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1

Solnica, Bogdan, Grażyna Sygitowicz, Dariusz Sitkiewicz, et al. "Wytyczne Polskiego Towarzystwa Diagnostyki Laboratoryjnej i Polskiego Towarzystwa Lipidologicznego dotyczące diagnostyki laboratoryjnej zaburzeń gospodarki lipidowej." Diagnostyka Laboratoryjna 55, no. 4 (2020): 239–56. http://dx.doi.org/10.5604/01.3001.0014.1296.

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Na rutynowo wykonywany w celu oceny ryzyka sercowo-naczyniowego profil lipidowy składają się oznaczenia/wyliczenia stężenia w surowicy/osoczu cholesterolu całkowitego (TC), cholesterolu lipoprotein o dużej gęstości (HDL-C), cholesterolu lipoprotein o małej gęstości (LDL-C), triglicerydów (TG) oraz cholesterolu nie-HDL (nie-HDL-C), chociaż wciąż największe znaczenie ma stężenie LDL-C, zarówno w rozpoznawaniu, predykcji jak i monitorowaniu przebiegu i leczenia zaburzeń lipidowych [1, 2, 3, 8]. Wyniki tych oznaczeń/wyliczeń pośrednio i w przybliżeniu odzwierciedlają zawartość we krwi odpowiednich lipoprotein. Szczególne znaczenie w laboratoryjnej ocenie gospodarki lipidowej i ryzyka postępu miażdżycy ma ilościowe oznaczenie zawartości we krwi lipoprotein o działaniu aterogennym: LDL, lipoproteiny (a) [Lp(a)] oraz remnantów chylomikronów (CM) i remnantów lipoprotein o bardzo małej gęstości (VLDL) [2, 3]. Stąd profil lipidowy, określający jedynie zawartość LDL, powinien być uzupełniany, jeśli tylko jest to możliwe, o wykonywanie zgodnie ze wskazaniami oznaczeń Lp(a) oraz remnantów CM i remnantów VLDL. Lipoproteiny stanowią rodzinę wielkocząsteczkowych struktur złożonych z „koperty”, zawierającej fosfolipidy i wolny cholesterol oraz rdzenia złożonego z TG i estrów cholesterolu. Lipidowa część jest związana ze swoistymi białkami – apolipoproteinami (apo), które determinują fizyczne i biologiczne właściwości lipoprotein. Lipidy i białka nie są ze sobą związane kowalencyjnie. Struktura lipoprotein jest utrzymywana w większości przez hydrofobowe interakcje pomiędzy niepolarnymi komponentami lipidów oraz białek. Klasyfikacja lipoprotein odzwierciedla zarówno rozmiar ich cząstek, jak i gęstość w wodnym środowisku osocza, a także zawartość apolipoprotein (ryc. 1). Bogate w triglicerydy CM, VLDL oraz remnanty CM i remnanty VLDL wykazują gęstość poniżej 1,006 g/ml. Pozostałe lipoproteiny o gęstości powyżej 1,006 g/ml to LDL, HDL oraz Lp(a). System transportu lipidów z udziałem lipoprotein spełnia dwie podstawowe funkcje: <br>––transport triglicerydów z jelit i wątroby do tkanki tłuszczowej i mięśni (szlak jelitowy); <br>––dostarczanie do tkanek obwodowych cholesterolu, niezbędnego do formowania błon komórkowych, biosyntezy hormonów steroidowych a także do wątroby w celu syntezy kwasów żółciowych (szlak wątrobowy) (ryc. 2). null ABC A1 – zależny od ATP transporter A1, CETP – białko transportujące estry cholesterolu, EL – lipaza śródbłonkowa, HL – lipaza wątrobowa, LCAT – acylotransferaza lecytyna: cholesterol, LPL – lipaza lipoproteinowa, PLTP – białko transportujące fosfolipidy, TG – triglicerydy. TG pokarmowe są w jelicie hydrolizowane do wolnych kwasów tłuszczowych (WKT), mono – i diglicerydów, wchłanianych wraz z egzogennym cholesterolem do enterocytów, w których powstają transportujące je CM, docierające przez układ chłonny do krwi krążącej. Lipaza lipoproteinowa (LPL) związana ze śródbłonkiem kapilar tkanki tłuszczowej i mięśniowej hydrolizuje zawarte w nich TG do glicerolu i WKT, z wytworzeniem remnantów CM zawartych w lipoproteinach o pośredniej gęstości (IDL). Endogenne TG są syntetyzowane w hepatocytach i tam razem z cholesterolem i apolipoproteinami (apoB 100, apoE, apoC) są budulcem dla VLDL wydzielanych do krwi, gdzie pod działaniem lipazy śródbłonkowej (EL; ang. <i>endothelial lipase</i>) powstają ich remnanty (IDL). LDL powstają z IDL przy udziale lipazy wątrobowej (HL; ang. <i>hepatic lipase</i>) i są wzbogacone cholesterolem z HDL przy udziale białka transportującego estry cholesterolu (CETP; ang. <i>cholesterol ester transfer protein</i>). Cząstki HDL powstają w wątrobie i jelicie oraz w toku degradacji CM i VLDL, z ich powierzchniowych fosfolipidów i wolnego cholesterolu. Wolny cholesterol jest pobierany z komórek obwodowych (w tym makrofagów w ścianie naczyniowej) przez nowopowstałe HDL (ang. <i>nascent-HDL</i>) i HDL3, z udziałem zależnego od ATP transportera ATP-A1 (ABCA1; ang. <i>ATP binding cassette transporter A1</i>) wiążącego się z apoA-I, a następnie estryfikowany przy udziale osoczowego enzymu acylotransferazy lecytyna:cholesterol (LCAT). Estry cholesterolu są transportowane przez dojrzałe HDL2 wiązane przez receptor SR-B1 hepatocytów, gdzie są wykorzystane w syntezie kwasów żółciowych. Jest to tzw. bezpośredni mechanizm zwrotnego transportu cholesterolu. W tzw. mechanizmie pośrednim CETP przenosi je z HDL do zawierających apoB lipoprotein z wymianą na TG. Lipoproteiny zawierające apoB są wychwytywane przez wątrobę za pośrednictwem receptorów LDL, a także innych błonowych receptorów (receptor VLDL, receptor apoE). Hydroliza TG w HDL2 przez HL prowadzi do powstania HDL3 (ryc. 2). Dostępne aktualnie metody analityczne dają jedynie pośredni, przybliżony wgląd w przemiany zarówno cholesterolu i TG, jak i w metabolizm i funkcje lipoprotein. Diagnostyka zaburzeń gospodarki lipidowej stanowi w praktyce klinicznej część oceny i kontroli ryzyka miażdżycy oraz związanych z nią chorób sercowo- naczyniowych. Stąd głównym celem diagnostyki laboratoryjnej dyslipidemii, definiowanej jako stan, w którym stężenia lipidów i lipoprotein we krwi odbiegają od wartości pożądanych, jest ocena zawartości we krwi lipoprotein o działaniu aterogennym. Metodyczne podejście do badania lipoprotein jest obecnie zróżnicowane – można ich zawartość we krwi oznaczać bezpośrednio jako liczbę cząstek [LDL-P, HDL-P, Lp(a)-P] lub ich stężenie, bądź też oceniać w sposób pośredni poprzez oznaczanie stężenia składników poszczególnych lipoprotein – cholesterolu lub apolipoprotein (apoB, apoA-I).
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2

