Academic literature on the topic 'LPC lipids'
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Journal articles on the topic "LPC lipids":
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Luo, Jixun, Lei Liu, Christine Konik-Rose, Lijun Tian, Surinder Singh, Crispin A. Howitt, Zhongyi Li, and Qing Liu. "Down-Regulation of FAD2-1 Gene Expression Alters Lysophospholipid Composition in the Endosperm of Rice Grain and Influences Starch Properties." Foods 10, no. 6 (May 23, 2021): 1169. http://dx.doi.org/10.3390/foods10061169.
Abstract:
Small quantities of lipids accumulate in the white rice grains. These are grouped into non-starch lipid and starch lipid fractions that affect starch properties through association with starch. Lysophosphatidylcholine (LPC) and lysophosphatidylethanolamine (LPE) are two major lipid classes in the two fractions. Using high-oleic rice grains, we investigated the fatty-acid composition in flour and starch by LC-MS and evaluated its impact on starch properties. In the wild-type grain, nearly 50% of fatty acids in LPC and LPE were palmitic acid (C16:0), over 20% linoleic acid (C18:2) and less than 10% oleic acid (C18:1). In the high-oleic rice grain, C18:1 increased at the expense of C18:2 and C16:0. The compositional changes in starch lipids suggest that LPC and LPE are transported to an amyloplast with an origin from endoplasmic reticulum-derived PC and PE during endosperm development. The high-dissociation temperature of the amylose-lipid complex (ALC) and restricted starch swelling power in the high-oleic rice starch indicates that the stability of the ALC involving C18:1 is higher than that of C18:2 and C16:0. This study provides insight into the lipid deposition and starch properties of rice grains with optimized fatty-acid composition.
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Kuang, Alan, Iris Erlund, Christian Herder, Johan Westerhuis, Jaakko Tuomilehto, and Marilyn Cornelis. "Lipidomic Response to Coffee Consumption." Nutrients 10, no. 12 (December 1, 2018): 1851. http://dx.doi.org/10.3390/nu10121851.
Abstract:
Coffee is widely consumed and contains many bioactive compounds, any of which may impact pathways related to disease development. Our objective was to identify individual lipid changes in response to coffee drinking. We profiled the lipidome of fasting serum samples collected from a previously reported single blinded, three-stage clinical trial. Forty-seven habitual coffee consumers refrained from drinking coffee for 1 month, consumed 4 cups of coffee/day in the second month and 8 cups/day in the third month. Samples collected after each coffee stage were subject to quantitative lipidomic profiling using ion-mobility spectrometry–mass spectrometry. A total of 853 lipid species mapping to 14 lipid classes were included for univariate analysis. Three lysophosphatidylcholine (LPC) species including LPC (20:4), LPC (22:1) and LPC (22:2), significantly decreased after coffee intake (p < 0.05 and q < 0.05). An additional 72 species mapping to the LPC, free fatty acid, phosphatidylcholine, cholesteryl ester and triacylglycerol classes of lipids were nominally associated with coffee intake (p < 0.05 and q > 0.05); 58 of these decreased after coffee intake. In conclusion, coffee intake leads to lower levels of specific LPC species with potential impacts on glycerophospholipid metabolism more generally.
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Chapman, M. John, Alexina Orsoni, Ricardo Tan, Natalie A. Mellett, Anh Nguyen, Paul Robillard, Philippe Giral, Patrice Thérond, and Peter J. Meikle. "LDL subclass lipidomics in atherogenic dyslipidemia: effect of statin therapy on bioactive lipids and dense LDL." Journal of Lipid Research 61, no. 6 (April 15, 2020): 911–32. http://dx.doi.org/10.1194/jlr.p119000543.
Abstract:
Atherogenic LDL particles are physicochemically and metabolically heterogeneous. Can bioactive lipid cargo differentiate LDL subclasses, and thus potential atherogenicity? What is the effect of statin treatment? Obese hypertriglyceridemic hypercholesterolemic males [n = 12; lipoprotein (a) <10 mg/dl] received pitavastatin calcium (4 mg/day) for 180 days in a single-phase unblinded study. The lipidomic profiles (23 lipid classes) of five LDL subclasses fractionated from baseline and post-statin plasmas were determined by LC-MS. At baseline and on statin treatment, very small dense LDL (LDL5) was preferentially enriched (up to 3-fold) in specific lysophospholipids {LPC, lysophosphatidylinositol (LPI), lysoalkylphosphatidylcholine [LPC(O)]; 9, 0.2, and 0.14 mol per mole of apoB, respectively; all P < 0.001 vs. LDL1-4}, suggesting elevated inflammatory potential per particle. In contrast, lysophosphatidylethanolamine was uniformly distributed among LDL subclasses. Statin treatment markedly reduced absolute plasma concentrations of all LDL subclasses (up to 33.5%), including LPC, LPI, and LPC(O) contents (up to −52%), consistent with reduction in cardiovascular risk. Despite such reductions, lipotoxic ceramide load per particle in LDL1-5 (1.5–3 mol per mole of apoB; 3–7 mmol per mole of PC) was either conserved or elevated. Bioactive lipids may constitute biomarkers for the cardiometabolic risk associated with specific LDL subclasses in atherogenic dyslipidemia at baseline, and with residual risk on statin therapy.
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Stiasny, Karin, and Franz X. Heinz. "Effect of Membrane Curvature-Modifying Lipids on Membrane Fusion by Tick-Borne Encephalitis Virus." Journal of Virology 78, no. 16 (August 15, 2004): 8536–42. http://dx.doi.org/10.1128/jvi.78.16.8536-8542.2004.
Abstract:
ABSTRACT Enveloped viruses enter cells by fusion of their own membrane with a cellular membrane. Incorporation of inverted-cone-shaped lipids such as lysophosphatidylcholine (LPC) into the outer leaflet of target membranes has been shown previously to impair fusion mediated by class I viral fusion proteins, e.g., the influenza virus hemagglutinin. It has been suggested that these results provide evidence for the stalk-pore model of fusion, which involves a hemifusion intermediate (stalk) with highly bent outer membrane leaflets. Here, we investigated the effect of inverted-cone-shaped LPCs and the cone-shaped oleic acid (OA) on the membrane fusion activity of a virus with a class II fusion protein, the flavivirus tick-borne encephalitis virus (TBEV). This study included an analysis of lipid mixing, as well as of the steps preceding or accompanying fusion, i.e., binding to the target membrane and lipid-induced conformational changes in the fusion protein E. We show that the presence of LPC in the outer leaflet of target liposomes strongly inhibited TBEV-mediated fusion, whereas OA caused a very slight enhancement, consistent with a fusion mechanism involving a lipid stalk. However, LPC also impaired the low-pH-induced binding of a soluble form of the E protein to liposomes and its conversion into a trimeric postfusion structure that requires membrane binding at low pH. Because inhibition is already observed before the lipid-mixing step, it cannot be determined whether impairment of stalk formation is a contributing factor in the inhibition of fusion by LPC. These data emphasize, however, the importance of the composition of the target membrane in its interactions with the fusion peptide that are crucial for the initiation of fusion.
