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Academic literature on the topic 'Métabolisme des HDL'
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Journal articles on the topic "Métabolisme des HDL"
Gautier, T., D. Masson, and L. Lagrost. "Métabolisme des lipoprotéines de haute densité (HDL)." Archives of Cardiovascular Diseases Supplements 3, no. 4 (2011): 267–72. http://dx.doi.org/10.1016/s1878-6480(11)70785-6.
Full textBouillet, Benjamin, Pauline Tscherter, Pauline Legris, Alexia Rouland, Jean-Michel Petit, and Bruno Vergès. "Effets de la corticothérapie systémique sur le métabolisme des HDL." Médecine des Maladies Métaboliques 14, no. 6 (2020): 529–35. http://dx.doi.org/10.1016/j.mmm.2020.06.014.
Full textShi, Y., M. de Groh, and C. Bancej. "Gradients socioéconomiques du risque cardiovasculaire chez les enfants et les adolescents canadiens." Promotion de la santé et prévention des maladies chroniques au Canada 36, no. 2 (2016): 22–36. http://dx.doi.org/10.24095/hpcdp.36.2.02f.
Full textChristen, L., D. Detue, and Y. Yeuillaz. "Dépistage et prise en charge du syndrome métabolique chez des patients bénéficiant d’un neuroleptique d’action prolongée." European Psychiatry 28, S2 (2013): 49. http://dx.doi.org/10.1016/j.eurpsy.2013.09.128.
Full textSossa, Charles Jérôme, Victoire Agueh, Colette Sylvie Azandjèmè, et al. "Performances comparées du HDL-cholestérol et du ratio cholestérol total/HDL pour le dépistage du syndrome métabolique chez des adultes du Sud-Bénin (Afrique de l’Ouest)." International Journal of Biological and Chemical Sciences 10, no. 4 (2017): 1773. http://dx.doi.org/10.4314/ijbcs.v10i4.26.
Full textDenimal, D., A. Nguyen, J. Pais de Barros, et al. "CO-74: Altérations majeures du sphingophospholipidome des lipoprotéines de haute densité (HDL) de patients avec syndrome métabolique et glycémie normale." Diabetes & Metabolism 42 (March 2016): A22. http://dx.doi.org/10.1016/s1262-3636(16)30092-1.
Full textMacPherson, M., M. de Groh, L. Loukine, D. Prud'homme, and L. Dubois. "Prévalence du syndrome métabolique et de ses facteurs de risque chez les enfants et les adolescents canadiens : Enquête canadienne sur les mesures de la santé, cycle 1 (2007-2009) et cycle 2 (2009-2011)." Promotion de la santé et prévention des maladies chroniques au Canada 36, no. 2 (2016): 37–45. http://dx.doi.org/10.24095/hpcdp.36.2.03f.
Full textMaïga, S., A. Gaaya, L. Fourchaud, N. Fournier, M. Chabert, and A. D. Kalopissis. "O16 Effet d’un régime hyperlipidique sur la concentration des HDL et l’efflux du cholestérol des macrophages péritonéaux dans un modèle murin de syndrome métabolique." Diabetes & Metabolism 35 (March 2009): A5. http://dx.doi.org/10.1016/s1262-3636(09)71708-2.
Full textLEBRET, B., L. LEFAUCHEUR, and J. MOUROT. "La qualité de la viande de porc. Influence des facteurs d’élevage non génétiques sur les caractéristiques du tissu musculaire." INRAE Productions Animales 12, no. 1 (1999): 11–28. http://dx.doi.org/10.20870/productions-animales.1999.12.1.3851.
Full textHarnafi, M., I. Touiss, S. Khatib, et al. "L’extrait phénolique de l’enveloppe charnue d’amande (Prunus amygdalus L.) restaure le métabolisme lipidique chez la souris hyperlipidémique et prévient l’oxydation des lipoprotéines plasmatiques." Phytothérapie, 2019. http://dx.doi.org/10.3166/phyto-2019-0207.
Full textDissertations / Theses on the topic "Métabolisme des HDL"
Dubois, Denis. "Contribution à l'étude du métabolisme des HDL chez l'être humain: mise en évidence des fonctions spécifiques des HDL en dehors du "reverse cholesterol transport"." Doctoral thesis, Universite Libre de Bruxelles, 1993. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212863.
Full textCardouat, Guillaume. "Rôle de l’autophagie et du métabolisme nucléotidique extracellulaire dans la régulation de la voie ecto-F1-ATPase d’endocytose des HDL." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30215.