Vaverková, Helena, and David Karásek. "Lipoprotein-associated phospholipase A2 (Lp-PLA2) as a marker of atherosclerotic activity and a potential therapeutic target." Cor et Vasa 53, no. 4-5 (2011): 234–38. http://dx.doi.org/10.33678/cor.2011.052.

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3

Beňovská, M., L. Babušíková, J. Pařenica, and J. Tůmová. "Lipoprotein-associated phospholipase A<sub>2</sub> - significance, method of determination and clinical monitoring." Klinická biochemie a metabolismus 18, no. 1 (2010): 38–44. https://doi.org/10.61568/kbm.2010.010.

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4

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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5

Soška, Vladimír, David Karásek, Vladimír Blaha, et al. "A summary of the EAS consensus concerning the causal relationship between low-density lipoproteins and atherosclerotic cardiovascular diseases, prepared by the Board of the Czech Society for Atherosclerosis." Vnitřní lékařství 64, no. 12 (2018): 1124–28. http://dx.doi.org/10.36290/vnl.2018.160.

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6

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 native highdensity lipoproteins, low-density lipoproteins, glycated low-density lipoproteins/glycated high-density lipoproteins were added to ADP-induced platelets. Oxidative parameters, caspase-3/9 and nitric oxide levels were measured spectrophotometrically; CD62-P/ annexin-V expression was determined by flow cytometry. In glycated low-density lipoprotein/glycated high-density lipoprotein-treated groups, platelet malondialdehyde/ protein carbonyl, P-selectin, annexin-V, caspase-3/9 levels were increased (ranging from P &lt; 0.001 to P &lt; 0.01); glutathione and nitric oxide levels were reduced (ranging from P &lt; 0.001 to P &lt; 0.01). In glycated low-density lipoprotein/glycated high-density lipoprotein-treated groups, melatonin treatment reduced malondialdehyde, protein carbonyl, CD62-P, annexin-V and caspase-3/9 (P &lt; 0.001, P &lt; 0.01) levels and elevated nitric oxide (only glycated low-density lipoproteins). In glycated low-density lipoprotein/glycated high-density lipoprotein-treated groups, native high-density lipoprotein treatment reduced malondialdehyde, protein carbonyl, annexin-V, caspase-3/9 levels (P &lt; 0.001, P &lt; 0.01) and increased glutathione; nitric oxide levels (only with gly-HDL). Both melatonin and high-density lipoproteins should be regarded as novel promising mechanism-based potential therapeutic targets to prevent atherothrombosis in diabetics.
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7

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 studies have discovered that the triglyceriderich lipoproteins and their remnants are linked with cardiovascular disease risk. In this review, we describe the potential mechanisms by which the triglyceride-rich remnant lipoproteins can contribute to the development of atherosclerotic lesions, and highlight the differences in the atherogenicity between low-density lipoproteins and the remnant lipoproteins.
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8

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 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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9

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, providing intense edge contrast. The results show that LPs have a continuous frequency distribution of sizes, extending from LDL (&gt; 15 nm) to intermediate density lipoprotein (IDL) and very low-density lipoproteins (VLDL). Furthermore, mixed metal staining produces striking “positive” contrast of specific antibodies attached to lipoproteins providing quantitative data on apolipoprotein(a)-positive Lp(a) or apolipoprotein B (ApoB)-positive particles. To enable automatic particle characterization, we also demonstrated efficient segmentation of lipoprotein particles using deep learning software characterized by a Mask Region-based Convolutional Neural Networks (R-CNN) architecture with transfer learning. In future, EM and machine learning could be combined with microarray deposition and automated imaging for higher throughput quantitation of lipoproteins associated with CVD risk.
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10

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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11

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 high lipoprotein lipase activity is a principal site for generation of remnant lipoproteins. Under circumstances of reduced efficiency in the removal of triacylglycerols from lipoproteins, there is accumulation of remnant lipoproteins, which are potentially atherogenic.
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12

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 lipoproteins as well as lipoprotein-processing enzymes were expressed by E. chaffeensis cultured in the human promyelocytic leukemia cell line HL-60. Consistent with this observation, a signal peptidase II inhibitor, globomycin, was found to inhibit E. chaffeensis infection and lipoprotein processing in HL-60 cell culture. To study in vivo E. chaffeensis lipoprotein expression and host immune responses to E. chaffeensis lipoproteins, 13 E. chaffeensis lipoprotein genes were cloned into a mammalian expression vector. When the DNA constructs were inoculated into naïve dogs, or when dogs were infected with E. chaffeensis, the animals developed delayed-type hypersensitivity reactions at cutaneous sites of the DNA construct deposition and serum antibodies to these lipoproteins. This is the first demonstration of lipoprotein expression and elicitation of immune responses by a member of the order Rickettsiales. Multiple lipoproteins expressed by E. chaffeensis in vitro and in vivo may play key roles in pathogenesis and immune responses in HME.
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13