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Diehl, Philipp, Frederik Nienaber, Maria T. K. Zaldivia, Johannes Stamm, Patrick M. Siegel, Natalie A. Mellett, Marius Wessinger, et al. "Lysophosphatidylcholine is a Major Component of Platelet Microvesicles Promoting Platelet Activation and Reporting Atherosclerotic Plaque Instability." Thrombosis and Haemostasis 119, no. 08 (August 2019): 1295–310. http://dx.doi.org/10.1055/s-0039-1683409.
Abstract:
Background Microvesicles (MVs) are small cell-derived vesicles, which are mainly released by activated cells. They are part of a communication network delivering biomolecules, for example, inflammatory molecules, via the blood circulation to remote cells in the body. Platelet-derived MVs are known to induce vascular inflammation. Research on the mediators and mechanisms of their inflammatory effects has attracted major interest. We hypothesize that specific lipids are the mediators of vascular inflammation caused by platelet-derived MVs. Methods and Results Liquid chromatography electrospray ionization–tandem mass spectrometry was used for lipid profiling of platelet-derived MVs. Lysophosphatidylcholine (LPC) was found to be a major component of platelet-derived MVs. Investigating the direct effects of LPC, we found that it induces platelet activation, spreading, migration and aggregation as well as formation of inflammatory platelet–monocyte aggregates. We show for the first time that platelets express the LPC receptor G2AR, which mediates LPC-induced platelet activation. In a mouse model of atherosclerotic plaque instability/rupture, circulating LPC was detected as a surrogate marker of plaque instability. These findings were confirmed by matrix-assisted laser desorption ionization imaging, which showed that the LPC concentration of human plaques was highest in vulnerable plaque regions. Conclusion LPC is a major component of platelet-derived MVs and via its interaction with G2AR on platelets contributes to platelet activation, spreading, migration and aggregation and ultimately to vascular inflammation. Circulating LPC reports on atherosclerotic plaque instability in mice and is significantly increased in unstable areas of atherosclerotic plaques in both mice and humans, linking LPC to plaque instability.
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Küllenberg de Gaudry, Daniela, Lenka A. Taylor, Jessica Kluth, Tobias Hübschle, Jonas Fritzsche, Bernd Hildenbrand, Lars Pletschen, et al. "Effects of Marine Phospholipids Extract on the Lipid Levels of Metastatic and Nonmetastatic Prostate Cancer Patients." International Scholarly Research Notices 2014 (August 13, 2014): 1–12. http://dx.doi.org/10.1155/2014/249204.
Abstract:
High intake of omega-3 fatty acids (n-3 FAs) from fish has shown to reduce metastatic progression of prostate cancer. This clinical trial investigated the influence of high n-3 FA intake (marine phospholipids, MPL) on the FA composition of blood lipids, lysophosphatidylcholine (LPC), and on lipoproteins in prostate cancer patients and elderly men without prostate cancer. MPL supplementation resulted in a significant increase of n-3 FAs (eicosapentaenoic and docosahexaenoic acid) in blood lipids, while arachidonic acid (n-6 FA) decreased significantly. Low density lipoprotein (LDL) and high density lipoprotein (HDL) increased significantly, but the LDL increase was observed only in subjects with an inactive tumour. Similarly, LPC plasma concentration increased significantly only in patients without tumour. The missing increase of LDL and LPC after MPL supplementation in patients with actively growing (metastasizing) prostate cancer suggests that tumour cells have an elevated demand for LDL and LPC. Due to the MPL-induced increase of n-3 FAs in these blood lipids, it can be assumed that especially actively growing and metastasizing prostate cancer cells are provided with elevated amounts of these antimetastatic n-3 FAs. A hypothetic model explaining the lower incidence of metastatic progression in prostate cancer patients with high fish consumption is presented.
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Adibi, Shawn S., Joseph L. Alcorn, Kaori Ono, and Lenard M. Lichtenberger. "Gender and Smoking Correlations of Surfactant Lipids and Proteins in the Saliva of Dental Patients." Journal of Dental and Maxillofacial Surgery 1, no. 1 (October 22, 2018): 67–70. http://dx.doi.org/10.18314/jdms.v1i1.1385.
Abstract:
We sought to determine the effects of smoking on surfactant lipids and proteins in saliva. Levels of sphingomyelin (Sph) phosphatidylcholine (PC) and lyso-PC (LPC) were determined by thin layer chromatography. Levels of surfactant protein A (SP-A) were determined by western analysis using antibodies specific for SP-A. Significance of the results was determined by the student’s t-test. The LPC/PC ratio had a tendency to be much higher in smokers compared to nonsmokers. LPC levels were significantly higher in females smokers compared to male smokers. Additionally, levels of SP-A were significantly reduced in females smokers compared to non-smokers. Smoking alters surfactant protein and LPC/PC ratios in saliva. There is a significant difference in the effects in females compared to males. Findings suggest smoking alters the composition of saliva that may reduce protection of the oral cavity, which may explain why women smokers are at greater risk of developing oral mucositis.
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MILLANVOYE-VAN BRUSSEL, Elisabeth, Gökce TOPAL, Annie BRUNET, Thuc DO PHAM, Valérie DECKERT, Francine RENDU, and Monique DAVID-DUFILHO. "Lysophosphatidylcholine and 7-oxocholesterol modulate Ca2+ signals and inhibit the phosphorylation of endothelial NO synthase and cytosolic phospholipase A2." Biochemical Journal 380, no. 2 (June 1, 2004): 533–39. http://dx.doi.org/10.1042/bj20040069.