Full textThe cardioprotective effect of high-density lipoprotein cholesterol (HDL-C) is mostly attributed to their metabolic functions in reverse cholesterol transport (RCT), a process whereby excess cell cholesterol is taken up from peripheral cells and processed in HDL particles, and later delivered to the liver for further metabolism and bile excretion. ATP synthase, classically known to be located in the mitochondrial inner membrane, has been unexpectedly found expressed at the plasma membrane of hepatocytes, as a receptor for apoA-I, playing a role in HDL-cholesterol uptake. On hepatocytes, apoA-I binding to ecto-F1-ATPase stimulates extracellular ATP hydrolysis into ADP, which subsequently activates a P2Y13-mediated HDL endocytosis pathway. The strict dependence of HDL endocytosis on extracellular ADP level led us to study first, whether other plasma membrane proteins than ecto-F1-ATPase could regulate extracellular ADP level. We highlighted the presence on hepatocytes cell surface of Adenine Nucleotide Translocase (ANT), another transmembrane protein of the inner mitochondrial membrane. We showed that ecto-ANT activity could increase or reduce extracellular ADP level, depending on the extracellular ADP/ATP ratio. Furthermore, we demonstrated that pharmacological inhibition of ecto-ANT activity increased extracellular ADP level when ecto-F1-ATPase was activated by apoA-I. This increase in the bioavailability of extracellular ADP accordingly translated into an increase of HDL endocytosis in human hepatocytes. We then sought to explore the molecular mechanisms involved in targeting ecto-F1-ATPase to the plasma membrane. Indeed, F1-ATPase ectopic expression at the plasma membrane has been described on several cell types and has been related to several physiological and pathophysiological processes however, the pathway involved in its transport to the cell surface remains unknown
Espinosa, Delgado Sara. "Contribution respective des récepteurs P2Y13 et SR-BI dans le métabolisme du HDL-C et le développement de l'athérosclérose." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30053.
Full textThe atheroprotective effect of High Density Lipoproteins (HDL) is mostly attributed to their central role in Reverse Cholesterol Transport (RCT), a process whereby excess cholesterol is taken up from peripheral cells to be processed into HDL particles, then later delivered to the liver where it is preferentially secreted into the bile, either as free cholesterol or after transformation into bile acids, to be further excreted into the feces. Two independent pathways have been identified as being involved in the hepatic HDL uptake. The first one involves the ecto-F1-ATPase/P2Y13 pathway. Briefly, apoA-I (main HDL apolipoprotein) binds to the F1-ATPase expressed ectopically at the surface of the hepatocyte (ecto-F1-ATPase) and stimulates hydrolysis of extracellular ATP into ADP. The generated ADP selectively activates the purinergic receptor P2Y13 resulting in subsequent endocytosis of the HDL-holoparticle (i.e. protein and lipid moieties) through a low-affinity binding site distinct from SR-BI. Mice deficient for P2Y13 display decreased biliary lipids secretion associated to an impaired macrophage-to-feces RCT when fed a Chow Diet (CD), phenotype emphasized when fed a High Cholesterol Diet (HCD). Differently, the SR-BI pathway mediates selective HDL-cholesteryl ester uptake by the liver. Mice with liver-specific SR-BI deficiency (SR-BI-KOliver) display a hypercholesterolemia mainly due to an increase on HDL-C and develop atherosclerosis when fed a HCD. In a recent study, we showed that P2Y13 extinction in the pro-atherogenic mouse model apoE-KO resulted in an increase of atherosclerotic plaque development associated to a decreased biliary lipid secretion and macrophage-to-feces RCT. Moreover, in these mice, mRNA and protein level of hepatic SR-BI were consistently increased as compared to apoE KO mice, suggesting that a possible compensatory mechanism might exist between P2Y13 and SR-BI receptors. My thesis aimed to study the respective contribution of P2Y13 and hepatic SR-BI in HDL-C metabolism and atherosclerosis development. We crossbred P2Y13 KO with SR-BI KOliver mice and obtained double knockout mice (P2Y13 x SR-BIliver dKO). The phenotype of dKO mice was analysed with regards to HDL-C metabolism either on CD or after 20 weeks of HCD, and to atherosclerosis development on HCD. When fed a CD, dKO mice, showed an increase in plasma cholesterol compared to WT mice similar to that observed in SR-BI KOliver mice, mainly due to an increase in HDL-C. DKO, but not SR-BI KOliver mice, showed impaired biliary lipid secretion to the same extent than P2Y13 KO mice. HCD accentuated the metabolic phenotype of dKO mice, with an increase in atherosclerotic lipid lesions in dKO mice compared to SR-BI KOliver mice. The phenotypic features of P2Y13 x SR-BIliver dKO mice show that hepatic extinction of SR-BI essentially contributes to an increase of HDL-C levels. Conversely, P2Y13 extinction does not induce any change in plasma lipoprotein levels but mainly contributes to a decrease of hepato-biliary cholesterol secretions, which translates into an increased atherosclerosis development, on top of SR-BI hepatic extinction. These results support the concept that the dynamic flux of cholesterol transported by HDL from macrophage foam cells to the liver for further bile secretion is essential for athero-protection rather than steady-state HDL-C concentration. In the future of HDL-therapies, P2Y13 receptor activation constitutes an interesting therapeutic approach against atherosclerosis development
Tran, Dinh Alexy. "Rôle du SR-B1 dans les effets neuroprotecteurs des HDL à la phase aiguë de l'ischémie cérébrale." Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC310.