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 increased in STZ-induced diabetic hearts, but tissue residual LPL activity was decreased; moreover, diabetic lipoproteins stimulated HR-LPL activity in both diabetic and control hearts. Diabetic hearts oxidized lipoprotein-triacylglycerol (TAG) to a significantly greater extent than controls (&gt;80% compared with deposition as tissue lipid), and the oxidation rate of exogenous lipoprotein-TAG was increased significantly in diabetic hearts regardless of TAG source. Significantly increased intracardiomyocyte TAG accumulation was found in diabetic hearts, although cardiac mechanical function was not inhibited, suggesting that lipotoxicity precedes impaired cardiac performance. Glucose oxidation was significantly decreased in diabetic hearts; additionally, however, diabetic lipoproteins decreased glucose oxidation in diabetic and control hearts. These results demonstrate increased TAG-rich lipoprotein metabolism concomitant with decreased glucose oxidation in type 1 diabetic hearts, and the alterations in cardiac lipoprotein metabolism may be due to the properties of diabetic TAG-rich lipoproteins as well as the diabetic state of the myocardium. These changes were not related to cardiomyopathy at this early stage of diabetes.
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14

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: cholesterol acyltransferase (LCAT) activity was decreased. It is intriguing to suggest that the regenerating liver could regulated the blood lipoprotein pattern and the uptake of lipoproteins by modulating the surface expression of the receptors.
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15

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-density lipoprotein (LDL) remained in the supernatant liquid, and 30% of the high-density lipoprotein (HDL) was precipitated. These results indicate that, under these conditions, so-called HDL cholesterol may be a mixture of VLDL, LDL, and HDL, although the sum of the amount of these three fractions remaining in the supernate is fortuitously very close to the value for HDL cholesterol isolated by ultracentrifugation.
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16

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 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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17

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 remodeled *PE- and *Chol-labeled synthetic lipoprotein-X multilamellar vesicles (MLV) into a pre-β HDL-like particle containing *PE, *Chol, and *apoA-I. Fluorescent MLV-derived *PE specifically incorporated into plasma HDL, whereas MLV-derived *Chol incorporation into plasma lipoproteins was similar to direct *Chol incorporation, consistent with apoA-I-mediated remodeling of fluorescent MLV to HDL with concomitant exchange of *Chol between lipoproteins. Based on these findings, we developed a model system to study lipid transfer by depositing fluorescent *PE and *Chol-labeled on calcium silicate hydrate crystals, forming dense lipid-coated donor particles that are readily separated from acceptor lipoprotein particles by low-speed centrifugation. Transfer of *PE from donor particles to mouse plasma lipoproteins was shown to be HDL-specific and apoA-I-dependent. Transfer of donor particle *PE and *Chol to HDL in whole human plasma was highly correlated. Taken together, these studies suggest that cell-free *PE efflux monitors apoA-I functionality.
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18

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 low-density lipoprotein (LDL) increased PGI2 production in the short term (up to 24 h), but oxidized LDL caused an inhibition of PGI2-producing capacity in longer term incubations (48-72 h). Glycated (Glc) high-density lipoprotein 3 (HDL3) caused higher production of PGI2 in the short term (4-24 h) but reached similar levels as HDL3 over time. Glycation of high-density lipoprotein 2 had no effect on the PGI2-producing capacity of the lipoprotein. Thus modification of the lipoproteins affects their potential to induce PGI2 production in endothelial cells, and this may have an influence on vascular function in disease states such as diabetes and atherosclerosis. Although the changes appear to contradict data from long-term in vivo studies, these results from in vitro studies may reflect the situation in very early lesion development. GlcLDL, while causing an increase in endothelial cell PGI2 production, may be involved in compromised endothelial function, since GlcLDL is prone to oxidation.
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19

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 into the relative expression of lipoproteins. Twenty-six of the 68 predicted lipoproteins were specifically released into the extracellular proteome of the Δlgt strain, and this proved that deletion of lgt is an excellent approach for experimental verification of listerial lipoproteins. Consequently, we generated Δlgt ΔprfA double mutants to detect lipoproteins belonging to the main virulence regulon that is controlled by PrfA. Overall, we identified three lipoproteins whose extracellular levels are regulated and one lipoprotein that is posttranslationally modified depending on PrfA. It is noteworthy that in contrast to previous studies of Escherichia coli, we unambiguously demonstrated that lipidation by Lgt is not a prerequisite for activity of the lipoprotein-specific signal peptidase II (Lsp) in Listeria.
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Yousef, Malaz, Nadia Bou Chacra, Neal M. Davies, and Raimar Löbenberg. "Lipoproteins within the lymphatic system: Insights into health, disease, and therapeutic implications." Applied Chemical Engineering 6, no. 2 (2023): 2202. http://dx.doi.org/10.24294/ace.v6i2.2202.

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This analysis of contemporary findings aims to enhance our understanding of lipoprotein biology within the lymphatic system and its relevance to human health and disease. It delves into the complex interrelationship between lipoproteins and the lymphatic system, encompassing their diverse classes and pivotal roles in the absorption and transport of drugs, vitamins, and xenobiotics. Lipoproteins consist of a hydrophobic core comprising non-polar lipids and a hydrophilic membrane composed of phospholipids, free cholesterol, and apolipoproteins. The lymphatic system collaborates with lipoproteins in the absorption and transport of dietary lipids. Simultaneously, it plays a vital role in the regulation of body fluid levels and acts as a formidable defense mechanism against infections. Lipoprotein classes encompass chylomicrons, chylomicron remnants, very low-density lipoproteins, intermediate density lipoproteins, low-density lipoproteins, high-density lipoproteins, and lipoprotein (a). Understanding the intricate relationship between lipoproteins and the lymphatic system holds immense implications for comprehending the underlying pathological processes of various diseases such as atherosclerosis, diabetes and obesity among others. By shedding light on the interplay between lipoproteins and the lymphatic system, this report underscores the significance of conducting research that contributes to the advancement of our knowledge in this field. Ultimately, such research paves the way for potential therapeutic interventions and novel strategies to address numerous disorders.
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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 uric acid, creatinine, triglycerides, cholesterol, low-density lipoprotein, very low-density lipoprotein, and an increase in high-density lipoprotein (HDL) values.
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22

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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23