Abstract:
The oxidation of plasma LDLs (low-density lipoproteins) is a key event in the pathogenesis of atherosclerosis. LPC (lysophosphatidylcholine) and oxysterols are major lipid constitutents of oxidized LDLs. In particular, 7-oxocholesterol has been found in plasma from cardiac patients and atherosclerotic plaque. In the present study, we investigated the ability of 7-oxocholesterol and LPC to regulate the activation of eNOS (endothelial nitric oxide synthase) and cPLA2 (cytosolic phospholipase A2) that synthesize two essential factors for vascular wall integrity, NO (nitric oxide) and arachidonic acid. In endothelial cells from human umbilical vein cords, both 7-oxocholesterol (150 µM) and LPC (20 µM) decreased histamine-induced NO release, but not the release activated by thapsigargin. The two lipids decreased NO release through a PI3K (phosphoinositide 3-kinase)-dependent pathway, and decreased eNOS phosphorylation. Their mechanisms of action were, however, different. The NO release reduction was dependent on superoxide anions in LPC-treated cells and not in 7-oxocholesterol-treated ones. The Ca2+ signals induced by histamine were abolished by LPC, but not by 7-oxocholesterol. The oxysterol also inhibited (i) the histamine- and thapsigargin-induced arachidonic acid release, and (ii) the phosphorylation of both cPLA2 and ERK1/2 (extracellular-signal-regulated kinases 1/2). The results show that 7-oxocholesterol inhibits eNOS and cPLA2 activation by altering a Ca2+-independent upstream step of PI3K and ERK1/2 cascades, whereas LPC desensitizes eNOS by interfering with receptor-activated signalling pathways. This suggests that 7-oxocholesterol and LPC generate signals which cross-talk with heterologous receptors, effects which could appear at early stage of atherosclerosis.
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Cheng, Long, Xiao Han, and Yuguang Shi. "A regulatory role of LPCAT1 in the synthesis of inflammatory lipids, PAF and LPC, in the retina of diabetic mice." American Journal of Physiology-Endocrinology and Metabolism 297, no. 6 (December 2009): E1276—E1282. http://dx.doi.org/10.1152/ajpendo.00475.2009.
Abstract:
Platelet-activating factor (PAF) and lysophosphatidylcholine (LPC) are potent inflammatory lipids. Elevated levels of PAF and LPC are associated with the onset of diabetic retinopathy and neurodegeneration. However, the molecular mechanisms underlying such defects remain elusive. LPCAT1 is a newly reported lysophospholipid acyltransferase implicated in the anti-inflammatory response by its role in conversion of LPC to PC. Intriguingly, the LPCAT1 enzyme also catalyzes the synthesis of PAF from lyso-PAF with use of acetyl-CoA as a substrate. The present studies investigated regulatory roles of LPCAT1 in the synthesis of inflammatory lipids during the onset of diabetes. Our work shows that LPCAT1 plays an important role in the inactivation of PAF by catalyzing the synthesis of alkyl-PC, an inactivated form of PAF with use of acyl-CoA and lyso-PAF as substrates. In support of a role of LPCAT1 in anti-inflammatory responses in diabetic retinopathy, LPCAT1 is most abundantly expressed in the retina. Moreover, LPCAT1 mRNA levels and acyltransferase activity toward lyso-PAF and LPC were significantly downregulated in retina and brain tissues in response to the onset of diabetes in Ins2 Akita and db/db mice, mouse models of type 1 and type 2 diabetes, respectively. Conversely, treatment of db/db mice with rosiglitazone, an antidiabetes compound, significantly upregulated LPCAT1 mRNA levels concurrently with increased acyltransferase activity in the retina and brain. Collectively, these findings identified a novel regulatory role of LPCAT1 in catalyzing the inactivation of inflammatory lipids in the retina of diabetic mice.
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Wang, Yang, Chang-Tao Jiang, Jie-Yun Song, Qi-Ying Song, Jun Ma, and Hai-Jun Wang. "Lipidomic Profile Revealed the Association of Plasma Lysophosphatidylcholines with Adolescent Obesity." BioMed Research International 2019 (December 13, 2019): 1–9. http://dx.doi.org/10.1155/2019/1382418.
Abstract:
Objective. The human lipidomic profile reflects lipid metabolism, including the early phase of pathophysiological changes associated with diseases. An investigation of the association between the plasma lipidomic profile and adolescent obesity might provide new insights into the biological mechanisms of obesity. Therefore, we aimed to investigate the association of the plasma lipidome with obesity in Chinese adolescents using lipidomics. Methods. Using a combination of liquid chromatography and electrospray ionization tandem mass spectrometry, we quantified 328 lipid species from 24 lipid classes and subclasses in 100 male adolescents aged 14–16 years who were categorized into four groups: (1) normal weight with traditional normal clinical plasma lipid levels (NN); (2) normal weight with traditional abnormal clinical plasma lipid levels (NA); (3) obese with traditional normal clinical plasma lipid levels (ON); and (4) obese with traditional abnormal clinical plasma lipid levels (OA). The concentrations of all the lipid species were compared between obese and normal-weight adolescents at different traditional clinical plasma lipid levels using the Kruskal–Wallis test followed by the Mann–Whitney U test. A partial least squares discriminant analysis (PLS-DA) was applied to select lipids with a significant ability to discriminate adolescent obesity. Results. The lipidomic profile distinguished obese adolescents from normal-weight subjects. Regardless of whether traditional clinical plasma lipid levels were normal or abnormal, we observed a significant reduction in the levels of five lysophosphatidylcholines (LPC) species (LPC18:2, LPC18:1, LPC20:2, LPC20:1, and LPC20:0) in the obese group compared with the normal-weight group (difference = −31.29% to −13.19%; P=9.91×10−5 to 2.28×10−2). The ability of these five LPC species to discriminate adolescent obesity was confirmed in the PLS-DA model. Conclusions. The findings provided evidence for the association of some LPC species with adolescent obesity. The discriminatory effects of five LPC species were identified between normal-weight and obese adolescents, independent of traditional clinical plasma lipid levels. These results will provide a basis for validation in subsequent studies.
Dissertations / Theses on the topic "LPC lipids":
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Negm, Ahmed. "Étude du rôle des canaux ASIC3 dans l'hypersensibilité à la douleur associée à une alimentation riche en lipides." Thesis, Université Côte d'Azur (ComUE), 2019. http://theses.univ-cotedazur.fr/2019AZUR4046.
