1988): 6337–43. http://dx.doi.org/10.1016/s0021-9258(18)68791-5.

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Bakillah, Ahmed, Khamis Khamees Obeid, Maram Al Subaiee, et al. "Association of Advanced Lipoprotein Subpopulation Profiles with Insulin Resistance and Inflammation in Patients with Type 2 Diabetes Mellitus." Journal of Clinical Medicine 12, no. 2 (2023): 487. http://dx.doi.org/10.3390/jcm12020487.

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Plasma lipoproteins exist as several subpopulations with distinct particle number and size that are not fully reflected in the conventional lipid panel. In this study, we sought to quantify lipoprotein subpopulations in patients with type 2 diabetes mellitus (T2DM) to determine whether specific lipoprotein subpopulations are associated with insulin resistance and inflammation markers. The study included 57 patients with T2DM (age, 61.14 ± 9.99 years; HbA1c, 8.66 ± 1.60%; mean body mass index, 35.15 ± 6.65 kg/m2). Plasma lipoprotein particles number and size were determined by nuclear magnetic
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Zhao, Yang, James B. McCabe, Jean Vance, and Luc G. Berthiaume. "Palmitoylation of Apolipoprotein B Is Required for Proper Intracellular Sorting and Transport of Cholesteroyl Esters and Triglycerides." Molecular Biology of the Cell 11, no. 2 (2000): 721–34. http://dx.doi.org/10.1091/mbc.11.2.721.

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Apolipoprotein B (apoB) is an essential component of chylomicrons, very low density lipoproteins, and low density lipoproteins. ApoB is a palmitoylated protein. To investigate the role of palmitoylation in lipoprotein function, a palmitoylation site was mapped to Cys-1085 and removed by mutagenesis. Secreted lipoprotein particles formed by nonpalmitoylated apoB were smaller and denser and failed to assemble a proper hydrophobic core. Indeed, the relative concentrations of nonpolar lipids were three to four times lower in lipoprotein particles containing mutant apoB compared with those containi
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