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

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ABSTRACT Lipopolysaccharide (LPS), the major glycolipid component of gram-negative bacterial outer membranes, is a potent endotoxin responsible for pathophysiological symptoms characteristic of infection. The observation that the majority of LPS is found in association with plasma lipoproteins has prompted the suggestion that sequestering of LPS by lipid particles may form an integral part of a humoral detoxification mechanism. Previous studies on the biological properties of isolated lipoproteins used differential ultracentrifugation to separate the major subclasses. To preserve the integrity of the lipoproteins, we have analyzed the LPS distribution, specificity, binding capacity, and kinetics of binding to lipoproteins in human whole blood or plasma by using high-performance gel permeation chromatography and fluorescent LPS of three different chemotypes. The average distribution of O111:B4, J5, or Re595 LPS in whole blood from 10 human volunteers was 60% (±8%) high-density lipoprotein (HDL), 25% (±7%) low-density lipoprotein, and 12% (±5%) very low density lipoprotein. The saturation capacity of lipoproteins for all three LPS chemotypes was in excess of 200 μg/ml. Kinetic analysis however, revealed a strict chemotype dependence. The binding of Re595 or J5 LPS was essentially complete within 10 min, and subsequent redistribution among the lipoprotein subclasses occurred to attain similar distributions as O111:B4 LPS at 40 min. We conclude that under simulated physiological conditions, the binding of LPS to lipoproteins is highly specific, HDL has the highest binding capacity for LPS, the saturation capacity of lipoproteins for endotoxin far exceeds the LPS concentrations measured in clinical situations, and the kinetics of LPS association with lipoproteins display chemotype-dependent differences.
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24

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 lipoproteins), IDLs (intermediate-density lipoproteins), and light and dense LDLs (low-density lipoproteins) that do or do not contain apoE or apoC3. RESULTS: A major feature of the postprandial state is 50% lower secretion rate of triglyceride-rich lipoproteins and concurrent slowdown of their catabolism in circulation, as shown by 34% to 55% lower rate constants for the metabolic pathways of conversion by lipolysis from larger to smaller lipoproteins and direct clearance of lipoproteins from the circulation. In addition, the secretion pattern of apoB lipoprotein phenotypes was shifted from particles containing apoE and apoC3 in the fasting state to those without either protein in the postprandial state. CONCLUSIONS: Overall, during the fasting state, hepatic apoB lipoprotein metabolism is activated, characterized by increased production, transport, and clearance. After food intake, endogenous apoB lipoprotein metabolism is globally reduced as appropriate to balance dietary input to maintain the supply of energy to peripheral tissues.
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25

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 lipoprotein analysis will provide additional information on the accumulation of very low-density lipoproteins, intermediate density lipoproteins, chylomicrons, chylomicron-remnants and Lp(a) concentrations. Instead of measuring the cholesterol and triglyceride content of the lipoproteins, measurement of their apolipoproteins (apos) is more informative. Apos are either specific for a particular lipoprotein or for a group of lipoproteins. In particular measurement of apos in atherogenic particles is more biologically meaningful than the measurement of the cholesterol concentration contained in these particles. Applying apo profiling will not only improve characterization of the lipoprotein abnormality, but will also improve definition of therapeutic targets. Apo profiling aligns with the concept of precision medicine by which an individual patient is not treated as ‘average’ patient by the average (dose of) therapy. This concept of precision medicine fits the unmet clinical need for stratified cardiovascular medicine. The requirements for clinical application of proteomics, including apo profiling, can now be met using robust mass spectrometry technology which offers desirable analytical performance and standardization.
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26

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-density lipoprotein (HDL), P &lt; .00001, and 11.7-fold greater than that supported by LDL, P &lt; .00001. Oxidation of LDL increased lipoprotein-supported thrombin generation 12-fold compared to unmodified LDL, P &lt; .0001. We have shown that the phenomenon of lipoprotein-supported thrombin generation is mediated predominantly by specific phospholipids and is enhanced by oxidation of these phospholipids. The addition of vitamin E (α-tocopherol) markedly reduced the increase in thrombin generation observed after oxidation of LDL (822 ± 57 v 138 ± 47 nmol/L;P &lt; .0001). These effects suggest that lipoproteins are important in the production of thrombin and that vitamin E may confer protection from the detrimental effects of lipoprotein oxidation by limiting thrombin formation. These results suggest that atherogenic lipoproteins are linked to the development of atherosclerosis in part by their capacity to support thrombin generation.
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27

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 lipoprotein (HDL), P &lt; .00001, and 11.7-fold greater than that supported by LDL, P &lt; .00001. Oxidation of LDL increased lipoprotein-supported thrombin generation 12-fold compared to unmodified LDL, P &lt; .0001. We have shown that the phenomenon of lipoprotein-supported thrombin generation is mediated predominantly by specific phospholipids and is enhanced by oxidation of these phospholipids. The addition of vitamin E (α-tocopherol) markedly reduced the increase in thrombin generation observed after oxidation of LDL (822 ± 57 v 138 ± 47 nmol/L;P &lt; .0001). These effects suggest that lipoproteins are important in the production of thrombin and that vitamin E may confer protection from the detrimental effects of lipoprotein oxidation by limiting thrombin formation. These results suggest that atherogenic lipoproteins are linked to the development of atherosclerosis in part by their capacity to support thrombin generation.
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28

Heeren, J., W. Weber, and U. Beisiegel. "Intracellular processing of endocytosed triglyceride-rich lipoproteins comprises both recycling and degradation." Journal of Cell Science 112, no. 3 (1999): 349–59. http://dx.doi.org/10.1242/jcs.112.3.349.