Abstract:
L'obésité est un facteur de risque majeur pour de nombreux troubles métaboliques graves. Elle touche 13% de l'ensemble de la population adulte dans le monde, ce qui en fait un domaine de recherche important. L'obésité se caractérise par un indice de masse corporelle accru qui résulte d'un déséquilibre entre l'apport calorique et les dépenses énergétique. Cela peut être dû à une consommation accrue d'aliments riches en énergie, comme les aliments riches en graisses, qui correspondent à l'alimentation occidentale, en parallèle avec un faible niveau d’activité physique. Il est maintenant bien accepté que l'obésité induit une inflammation systémique chronique de bas grade, qui implique les adipokines et les cytokines libérées par l'intestin et le tissu adipeux. Cette inflammation de bas grade s'étend à d'autres tissus, entraînant des dysfonctionnements métaboliques systémiques. De plus, il a été démontré que l'obésité est corrélée à des douleurs chroniques, indépendamment des autres composantes du syndrome métabolique. Il n'est pas encore clairement établi comment cette douleur chronique est initiée et quels en sont les mécanismes. Notre étude s’est concentrée sur l'étude de l'effet de l'obésité sur l'activité des neurones sensoriels périphériques et la perception de la douleur, et la caractérisation des mécanismes cellulaires sous-jacents qui impliquent les canaux ioniques sensibles à l’acidose ASIC3. Méthodologie. Nous avons utilisé une alimentation riche en matières grasses composée essentiellement d'acides gras saturés pour induire l'obésité chez des souris juvéniles. Nous testons les seuils de perception des douleurs thermiques, mécaniques et chimiques chez les souris obèses à l'aide de tests de chaleur radiante Hargreaves, de von Frey dynamique et de formaline. Les approches électrophysiologiques, y compris les techniques de patch-clamp et l'enregistrement sur le nerf saphène, nous ont permis d'étudier l'effet l'obésité induite par un régime riche en graisses saturée sur l'excitabilité des neurones sensoriels périphériques. Résultats. Après 8 semaines d'alimentation riche en graisses (HFD), nous avons pu observer que les souris deviennent obèses. Ces souris sont prédiabétiques. Elles ont développé une dérégulation de l'homéostasie du glucose par rapport aux souris maigres nourries en régime standard. De plus, les souris obèses présentent une hypersensibilité thermique une fois l'obésité bien établie, alors que les autres modalités sensorielles ne sont pas affectées. Nous avons observé une surexpression des cytokines inflammatoires chez des souris obèses non seulement dans le tissu adipeux mais aussi dans d'autres tissus impliqués dans la voie de la douleur (c'est-à-dire les ganglions radiculaires dorsaux et la moelle épinière). Le régime alimentaire riche en lipides a provoqué une dyslipidémie avec une concentration accrue de plusieurs espèces de lipides dans le sérum des souris obèses, dont le lysophosphatidylcholine. Nous montrons que le sérum de souris obèses active directement les canaux ASIC3 et potentialise les réponses à une acidification modérée (pH 7). L'obésité augmente la réponse des fibres C mechano et thermosensibles cutanées à la chaleur. L’absence des canaux ASIC3 chez les souris knockout protège ces souris de l'hyperalgésie à la chaleur. Conclusions. Nos expériences ont mis en lumière l'impact de l'inflammation chronique de bas grade et de la dysrégulation métabolique induite par une alimentation riche en graisses, induisant l’obésité sur le système nerveux périphérique et la douleur. Nous démontrons le rôle des canaux ASIC3 dans sur l’excitation des neurones sensorielles et l’hyperalgésie thermique. Nos résultats donnent une portée clinique intéressante et suggèrent que l'hypersensibilité thermique associée à l'obésité induite par les lipides pourrait être traitée pharmacologiquement en bloquant ASIC3Obesity is a major risk factor for many serious disorders. It affects 13% of the whole adult population worldwide making it an important field for research. Obesity is characterized by an increased body mass index resulting from an energy imbalance between caloric intake and expenditure. This can be caused by an increased consumption of energy-dense foods such as food rich in fat, which corresponds to occidental diet. It is now well accepted that obesity induces chronic systemic low-grade inflammation, which is mediated by Adipokines and cytokines released from the gut and adipose tissue. This low-grade inflammation extends to other tissue leading to systemic metabolic dysfunctions. In addition, obesity was shown to be correlated to chronic pain regardless of other components of the metabolic syndrome. It is not yet clear how this chronic pain is initiated and what mechanisms are involved. Our study focuses on investigating the effect of obesity on peripheral sensory neurons activity and pain perception, followed by deciphering the underlying cellular and molecular mechanisms that involve the Acid Sensing Ion Channels ASIC3. Methods. Mice were fed with a high-fat diet composed of saturated fatty acids to induce obesity. We are using pain behavioral tests to measure the thermal, mechanical and chemical perception in obese mice using radiant heat Hargreaves test, dynamic von Frey, and formalin tests. Electrophysiological approaches including patch-clamp techniques and skin-saphenous nerve recording preparation allowed us to study the effect of high-fat diet and obesity on peripheral sensory neurons excitability, while qPCR and Immunohistochemistry chemistry were used in investigating the changes in pro-inflammatory factors expression. Results. After 8 weeks of high-fat diet (HFD), we observe that mice become obese. These mice developed a deregulation of glucose homeostasis compared to lean mice fed on standard regime. In addition, obese mice showed a long-lasting thermal hypersensitivity once the obesity was well established, while other sensory modalities were not affected. We found an overexpression of the inflammatory cytokines in obese mice not only in the adipose tissue but also in other tissues involved in the pain pathway (i.e. Dorsal root ganglions and spinal cord). In addition, the lipid rich diet induced dyslipidemia with increased concentration of several lipid species in the serum of obese mice. Delivering the serum from obese mice to recombinant ASIC3 channels directly activated the channels and potentiated the channels responses to moderate acidification (pH 7). Obesity led to increased firing of heat sensitive C-fibers. The genetic deletion of ASIC3 channels in ASIC3 knockout mice protected these mice from thermal hypersensitivity. Conclusions. Our experiments shed light on the impact of the chronic low-grade inflammation and metabolic dysregulation induced by fat-rich diet on the peripheral nervous system and pain, and on the role of ASIC3 channels in these conditions. Our results give an interesting clinical scope and suggest that the thermal hypersensitivity associated with lipid induced obesity could be treated pharmacologically by blocking ASIC3
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Robitaille, Nicole. "Polymorphisme de l'apolipoprotéine E au sein de la population du Lac St-Jean Chibougamau /." Thèse, Chicoutimi : Université du Québec à Chicoutimi, 1994. http://theses.uqac.ca.
Abstract:
Mémoire (M.Med.Exp.)-- Université du Québec à Chicoutimi, 1994.Ce mémoire a été réalisé à l'Université du Québec à Chicoutimi dans le cadre du programme de maîtrise en médecine expérimentale de l'Université Laval extensionné à l'UQAC. CaQCU Document électronique également accessible en format PDF. CaQCU
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Paquette, Sara Montminy. "Evasion of LPS-TLR4 Signaling as a Virulence Determinate for Yersinia pestis." eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/458.