Full textStroke is a major concern of public health. Etiological treatment is limited to me recanalization of the thrombosed artery (intravenous or intra-arterial thrombolysis by a recombinant of tissue plasminogen activator (rt-PA) and mechanical clot extraction). New neuroprotective drugs are needed to attenuate the deleterious effects of ischemic cascade. High-density lipoproteins (HDLs) are complex molecules having multiple protective activities as reverse cholesterol transport from peripheral tissues back to the liver and the struggle against oxidation, inflammation, apoptosis and thrombosis. These pleiotropic effects confer to HDLs a protective function for vascular endothelium via the interaction with an endothelial receptor, the scavenger receptor class B type 1 (SR-B1). We showed in a murine model of cerebral ischemia that the perfusion of HDL decreased the infarct volume and the blood-brain barrier (BBB) leakage. The neuroprotective effect of HDLs was dependent of their interaction with endothelial SR-B1. The vasculoprotective effect of HDLs on the BBB and the rnle of SR-B1 were confirmed in vitro using a monocellular model of human BBB
Malaval, Camille. "Régulation de la captation hépatique des HDL : la voie F1-ATPase/P2Y13 : de la caractérisation cellulaire au modèle animal." Toulouse 3, 2008. http://thesesups.ups-tlse.fr/390/.
Full textHDL mediate the elimination of cholesterol thanks to their internalization by hepatocytes. We identified in hepatocytes a new pathway for HDL endocytosis as following: stimulation of an ectopic cell surface F1-ATPase by the HDL apolipoprotein A-I, induces the production of ADP which in turn activates the purinergic receptor P2Y13, triggering HDL endocytosis through unknown low affinity receptor(s). In one hand, we identified a major role of the small GTPase RhoA and its effector ROCK1 downstream P2Y13. This cell signalling stimulates the HDL endocytosis by remodelling actin cytoskeleton. In other hand, the study in mice showed the crucial role of P2Y13 in HDL catabolism and in the subsequent cholesterol biliary elimination. Taking together, these results demonstrate the importance of the receptor P2Y13 in cholesterol metabolism. Thus, P2Y13 appears as a new pharmacological target to control reverse cholesterol transport and prevent hypercholesterolemia
Do, Hong Quang. "Régulation du cholestérol HDL : approche génétique et nutritionnelle : intérêt de stérols d'origine marine." Nantes, 2008. https://archive.bu.univ-nantes.fr/pollux/show/show?id=bfff3c8b-f4f0-40af-8c8d-4a9ea70c3bb1.
Full textEpidemiologic and experimental studies showed that genetic polymorphisms (non modifiable factors) and lifestyle (modifiable factors) could modulate the concentrations of cholesterol, HDL-C and then the individual susceptibility to atherosclerosis, the major cause of death in the developed countries. In our studies, we evaluated 1) the potential associations between the genetic polymorphisms (APOAI, APOE, CETP, PPARA) and the concentrations of HDL-C in 857 individuals free of cardiovascular disease from the PRIME prospective cohort study and 2) the in vitro influence of sterols extracted from sponge (Ciocallypta sp. ) on the intestinal absorption of cholesterol. In the PRIME study, we found significant associations between the polymorphism CETP A373P and the concentrations of HDL-C, ApoAI, LpAI and LpAIAII. In fact, the rare allele c was less frequent in the high-HDL-C group. The association disappeared when adjusted for triglycerides. Another positive association has been found between allele 2 of apo E and ApoAI and LpAI. The other polymorphisms are absent in the cohort or have no effect on HDL-C. In the study of the influence of sponge sterols on intestinal absorption of cholesterol, we found that the 24-isopropylcholesterol reduces the absorption of cholesterol and increase the expression of ABCA-1, the carrier playing a major role in cholesterol efflux and in HDL biogenesis. The results highlight the importance of different factors in HDL level determination and in intestinal absorption of cholesterol
Verdier, Céline. "De la souris à l'homme : de l'endocytose des lipoprotéines HDL via la voie de la F1ATPase-P2Y13 aux variants géniques impactant le métabolisme du HDL et leur association au risque cardio-vasculaire." Toulouse 3, 2014. http://thesesups.ups-tlse.fr/3074/.