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The current study was performed to investigate the intracellular fate of triglyceride-rich lipoproteins. Triglyceride-rich lipoproteins are responsible for the delivery of lipids to various tissues, however, their intracellular pathway has not yet been elucidated. Here radiolabeled triglyceride-rich lipoproteins, associated with lipoprotein lipase, were used for the quantitative evaluation of the intracellular metabolism. Pulse chase experiments showed that after 90 minutes approximately 60% of the labeled protein, mainly apoproteins E and C, was released intact into the medium, where it re-associates with lipoproteins. Apoprotein B, in contrast, was degraded, following the same pathway as the apoprotein B from low density lipoproteins. In kinetic experiments uptake and intracellular fate of triglyceride-rich lipoproteins was compared to that of transferrin and low density lipoproteins. These experiments revealed that apoproteins were retained inside the cell much longer than transferrin, and unlike low density lipoproteins were not degraded. Using immunofluorescence it was shown that apoprotein E and lipoprotein lipase follow a distinct route from the sorting compartment to the surface, which is clearly distinguishable from the perinuclear transferrin recycling compartment. In contrast, the fluorescence labeled lipids were delivered to lysosomal compartments. The data presented here show that surface proteins of triglyceride-rich lipoproteins, such as apoproteins E and C and lipoprotein lipase follow a recycling pathway, whereas lipids and high molecular mass core proteins are degraded.
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29

Rácz, Oliver, Daniel Pella, and Erika Bilá. "Súlad a nesúlad medzi základnými ukazovateľmi lipidového metabolizmu stanovenými rutinnými laboratórnymi metódami a metódou protónovej nukleárnej magnetickej rezonančnej spektroskopie v náhodne vybranej populačnej vzorke." Laboratórna Diagnostika XXVI, no. 1/2021 (2021): 79–85. https://doi.org/10.5281/zenodo.4780837.

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S&Uacute;HRN Prot&oacute;nov&aacute; nukle&aacute;rna magnetick&aacute; rezonančn&aacute; spektroskopia umožňuje meranie počtu čast&iacute;c jednotliv&yacute;ch lipoprote&iacute;nov a ich rozmer. Cieľom na&scaron;ej pilotnej &scaron;t&uacute;die bolo vy&scaron;etrenie n&aacute;hodne vybranej skupiny probandov bez klinicky zjavn&yacute;ch pr&iacute;znakov aterosklerotickej choroby srdca touto met&oacute;dou a porovnanie v&yacute;sledkov s hodnotami z&aacute;kladn&eacute;ho lipidov&eacute;ho panelu meran&yacute;mi bežn&yacute;mi met&oacute;dami. V&yacute;sledky korelačnej anal&yacute;zy medzi v&yacute;sledkami prot&oacute;novej nukle&aacute;rnej magnetickej rezonančnej spektroskopie a z&aacute;kladn&yacute;mi ukazovateľmi lipidov&eacute;ho metabolizmu potvrdili predpoklad o pridanej hodnote novej met&oacute;dy vo vzťahu k ateroskler&oacute;ze. Medzi vybran&yacute;mi parametrami v&yacute;sledkov prot&oacute;novej nukle&aacute;rnej magnetickej rezonančnej spektroskopie a z&aacute;kladn&yacute;mi ukazovateľmi lipidov&eacute;ho metabolizmu bol v&yacute;znamn&yacute; nes&uacute;lad. Na z&aacute;klade počtu LDL čast&iacute;c bolo 70 % probandov zaraden&yacute;ch do hor&scaron;ej rizikovej triedy, ako na z&aacute;klade LDL cholesterolu. V pr&iacute;pade HDL bol nes&uacute;lad menej čast&yacute; a približne polovica probandov bola zaraden&aacute; do niž&scaron;ej rizikovej skupiny podľa počtu čast&iacute;c v porovnan&iacute; s HDL cholesterolom. ABSTRACT Proton nuclear magnetic resonance spectroscopy makes measurement of individual lipoprotein particle number and size possible. The aim of our pilot study was the assessment of a randomly selected group of probands without clinically manifest symptoms of atherosclerotic cardiovascular with this method and the comparison of results with values of basic lipid parameters measured by routine laboratory methods. The correlation analysis between results of proton nuclear magnetic resonance spectroscopy and basic parameters of lipid metabolism confirmed our assumption about the added value of the new method in relation to atherosclerosis. There was a significant discordance between results of selected parameters of proton nuclear magnetic resonance spectroscopy and basic parametres of lipid metabolism. 70 % of probands were ranked into&nbsp;worse risk classes according to LDL particle number as compared with the LDL cholesterol values. In case of HDL the discordance was less common and about half of the probands was ranked into a better risk class according the particle number as compared with HDL cholesterol values. &nbsp;
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30

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-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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31

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 role in the modulation of fibrinolysis. Several aspects of lipoproteins and lipoprotein metabolism will be examined. Emphasis will be placed on the proatherogenic and thrombogenic effects of oxidized LDL.
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32

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 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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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 metabolism by lipoprotein metabolism. We observed that moderate amounts of glycero-lysophospholipids, with the exception of lysophosphatidylserine, were distributed on the LDL and HDL fractions, and glycero-lysophospholipids that had bound to albumin were observed in lipoprotein fractions when they were co-incubated. The overexpression of cholesteryl ester transfer protein decreased the plasma levels of lysophosphatidylcholine, lysophosphatidylethanolamine, lysophosphatidylglycerol, and lysophosphatidylinositol and it increased their contents in apoB-containing lipoproteins, while it decreased their contents in HDL and lipoprotein-depleted fractions in mice. The overexpression of the LDL receptor (LDLr) decreased the plasma levels of lysophosphatidylcholine, lysophosphatidylethanolamine, lysophosphatidylglycerol, and lysophosphatidylinositol and decreased the contents of these compounds in the LDL, HDL, and lipoprotein-depleted fractions, while the knockdown of the LDLr increased them. These results suggest the potential importance of glycero-lysophospholipids in the pleiotropic effects of lipoproteins as well as the importance of lipoprotein metabolism in the regulation of glycero-lysophospholipids.
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34

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 ingestion of DAI and daidzein-7-O-β-d-glucoside (DG) (1 mg DAI aglycone equivalents/kg body weight) blood samples were drawn before isoflavone administration as well as 1, 2, 3, 4·5, 6, 8, 10, 12, 24 and 48 h post-dose. Concentrations of DAI in the different lipoprotein fractions (chylomicrons, VLDL, LDL, HDL) and in the non-lipoprotein fraction were analysed using isotope dilution capillary GC/MS. The lipoprotein fraction profiles were similar for all subjects and resembled those obtained for plasma in our previously published study. The lipoprotein distribution based on the area under the concentration–time profiles from 0 h to infinity in the different fractions were irrespective of the administered form: non-lipoprotein fraction (53 %) &gt; LDL (20 %) &gt; HDL (14 %) &gt; VLDL (9·5 %) &gt; chylomicrons (2·5 %). Of DAI present in plasma, 47 % was associated to lipoproteins. Concentrations in the different lipoprotein fractions as well as in the non-lipoprotein fraction were always higher after the ingestion of DG than of DAI. Taken together, these results demonstrate an association between isoflavones and plasma lipoproteins in vivo.
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35

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 &amp; 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&lt;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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36

Huemer, H. P., H. J. Menzel, D. Potratz, et al. "Herpes Simplex Virus Binds to Human Serum Lipoprotein." Intervirology 29, no. 2 (1988): 68–76. http://dx.doi.org/10.1159/000150031.