Abstract:
Yersinia pestis, the gram-negative causative agent of plague, is a master of immune evasion. The bacterium possesses a type three secretion system which translocates Yop effector proteins into host immune cells to inhibit a number of immune and cell signaling cascades. Interestingly, this apparatus is not expressed at low temperatures such as those found within the flea vector and is therefore neither in place nor functional when the bacteria are first transmitted into a mammalian host. However, the bacterium is still able to avoid activating the immune system, even very early during infection.
When grown at 37°C (human body temperature) Y. pestis produces a tetra-acyl lipid A molecule, which is antagonistic to the human Toll like receptor 4/MD2, the major lipopolysaccharide recognition receptor. Although tetra-acyl lipid A binds this receptor complex, it does not induce signaling, and in fact inhibits the receptors interaction with other stimulatory forms of lipid A. The work undertaken in this thesis seeks to determine if the production of tetra-acyl lipid A by Y. pestis is a key virulence determinant and was a critical factor in the evolution of Y. pestis from its ancestral parent Yersinia pseudotuberculosis.
By examining the enzymes involved in the lipid A biosynthesis pathway, it has been determined that Y. pestis lacks LpxL, a key enzyme that adds a secondary acyl chain on to the tetra acyl lipid A molecule. In the absence of this enzyme, Y. pestis cannot produce a TLR4 stimulating form of lipid A, whereas Y. pseudotuberculosis does contain the gene for LpxL and produces a stimulatory hexa acyl lipid A. To determine if the absence of LpxL in Y. pestis is important for virulence, LpxL from E. coli and Y. pseudotuberculosis were introduced into Y. pestis. In both cases the addition of LpxL led to bacterium which produced a hexa-acylated lipid A molecule and TLR4/MD2 stimulatory LPS. To verify the LpxL phenotype, lpxL was deleted from Y. pseudotuberculosis, resulting in bacteria which produce tetra-acylated lipid A and nonstimulatory LPS. Mice challenged with LpxL expressing Y. pestis were found to be completely resistant to infection. This profound attenuation in virulence is TLR4 dependent, as mice deficient for this receptor rapidly succumb to disease. These altered strains of the bacterium also act as vaccines, as mice infected with Y. pestis expressing LpxL then challenged with wild type Y. pestis do not become ill. These data demonstrate that the production of tetra-acyl lipid A is a critical virulence determinant for Y. pestis, and that the loss of LpxL formed a major step in the evolution of Y. pestis from Y. pseudotuberculosis.
These bacterial strains were also used as tools to determine the contributions of different innate immune receptors and adaptor molecules to the host response during Y. pestis infection. The use of LpxL expressing Y. pestis allowed identification of the innate immune pathways critical for protection during Y. pestis infection. This model also established that CD14 recognition of rough LPS is critical for protection from Y. pestisexpressing LpxL, and activation of the IL-1 receptor and the induction of IL-1β plays a major role in this infection as well.
The lipid A acylation profile of gram negative bacteria can have a direct and profound effect on the pathogenesis of the organism. This work illustrates a previously unknown and critical aspect of Y. pestis pathogenesis, which can be extended to other gram-negative pathogens. The greater detail of the contributions which different host adaptor and receptor molecules make to the overall innate immune signaling pathway will allow a better insight into how gram negative infections progress and how they are counteracted by the immune system. Alterations of the lipid A profile of Y. pestis have important implications for the production of vaccines to Y. pestis and other gram negative pathogens. Taken together, this work describes a novel mechanism for immune evasion by gram negative bacteria with consequences for understanding the immune response and the creation of more effective vaccines, both of which will decrease the danger posed by this virulent pathogen.
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Garcia-Murillas, Isaac. "Functional analysis of lipid phosphate phosphohydrolases (LPP) in Drosophila melanogaster phototransduction cascade." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.613148.
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Pohl, Antje Heide. "Lipid transport by ABC proteins." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2002. http://dx.doi.org/10.18452/14784.
Abstract:
In eukaryotischen Zellen sind die Lipidspezies häufig asymmetrisch zwischen den Hälften der Plasmamembran verteilt. Insbesondere Phosphatidylserin (PS) weist oft eine ausgeprägte transversale Asymmetrie auf, da es fast ausschliesslich auf die innere Hälfte der Plasmamembran beschränkt ist. In den letzten Jahren wurden mehrere Proteine diskutiert, die Lipide zwischen den Membranhälften transportieren und möglicherweise die transversale Lipidasymmetrie sowie damit verbundene Zelleigenschaften beeinflussen. Im Mittelpunkt der vorliegenden Promotion steht der Auswärtstransport fluoreszierender (C6-NBD-) Lipid-Analoga und endogener Lipide durch das Multidrug Resistance 1 P-Glycoprotein (MDR1 Pgp), das der ATP Binding Cassette (ABC) Transporter Superfamilie angehört. Interessanter Weise wird für MDR1 Pgp eine ungewöhnlich breite Substratspezifität angenommen. Das anionische Lipid PS war hier von besonderem Interesse, obgleich es in vorhergehenden Arbeiten nicht als MDR1 Pgp Substrat betrachtet wurde. Der Auswärtstransport von Phosphatidylcholin-, Phosphatidylethanolamin-, Glucosylceramid- und Sphingomyelin-Analoga durch MDR1 Pgp konnte in einer humanen Magenkarzinomlinie (EPG85-257), die MDR1 überexprimiert, mittels Fluoreszenzspektroskopie bestätigt werden. Zudem legt die verringerte Akkumulation von Diacylglycerol- und Ceramid-Analoga den Transport dieser Lipidspezies durch MDR1 Pgp nahe. Im Anschluß an die intrazelluläre Markierung mit C6-NBD-PS mittels eines neuen Verfahrens konnte der signifikant erhöhte Auswärtstransport dieses Analogons in MDR1 überexprimierenden Zellen durch Verwendung spezifischer Inhibitoren MDR1 Pgp zugeschrieben werden. In flusscytometrischen Versuchen war die Exponierung von endogenem PS auf der äusseren Membranhälfte von MDR1 überexprimierenden Zellen signifikant höher als in Kontrollzellen. Verringerung der PS-Exponierung durch einen Inhibitor von MDR1 Pgp deutet auf den Transport von endogenem PS durch MDR1 Pgp hin. Zusätzlich wurde hier der Transport von C6-NBD-PS in vier weiteren Zellinien mit verschiedener Spezies- und Gewebezugehörigkeit charakterisiert, die unterschiedliche Mengen an MDR1 Pgp synthetisieren. Wie Experimente in einer BCRP überexprimierenden EPG85-257-Sublinie nahelegen, ist ausser