Full textThe atheroprotective properties of HDL particles are mostly attributed to their role in the reverse cholesterol transport (RCT), a process whereby excess cell cholesterol is taken up from the arterial wall and processed into HDL for further uptake and catabolism by the liver. We previously described a new pathway for HDL uptake by hepatocytes: apolipoprotein A-I binding to an ecto-F1-ATPase generates extracellular ADP, which specifically activates the P2Y13 receptor and finally triggers HDL holoparticle uptake (protein and lipid moieties). In the present work, hepatic expression of genes involved in cholesterol metabolism was analysed in mice, following inactivation or stimulation of P2Y13. Inactivation of P2Y13 was obtained by gene deletion (knock-out) and stimulation of P2Y13 was achieved by using cangrelor, a partial agonist of P2Y13. The importance of P2Y13 receptor in RCT was confirmed since we observed in these conditions that different hepatic genes involved in lipid metabolism were modulated. In parallel, the case-control study GENES on coronary stable patients allowed us to link a single nucleotide polymorphism (SNP rs1500588) of hepatic lipase to coronary heart disease in normotriglyceridemic patients. Furthermore, rs3732757 (synonymous mutation, I80i) located in the P2RY13 gene was found associated to a cardioprotective phenotype. Altogether these results confirm the potential physiological relevance of the P2Y13 pathway in HDL metabolism in human
Chetiveaux, Maud. "Nouvelle approche de l'étude cinétique du métabolisme des HDL par marquage endogène de l'Apo A-I par des isotopes stables chez l'homme." Nantes, 2004. http://www.theses.fr/2004NANT17VS.
Full textHDL-cholesterol is inversely correlated to the cardiovascular risk. HDL display anti-atherogenic properties in part by promoting cholesterol reverse transport from peripheral tissues to the liver. Kinetic investigations, because of their dynamic properties, are a powerful tool for studying lipoproteins metabolism. Most of kinetic studies have been investigated by using total HDL isolated by ultracentrifugation, technique known to alter HDL subclasses. The aim of this study was to assess the isolation of HDL by FPLC. This technique of gel filtration respects the integrity of lipoproteins and allows the distinction of enrichments of Apo A-I in preβ1 and αHDL from total HDL previously used. A new multi-compartmental model was created, including two distinct compartments of preβ1 and αHDL, which allow the measurement of conversion rate between these lipoproteins. To validate this model, this methodology has been applied to study kinetic disorders of Apo A-I - HDL subclasses metabolism in physiopathology state (type II diabetes) and in physiology state (post prandial study). In type II diabetes, αHDL as well as plasma Apo A-I concentration were decreased because of the increase of protein catabolism. The relative contribution of Apo A-I in preβ1 HDL was significantly increased and was related to an increase of the recycling rate of αHDL to preβ1 HDL. In a second time, the preβ1 and αHDL metabolism has been studied in post prandial state to determine the relative contribution of the intestine in the Apo A-I synthesis. Apo A-I synthesised by the intestine represented 10-20% of the total Apo A-I and was incorporated in HDL after an exchange with triglycerides rich lipoproteins. A direct contribution of the intestine
Guay, Simon-Pierre. "Étude des déterminants épigénétiques de facteurs de risque de la maladie cardiovasculaire." Thèse, Université de Sherbrooke, 2014. http://savoirs.usherbrooke.ca/handle/11143/5304.
Full textFlorens, Nans. "Modifications post-traductionnelles des lipoprotéines de haute densité (HDL) et risque cardio-vasculaire dans l’insuffisance rénale chronique." Thesis, Lyon, 2020. http://www.theses.fr/2020LYSE1034.
Full textCardiovascular complications remain the main problem in chronic kidney disease (CKD) but all the reasons of this risk are not fully understood. there is an addition of traditional risk factors and uremia-related ones. Among the latter, the generation of post-translational modifications of HDL could play a role. In this work, we highlighted an excess of carbonylation by 4-HNE onto the protein part of HDL in CKD in a rabbit model of CKD and in hemodialysis and peritoneal dialysis patients. This carbonylation by 4-HNE is responsible for ablunted anti-aggregant properties of HDL mediated by a CD36-dependant pathway. We also showed that the proteome of HDL from non diabetic hemodialysis patients is deeply modified and that there were several post-translational modifications onto the protein cargo of these HDL. The generation of carboxylate-methyl-lysine from non-enzymatic glycation processes was the main modification in our patients. The origin of such glycation could be from a favorable chemical environment but a potential load from hemodialysis fluids should be addressed