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Binding of herpes simplex virus (HSV) type 1 to the various subclasses of human serum lipoproteins was investigated. Studies were performed with human serum lipoproteins purified by differential ultracentrifugation and artificial proteoliposomes containing only one type of apolipoprotein (Al5 E) by using an enzyme-linked immunosorbent assay technique, column chromatography, and electron microscopy. All tested lipoprotein subclasses (very low, low-, high-density lipoproteins; VLDL, LDL, HDL, HDLi) showed significant binding of purified HSV type 1. Furthermore, HSV bound to all different synthetic proteoliposomes. Adsorption of envelope proteins isolated from purified HSV to Sepharose-bound lipoproteins revealed binding of HSV glycoprotein B. Based on these results we reached the conclusion that in HSV-lipoprotein complex formation the lipid component in the lipoproteins and the glycoprotein B in HSV are the preferential reaction partners.
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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 between the twin pairs for all lipids and lipoproteins measured, particularly lipoprotein (a), for which identical apoprotein (a) isoforms were also found. 4. Correlations existed between the non-diabetic twins and the control subjects for high-density lipoprotein cholesterol and apoprotein A-I, probably due to the rigorous matching of control subjects. 5. The similarity between values for lipids and lipoproteins in the non-diabetic twins and control subjects suggested no effect of a genetic susceptibility to insulin-dependent diabetes mellitus. The differences in lipoproteins we describe for the identical twins discordant for insulin-dependent diabetes mellitus, in whom there was no evidence of a raised urinary albumin excretion rate, does not appear to explain the excess mortality from cardiovascular disease reported in patients with this disease.
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38

Radolf, J. D., M. V. Norgard, M. E. Brandt, R. D. Isaacs, P. A. Thompson, and B. Beutler. "Lipoproteins of Borrelia burgdorferi and Treponema pallidum activate cachectin/tumor necrosis factor synthesis. Analysis using a CAT reporter construct." Journal of Immunology 147, no. 6 (1991): 1968–74. http://dx.doi.org/10.4049/jimmunol.147.6.1968.

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Abstract Lipoproteins from two pathogenic spirochetes (Borrelia burgdorferi and Treponema pallidum) induced the biosynthesis of TNF in murine macrophages and in permanently transformed macrophages of the cell line RAW 264.7. Induction was studied by measuring the secretion of biologically active TNF and by measuring the activity of the reporter enzyme chloramphenicol acetyltransferase (CAT) produced within macrophages transfected with an endotoxin-responsive CAT construct. Several lines of evidence indicated that the induction of TNF and CAT was attributable to the spirochete lipoproteins rather than to contaminating or endogenous LPS: 1) the dose response curves observed for the lipoproteins were markedly different from those obtained with LPS; 2) lipoprotein-mediated activation was unaffected by amounts of polymyxin B that completely neutralized the induction of TNF and CAT by LPS, 3) low concentrations of the lipoproteins induced TNF in macrophages from endotoxin-unresponsive C3H/HeJ mice as effectively as in macrophages from normal C3H/HeN mice, and 4) isolated spirochete lipoproteins, but not a non-lipoprotein immunogen, were potent inducers of CAT in the transformed macrophages. Moreover, LPS was not detected in the B. burgdorferi lipoprotein mixtures by Limulus amebocyte lysate assay. Proteolytic digestion of the intact bacterial protein preparations only modestly diminished their ability to activate the cells, suggesting that small lipopeptides comprise the biologically active portions of the molecules, as is the case with the murein lipoprotein of Escherichia coli. Through their ability to induce TNF production by macrophages, spirochete lipoproteins may play important roles in the development of the local inflammatory changes and the systemic manifestations that characterize syphilis and Lyme disease.
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39

Imamura, Hiroyuki, Keiko Mizuuchi, and Reika Oshikata. "Physical Activity and Blood Lipids and Lipoproteins in Dialysis Patients." International Journal of Nephrology 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/106914.

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The relationship between physical activity and blood lipids and lipoproteins in dialysis patients is reviewed in the context of the potentially confounding factors such as nutritional intake, cigarette smoking, obesity, alcohol intake, and physical activity levels in the general population and additional confounding factors such as mode of dialysis and diabetes in dialysis patients. The known associations in the general population of physical activity with high-density-lipoprotein cholesterol subfractions and apolipoprotein A-I are more pronounced in hemodialysis patients than in peritoneal dialysis patients even after adjusting for these confounding factors. Examining studies on the effects of physical activity on blood lipids and lipoproteins, the most consistent observation is the noted decrease in triglycerides and increase in high-density-lipoprotein cholesterol and insulin sensitivity in hemodialysis patients. The changes in lipids and lipoproteins in hemodialysis patients could be caused by changes in activity levels of lipoprotein lipase, insulin sensitivity, and/or glucose metabolism. Future research investigating the relationship between physical activity and blood lipids and lipoproteins in dialysis patients should direct research towards the underlying mechanisms for changes in blood lipids and lipoproteins.
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40

Narita, Shin-ichiro, Kimie Tanaka, Shin-ichi Matsuyama, and Hajime Tokuda. "Disruption of lolCDE, Encoding an ATP-Binding Cassette Transporter, Is Lethal for Escherichia coli and Prevents Release of Lipoproteins from the Inner Membrane." Journal of Bacteriology 184, no. 5 (2002): 1417–22. http://dx.doi.org/10.1128/jb.184.5.1417-1422.2002.