MDR1 Pgp möglicherweise ebenfalls der ABC Halb-Transporter Breast Cancer Resistance Protein (BCRP) am Transport von C6-NBD-PS und an der verstärkten Exponierung von endogenem PS beteiligt.In eukaryotic cells, the lipid species are frequently distributed asymmetrically between the plasma membrane leaflets. Phosphatidylserine (PS), in particular, often exhibits a distinct transverse asymmetry, being restricted almost exclusively to the inner leaflet. In the past years, several proteins were suggested to transport lipids between the leaflets of a membrane, and to potentially influence transverse lipid asymmetry and related cell properties. This thesis focuses on outward transport of fluorescent (C6-NBD-) lipid analogs and endogenous lipids by the Multidrug Resistance 1 P-Glycoprotein (MDR1 Pgp), a member of the ATP binding cassette (ABC) transporter superfamily. Interestingly, MDR1 Pgp has been suggested to exhibit an unusually broad substrate specificity. Here, the anionic PS was of particular concern, although previously reported not to be an MDR1 Pgp substrate. In a human gastric carcinoma cell line (EPG85-257) overexpressing MDR1, outward transport of phosphatidylcholine, phosphatidylethanolamine, glucosylceramide and sphingomyelin analogs via MDR1 Pgp was confirmed using fluorescence spectroscopy. In addition, decreased accumulation of analogs of diacylglycerol and ceramide suggest MDR1 Pgp mediated transport of these lipid species. Upon intracellular labelling with C6-NBD-PS using a novel approach, significantly increased outward transport of this analog in MDR1 overexpressing cells could be attributed to MDR1 Pgp by employing specific inhibitors. In a flow cytometry setup, the exposure of endogenous PS on the outer plasma membrane leaflet was significantly elevated in MDR1 overexpressing cells compared to controls. Reduction of PS exposure by an MDR1 Pgp inhibitor suggests transport of endogenous PS by MDR1 Pgp. Transport of C6-NBD-PS was furthermore characterized here in four additional cell lines of different species and tissue origin with varying synthesis levels of MDR1 Pgp. Besides MDR1 Pgp, the ABC half-size transporter Breast Cancer Resistance Protein (BCRP) is possibly also involved in transport of C6-NBD-PS and in increased exposure of endogenous PS, as found in a BCRP overexpressing EPG85-257 subline.
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Chi, Xun. "Extracellular regulation of LPL activity by angiopoietin-like proteins." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/5729.
Abstract:
Dyslipidemia often accompanies metabolic diseases such as obesity and type II diabetes mellitus and represents a risk factor for cardiovascular disease. Clearance of triglycerides from the plasma is mediated by lipoprotein lipase (LPL), which hydrolyzes the triglycerides in chylomicrons and VLDL, liberating fatty acids for tissue uptake. LPL functions in the capillaries of the heart, adipose tissue, and skeletal muscle where LPL is anchored to the capillary wall by its endothelial cell transporter GPIHBP1. LPL activity is regulated by several factors including three members of the angiopoietin-like (ANGPTL) family–ANGPTL3, ANGPTL4, and ANGPTL8. How these proteins interact with LPL, especially in the physiological context of LPL anchored to endothelial cells by GPIHBP1, has not been well characterized. In my studies of ANGPTL4, I found when LPL is bound to GPIHBP1, it is partially, but not completely, protected from inactivation by ANGPTL4. Inactivation of LPL by ANGPTL4 leads to the dissociation of active LPL dimers into inactive monomers and I found that these monomers have a greatly reduced affinity for GPIHBP1. ANGPTL4 can be cleaved in vivo, separating the N-terminal coiled-coil domain from the C-terminal fibrinogen like-domain. I found the N-terminal domain alone is a much more potent LPL inhibitor than the full-length protein, even though both appear to have similar binding affinities for LPL-GPIHBP1 complexes. When I investigated ANGPTL3, I found ANGPTL3 itself is not a potent inhibitor of LPL at physiological concentrations, and unlike ANGPTL4, cleavage of ANGPTL3 does not improve its ability to inhibit LPL. Instead I found that ANGPTL3 forms a complex with ANGPTL8, a complex that only forms efficiently when the two proteins are co-expressed, and that this complex allows ANGPTL3 to bind and inhibit LPL. My data provide new insights into how ANGPTL proteins regulate LPL activity and the delivery of fat to tissues.
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Pott, Markus Philipp. "Organic hydroperoxide-induced lipid peroxidation (LPO) and signal transduction pathways in human keratinocytes." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=96545293X.
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Ciesielski, Filip I. "Bacterial outer membranes : LPS and the role of lipid rafts in mediating host invasion." Thesis, University of Nottingham, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604885.
Abstract:
Lipopolysaccharide is an essential component of outer membranes in Gram-negative bacteria and there is increasing evidence that it might be involved in mediating host invasion via a direct interaction with host cell membrane. Also, many pathogenic intracellular bacteria, such as Brucella spp., use lipid rafts-dependent entry to mimic endocytic pathway and avoid lysosoma l degradation. In th is project, solid state NMR (ssNMR) spectroscopy and fluorescence spectroscopy are used to investigate possible interactions between bacterial LPS and membranes with raft-like composition. A ssNMR technique for studying changes in lipid dynamics during LPS/ membrane interactions was first developed and J- resolved 13C MAS NMR was used to study changes to DPPC membranes in response to temperature variation and in the absence of isotopic enrichment. J- resolved 20 HETCOR NMR spectroscopy was also developed to investigate more complex lipid membranes and was applied to DOPC/cholesterol and triple mixture DOPC/ SM/Chol, a model membrane used to mimic lipid rafts. Interactions between membrane-incorporated LPS and raft- like membranes were then investigated using 13C MAS NMR as well as 31p NMR spectroscopy. Results revealed that endotoxins undergo significant mobility restrictions in the presence of sphingomyelin and cholesterol suggesting that they partition into the liquid-ordered phase. Fluorescence spectroscopy was then used to study interactions between free LPS and membranes with and without latera l domains showing a preferred affin ity of endotoxins towards bilayers with raft-like composition over plain PC membranes, in agreement with the NMR data. ; ..
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Dalko, Peter I. "Synthèse d'analogues carbocycliques du N-acetyl-muramyl-dipeptide (MDP) et du lipide X (LPX), immunomodulateurs potentiels." Paris 11, 1989. http://www.theses.fr/1989PA112001.