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ABSTRACT ATP-binding cassette transporter LolCDE was previously identified, by using reconstituted proteoliposomes, as an apparatus catalyzing the release of outer membrane-specific lipoproteins from the inner membrane of Escherichia coli. Mutations resulting in defective LolD were previously shown to be lethal for E. coli. The amino acid sequences of LolC and LolE are similar to each other, but the necessity of both proteins for lipoprotein release has not been proved. Moreover, previous reconstitution experiments did not clarify whether or not LolCDE is the sole apparatus for lipoprotein release. To address these issues, a chromosomal lolC-lolD-lolE null mutant harboring a helper plasmid that carries the lolCDE genes and a temperature-sensitive replicon was constructed. The mutant failed to grow at a nonpermissive temperature because of the depletion of LolCDE. In addition to functional LolD, both LolC and LolE were required for growth. At a nonpermissive temperature, the outer membrane lipoproteins were mislocalized in the inner membrane since LolCDE depletion inhibited the release of lipoproteins from the inner membrane. Furthermore, both LolC and LolE were essential for the release of lipoproteins. On the other hand, LolCDE depletion did not affect the translocation of a lipoprotein precursor across the inner membrane and subsequent processing to the mature lipoprotein. From these results, we conclude that the LolCDE complex is an essential ABC transporter for E. coli and the sole apparatus mediating the release of outer membrane lipoproteins from the inner membrane.
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41

Chaudhary, Jaideep, Joseph Bower, and Ian R. Corbin. "Lipoprotein Drug Delivery Vehicles for Cancer: Rationale and Reason." International Journal of Molecular Sciences 20, no. 24 (2019): 6327. http://dx.doi.org/10.3390/ijms20246327.

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Lipoproteins are a family of naturally occurring macromolecular complexes consisting amphiphilic apoproteins, phospholipids, and neutral lipids. The physiological role of mammalian plasma lipoproteins is to transport their apolar cargo (primarily cholesterol and triglyceride) to their respective destinations through a highly organized ligand-receptor recognition system. Current day synthetic nanoparticle delivery systems attempt to accomplish this task; however, many only manage to achieve limited results. In recent years, many research labs have employed the use of lipoprotein or lipoprotein-like carriers to transport imaging agents or drugs to tumors. The purpose of this review is to highlight the pharmacologic, clinical, and molecular evidence for utilizing lipoprotein-based formulations and discuss their scientific rationale. To accomplish this task, evidence of dynamic drug interactions with circulating plasma lipoproteins are presented. This is followed by epidemiologic and molecular data describing the association between cholesterol and cancer.
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42

Otvos, J. D., E. J. Jeyarajah, L. W. Hayes, D. S. Freedman, N. A. Janjan, and T. Anderson. "Relationships between the proton nuclear magnetic resonance properties of plasma lipoproteins and cancer." Clinical Chemistry 37, no. 3 (1991): 369–76. http://dx.doi.org/10.1093/clinchem/37.3.369.

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Abstract We conducted a comprehensive investigation of the origin of nuclear magnetic resonance (NMR) lineshape variability of plasma lipids among healthy individuals and those with cancer. The methyl and methylene resonances of lipid in human plasma, whose linewidths have been reported to correlate with the presence of malignancy, are composed of the overlapping resonances of "mobile" protons from the major lipoproteins (very-low-, low-, and high-density lipoproteins). We tested two hypotheses for the origin of the narrower plasma linewidths observed for cancer patients: (a) malignancy-associated differences in the spectral properties (chemical shift, lineshape) of one or more of the lipoproteins, and (b) differences in the fraction of lipoprotein lipid giving rise to detectable NMR signal. Analysis of the concentrations of lipoprotein lipid and of 500 MHz NMR spectra of the lipoprotein constituents in greater than 100 plasma samples failed to provide support for either hypothesis. Although linewidths were found to be significantly narrower for the cancer group, the difference is entirely attributable to differences in the concentrations of the lipoproteins.
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43

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, analysing 112 lipoprotein subfractions. In plasma, we measured unspecific markers of neuronal damage and AD hallmark proteins using single molecule array technology. Additionally, clinical data and cerebrospinal fluid biomarker levels were also collected to enrich our data. Our findings, after adjusting for age and sex differences, highlight significant alterations in two specific lipoproteins; high-density lipoprotein (HDL)-1 Apo-A2 (H1A2) and HDL-2 Apo-A2 (H2A2), both with area under the curve (AUC) values of 0.67, 95% confidence interval (CI) = 0.52–0.82). These results indicate that these lipoprotein subfractions may have potential as indicators of AD-related metabolic changes.
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44

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 aorta induced by acetylcholine (ACh) and A23187 but did not inhibit relaxations induced by nitroglycerin or nitric oxide. These inhibitory activities were lost by delipidation of lipoproteins, and there were no differences in the inhibitory activity among these three lipoproteins on the basis of phospholipid concentration. Moreover, phospholipids such as phosphatidylcholine, phosphatidylinositol, and sphingomyelin reversed relaxations by ACh and A23187. Thus all lipoproteins inhibit endothelium-dependent relaxation, and this nonspecific inhibition seems to be due to the inhibition of production or release of endothelium-derived relaxing factor by phospholipids in the lipoprotein complex.
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45

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 proteins. There was no significant difference in the IL-4 content between the experimental and control groups of cows. In the subclinical form of ketosis in cows, abnormalities in lipid and lipoprotein metabolism were detected in the form of hypertriglyceridaemia and hyperlipoproteinaemia with very low-density lipoproteins, an increase in low-density lipoproteins, and a decrease in very high-density lipoproteins. This was verified by similar changes in β-lipoprotein levels and lipoprotein fractions and was specific to the first stage of lipomobilisation syndrome.
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46

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 multicompartmental modeling. Significant increases in total cholesterol, in ApoB-containing lipoproteins [very-low-density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and low-density lipoprotein (LDL)], and in triglycerides, but not in high-density lipoprotein (HDL), were observed. Lipoprotein particle composition remained unchanged. Mean fractional catabolic and production rates of ApoB-containing lipoproteins were not significantly different, although mean production rates of VLDL and IDL were substantially increased (+46 ± 139% and +30 ± 97%, respectively), whereas mean production of LDL remained unchanged (+2.1 ± 45.6%). Cholestanol in serum increased significantly but not the concentrations of plant sterols (campesterol, sitosterol) and the cholesterol precursors (lathosterol, mevalonic acid). There was a significant correlation between the decrease in free thyroxine and the increase in IDL cholesterol. Treatment with CBZ increases mainly ApoB-containing lipoproteins. CBZ seems not to influence endogenous cholesterol synthesis or intestinal absorption directly. The increase is neither related to increased ApoB production nor to decreased catabolism but is rather due to changes in the conversion cascade of IDL particles, most likely as an indirect effect through a decrease in thyroid hormones.
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47