Abstract:
Nous présentons dans la première partie de cette thèse une approche pour la synthèse d'aminocyclitols et de pseudo-amino-sucres. La méthode mise en jeu implique une substitution nucléophile des allyl-carbonates et acétates du conduritol-B, en présence de palladium(O). Nous avons montré que l’addition nucléophile sur le cation π-allylique est, dans certains cas, régiosélective. Dans la seconde partie, nous rapportons la préparation deux analogues carbocycliques du N-acétyl muramyl-dipeptide (MDP) à partir de la D-glucosamine. L'étape clef de la synthèse est la réaction de Ferrier, qui permet la transformation d'un dérivé sucre en cyclohexanone chirale hautement substituée. Pour préparer l'analogue carbocyclique du nor-MDP, nous avons mis au point deux méthodes conduisant respectivement en 12 et 15 étapes aux molécules cibles. La synthèse de l'analogue carbocyclique du MDP possédant un cycle oxazolidinone a été réalisée en 16 étapes. Dans le troisième chapitre nous décrivons la préparation de deux dérivés carbocycliques du lipide X (LPX). Les analogues carbocycliques du nor-LPX et du LPX ont été synthétisés respectivement en 18 et 21 étapes. Les analogues carbocycliques synthétisés possèdent des propriétés immunomodulateursWe describe in the first part of this thesis an exploratory approach for the synthesis of aminocyclitols and pseudo-amino-sugars. The method consists of a nucleophilic substitution in the presence of palladium (O) on the allyl-acetate, or carbonate, of conduritol-B. We present here the evidence that the substitution with chiral nucleophiles on the π-allylic cation proceedes in certain cases in a regioselective fashion. In the second part, we report the preparation of two carbocyclic analogues of N-acetyl-muramyl-dipeptide (MDP) using D-glucosamine as starting material. The key step in the synthetic sequence is the Ferrier transformation of the carbohydrate into the corresponding chiral cyclohexanone. From the latter, we prepared the carbocyclic analogues of nor-MDP by two methods using a sequence of 12 and 15 steps, respectively. In addition a carbocyclic analogue of MDP, containing an oxazolidinone ring was also prepared in 16 steps. In the third part we present the synthesis of two carbocyclic analogues of lipid X (LPX) also from aminocyclohexanones. The carbocyclic analogues of nor-LPX and LPX were synthesized in a sequence of 18 and 21 steps, respectively. The carbocyclic analogues synthesized show immunological properties
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Cody, West Kime. "Autotaxin-mediated lipid signaling intersects with LIF and BMP signaling to promote the naive pluripotency transcription factor program." Kyoto University, 2018. http://hdl.handle.net/2433/232302.
Books on the topic "LPC lipids":
1
Wiklund, Olov, and Jan Borén. Pathogenesis of atherosclerosis: lipid metabolism. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0011.
Abstract:
Lipids are carried in plasma as microparticles, lipoproteins, composed of a core of hydrophobic lipids and a surface of amphipathic lipids. In addition, the particles carry proteins (i.e. apolipoproteins). The proteins have key functions in the metabolism as receptor ligands, enzymes or activators. Lipoproteins are classified based on density into: chylomicrons, VLDL, IDL, LDL, and HDL. Retention of apoB-containing lipoproteins (LDL, IDL, and VLDL) in the arterial intima is the initiating event in the development of atherosclerosis. Retention is mediated by binding of apoB to structural proteoglycans in the intima. Increased plasma concentration of apoB-containing lipoproteins is the main risk factor for atherosclerotic cardiovascular disease (CVD) and the causative role of LDL has been demonstrated in several studies. Lp(a) is a subclass of LDL and elevated Lp(a) is an independent risk-factor, primarily genetically mediated. Genetic data support that high Lp(a) causes atherosclerosis. Elevated triglycerides in plasma are associated with increased risk for CVD. Whether triglycerides directly induce atherogenesis is still unclear, but current data strongly support that remnant particles from triglyceride-rich lipoproteins are causal. HDL are lipoproteins that have been considered to be important for reversed cholesterol transport. Low HDL is a strong risk-factor for CVD. However, the causative role of HDL is debated and intervention studies to raise HDL have not been successful. Reduction of LDL is the main target for prevention and treatment, using drugs that inhibit the enzyme HMG-CoA reductase, i.e. statins. Other drugs for LDL reduction and to modify other lipoproteins may further reduce risk, and new therapeutic targets are explored.
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Claude, Bouchard, and Johnston Francis E. 1931-, eds. Fat distribution during growth and later health outcomes: A symposium held at Manoir St-Castin, Lac Beauport, Quebec, June 9-11, 1987. New York: Liss, 1988.
Book chapters on the topic "LPC lipids":
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Taniguchi, Masako, Toshihiro Sugiyama, and Naoyuki Taniguchi. "Abnormal Lipid Metabolism in LEC Rats." In The LEC Rat, 169–74. Tokyo: Springer Japan, 1991. http://dx.doi.org/10.1007/978-4-431-68153-3_19.
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Ueda, Hiroshi, and Hitoshi Uchida. "Lipid Mediator LPA-Induced Demyelination and Self-Amplification of LPA Biosynthesis in Chronic Pain Memory Mechanisms." In Bioactive Lipid Mediators, 223–36. Tokyo: Springer Japan, 2015. http://dx.doi.org/10.1007/978-4-431-55669-5_16.
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Voelker, Troy, and Roger Demers. "LC-MS Bioanalysis of Liposomal Drugs and Lipids." In Handbook of LC-MS Bioanalysis, 591–99. Hoboken, NJ, USA: John Wiley & Sons Inc., 2013. http://dx.doi.org/10.1002/9781118671276.ch46.
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Zhang, Quiping, Elisabeth Cavallero, Julian Cavanna, Andrea Kay, Aline Charles, Bernard Jacotot, and David J. Galton. "Environment-by-Gene Interactions: Polymorphisms at the Lipoprotein Lipase (Lpl) Locus." In Drugs Affecting Lipid Metabolism, 355–59. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0311-1_41.
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Sigrist, M., C. Zwillenberg-Fridman, Ch Giroud, W. Eichenberger, and A. Boschetti. "LHC II-Apoproteins of Chlamydomonas Reinhardii: Isolation, Isoelectric Focusing, Association with Lipids." In Techniques and New Developments in Photosynthesis Research, 149–52. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-8571-4_18.
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Salamatipour, Ashkan, Ian A. Blair, and Clementina Mesaros. "Targeted Lipid Biomarker Quantitation Using Liquid Chromatography-Mass Spectrometry (LC-MS)." In Targeted Biomarker Quantitation by LC-MS, 273–87. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781119413073.ch17.