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 was dependent on the cyclohexanedione concentration. Modification of 48% of lipoprotein lysine groups with malonaldehyde decreased the maximum activation by 20%, but three times as much lipoprotein was required to achieve this. Non-enzymic glycosylation of lipoprotein with glucose, under a variety of conditions resulting in up to 28 nmol of glucose/mg of protein, had no effect upon the ability to activate lipoprotein lipase. In contrast non-enzymic sialylation resulted in a time-dependent loss of up to 60% of ability to activate lipoprotein lipase. Reductive methylation and acetoacetylation of serum did not affect the ability to activate lipoprotein lipase. The results are compared to the effects of similar modifications to low density lipoproteins on receptor-mediated endocytosis.
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48

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 did not possess the major outer membrane lipoprotein Lpp, suggesting that LolB is only important for the localization of Lpp in vivo. To examine the in vivo function of LolB, we constructed a chromosomal lolB null mutant harboring a temperature-sensitive helper plasmid carrying the lolBgene. At a nonpermissive temperature, depletion of the LolB protein due to loss of the lolB gene caused cessation of growth and a decrease in the number of viable cells irrespective of the presence or absence of Lpp. LolB-depleted cells accumulated the LolA-lipoprotein complex in the periplasm and the mature form of lipoproteins in the inner membrane. Taken together, these results indicate that LolB is the first example of an essential lipoprotein for E. coliand that its depletion inhibits the upstream reactions of lipoprotein trafficking.
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49

Dolphin, Peter J. "Lipoprotein metabolism and the role of apolipoproteins as metabolic programmers." Canadian Journal of Biochemistry and Cell Biology 63, no. 8 (1985): 850–69. http://dx.doi.org/10.1139/o85-107.

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The plasma lipoproteins are large spherical macromolecular structures containing hydrophobic core lipids with phospholipids, cholesterol, and specific proteins (apoproteins) providing an amphipathic interface with the hydrophilic environment of the plasma. The major function of these particles, which are biosynthesized by the intestine and liver, is the transport of dietary or endogenously synthesized lipids to those tissues which utilize exogenous lipids for oxidative metabolism, storage, steroid hormone biosynthesis, or maintenance of their membrane integrity. The triacylglycerol-rich lipoproteins are biosynthesized as metabolically inert particles which are catabolically programmed by postsecretory addition of apoproteins which activate the major lipolytic enzymes, inhibit premature removal, and ensure the later interaction of the degraded particles with specific cellular receptors. During the course of lipolysis, those apoproteins which activate catabolic enzymes are lost from the lipoprotein particles and are transferred to the high-density lipoproteins from which they were initially acquired. High-density lipoprotein also mediates the removal of cholesterol deposited in peripheral tissues as a result of uptake of degraded triacylglycerol-rich lipoproteins. Acquisition of cellular cholesterol by high-density lipoproteins results in its apoprotein-stimulated esterification and the later addition of an apoprotein which mediates receptor recognition and removal of the particle from the plasma. The presence or absence of specific apoproteins on the surface of a lipoprotein particle is modulated by the lipid-binding properties of the apoprotein, the surface lipid composition, and the size of the particle. The nature and mass ratios of these surface lipids are themselves dependent upon the activity of apoprotein-stimulated catabolic enzymes and other proteins which mediate the exchange of surface lipids between lipoprotein particles. Thus the apoproteins are effective programmers of lipoprotein metabolism and fulfil their role as such by cycling, in a directed fashion, between nascent and existing plasma lipoproteins. Genetic defects resulting in a perturbation of this intricate mechanism can lead to premature and pronounced atherosclerosis.
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50

POST, Sabine M., Jaap TWISK, L. V. D. FITS та ін. "Lipoprotein cholesterol uptake mediates up-regulation of bile-acid synthesis by increasing cholesterol 7α-hydroxylase but not sterol 27-hydroxylase gene expression in cultured rat hepatocytes". Biochemical Journal 341, № 2 (1999): 339–46. http://dx.doi.org/10.1042/bj3410339.

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Lipoproteins may supply substrate for the formation of bile acids, and the amount of hepatic cholesterol can regulate bile-acid synthesis and increase cholesterol 7α-hydroxylase expression. However, the effect of lipoprotein cholesterol on sterol 27-hydroxylase expression and the role of different lipoproteins in regulating both enzymes are not well established. We studied the effect of different rabbit lipoproteins on cholesterol 7α-hydroxylase and sterol 27-hydroxylase in cultured rat hepatocytes. β-Migrating very-low-density lipoprotein (βVLDL) and intermediate-density lipoprotein (IDL) caused a significant increase in the intracellular cholesteryl ester content of cells (2.3- and 2-fold, respectively) at a concentration of 200 μg of cholesterol/ml, whereas high-density lipoprotein (HDL, 50% v/v), containing no apolipoprotein E (apo E), showed no effect after a 24-h incubation. βVLDL and IDL increased bile-acid synthesis (1.9- and 1.6-fold, respectively) by up-regulation of cholesterol 7α-hydroxylase activity (1.7- and 1.5-fold, respectively). Dose- and time-dependent changes in cholesterol 7α-hydroxylase mRNA levels and gene expression underlie the increase in enzyme activity. Incubation of cells with HDL showed no effect. Sterol 27-hydroxylase gene expression was not affected by any of the lipoproteins added. Transient-expression experiments in hepatocytes, transfected with a promoter-reporter construct containing the proximal 348 nucleotides of the rat cholesterol 7α-hydroxylase promoter, showed an enhanced gene transcription (2-fold) with βVLDL, indicating that a sequence important for a cholesterol-induced transcriptional response is located in this part of the cholesterol 7α-hydroxylase gene. The extent of stimulation of cholesterol 7α-hydroxylase is associated with the apo E content of the lipoprotein particle, which is important in the uptake of lipoprotein cholesterol. We conclude that physiological concentrations of cholesterol in apo E-containing lipoproteins increase bile-acid synthesis by stimulating cholesterol 7α-hydroxylase gene transcription, whereas HDL has no effect and sterol 27-hydroxylase is not affected.
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