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Tigyi, G., D. J. Fisher, K. Lilion, Z. Guo, T. Virag, G. Sun, D. D. Miller, K. Murakami-Murofushi, S. Kobayashi, and J. R. Erickson. "Determinants of Receptor Subtype Specificity in the LPA-Like Lipid Mediator Family." In Advances in Experimental Medicine and Biology, 245–51. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4793-8_36.
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Zhang, Fan, and Hao-Ying Li. "Preparation of Lipid–Peptide–DNA (LPD) Nanoparticles and Their Use for Gene Transfection." In Methods in Molecular Biology, 91–98. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0319-2_6.
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Onur Yaman, Suzan, and Adnan Ayhanci. "Lipid Peroxidation." In Lipid Peroxidation [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95802.
Abstract:
Lipid peroxidation (LPO) is initiated by the attack of free radicals (eg OH ·, O2- and H2O2) on cellular or organelle membranes phospholipids or polyunsaturated fatty acids (PUFA), and with the formation of various types of aldehydes, ketones, alkanes, carboxylic acids and polymerization products. It is an autoxidation process that results. These products are highly reactive with other cellular components and serve as biological markers of LPO. Malondialdehyde (MDA), a toxic aldehyde end product of LPO, causes structural changes that mediate its oxidation, such as fragmentation, modification, and aggregation, especially in DNA and protein. The excessive binding of these reactive aldehydes to cellular proteins alters membrane permeability and electrolyte balance. Degradation of proteins leads to progressive degradation of the biological system mediated by oxidative stress. The chain reaction (CR) of LPO is initiated by the attack of free radicals on the PUFA of the cell membrane to form a carbon centered radical (R*). The O2 · - radical attacks the other lipid molecule to form lipid hydroperoxide (ROOH), thereby spreading the CR and forming the lipid peroxyl radical (ROO). These lipid hydroperoxides severely inhibit membrane functionality by allowing ions such as increased hardness and calcium to leak through the membrane. Damage to the lipid membrane and macromolecule oxidation can result in activation of necrotic or apoptotic tissue death pathways if severe enough.
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Oluwafemi Ezekiel, Kale. "Lipid Peroxidation and the Redox Effects of Polyherbal." In Lipid Peroxidation [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97625.
Abstract:
The use of more than one herb in a medicinal preparation also known as polyherbal has increased geometrically in recent times. Over a hundred thousand scientists have cited “herbal” to strengthen its ethnopharmacological relevance in literature. Polyherbal (PH) is effective potential therapeutic compound used globally to treat oxidative stress-induced injuries which give credence for their traditional applications. However, some issues related to safety and adverse reactions due to PH have raised important public health debates. Lipid peroxidation (LPO) assay is widely used to assess the toxic endpoint of PH. This paper discusses some important roles that PH plays during oxidation–reduction processes.
Conference papers on the topic "LPC lipids":
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Faulkner, M. F., and J. Brandon Dixon. "Engineered Model of the Intestine Suggests Active Transport of Lipid by Lymphatics." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53903.
Abstract:
The lymphatic system has long been thought of as little more than a series of passive ducts as they serve to return fluid and proteins from interstitial spaces back to the blood, provide a route for immune cell trafficking, and transport dietary lipid from the intestine to the blood. Recent evidence has revealed that the lymphatics play an active role in lipid trafficking, and alterations in this function have been correlated with the presence of lymphatic diseases (Dixon, 2010). Here we describe the use of a two-cell, tissue engineered model to explore mechanisms of lipid transport across lymphatic endothelial cells (LEC). Previously this model was demonstrated to recapitulate essential features of the intestinal-lacteal interface with in the mammalian gut (Dixon et al., 2009). With our model we demonstrate, not only that lipid transport across the lymphatics is transcellular and ATP dependent, but also, this mechanism of transport utilizes the molecular motors dynein and kinesin.
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Erzhen, Zen, Lu Yung-Cai, Wang Jain, Shi Fang, Lia Xiaoqing, Zhou Yulin, Jia Xudong, and Gou Zhaozheng. "EXPERIMENTAL STUDIES ON THE MECHANISM OF CHINESE MEDICINAL RHAPONTICUM UNIFLORUM DC IN PREVENTING CORONARY HEART DISEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643029.
Abstract:
The mechanism of Rhaponticum Uniflorum DC in preventing coronary heart disease was studied in vivo and in vitro. TBA fluorescent method was used to determine lipid peroxides (Lpo) and double analysis method was used to determine glutathione peroxidase (GSH-Px) activity and fluorescent polarization of DPH probed membrane fluidity of smooth muscle cell (SMC).Rabbits were fed with high fat diet for 120 days. At the end of experiment, all the animals acquired hyperlipidemia and developed atheroma lesions in aorta and/or coronary. It was found that hyperlipidemia caused a rising of Lpo in blood (from 2.6±0.56 in control up to 8.48±3.28 nmol/ml) and in arterial wall (from 6.75±0.59 in control up to 31.94±4.20 nmol/g protein) and a decreasing of GSH-Px activity in arterial wall (from 0.210±0.095 down to 0.056±0.026 EU/g protein); concomitantly, an increase in microviscosity of arterial SMC membrane (from 1.93±0.04 in control up to 3.49±0.92 poise) which reflects a decrease in fluidity of SMC membrane. Lpo level was higher in plaque area (113.70±46.14 nmol/g protein) than in non-plaque area (58.32±12.69 nmol/g protein). GSH-Px activity level was lower in plaque area (0.0052±0.0014 EU/g protein) than in non-plaque area (0.015+0.0014 EU/g protein). Microviscosity of SMC membrane was higher in plaque area (2.92±0.35 poise) than in non-plaque area (2.26±0.24 poise, p<0.02). By comparison, the rabbits received Rhaponticum Uniflorum DC and VE showed much lowering of Lpo level in arterial wall (down to 10.74±1.61 and 9.93±1.17 nmol/g protein) and decreasing of microviscosity (down to 2.05+0.45 and 2.08+0.50 poise) that is increasing of membrane fluidity of arterial SMC membrane, but GSH-Px activity in arterial wall was keeping at lower level (0.036±0.027 and 0.051±0.027 EU/g protein). The atheroma lesions develped in these two group animals were less severe and fewer in number.
Reports on the topic "LPC lipids":
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LAST, JULIE A., TINA HUBER, DARRYL Y. SASAKI, BRIAN SALVATORE, and SALVATORE J. TURCO. Atomic Force Microscopy Studies of Lipophosphoglycan (LPG) Molecules in Lipid Bilayers. Office of Scientific and Technical Information (OSTI), March 2003. http://dx.doi.org/10.2172/809989.