Добірка наукової літератури з теми "Métabolisme des dérivés du cholestérol"
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Статті в журналах з теми "Métabolisme des dérivés du cholestérol":
Brendel, C., JC Fruchart, J. Auwerx, and K. Schoonjans. "Régulation transcriptionnelle du métabolisme du cholestérol." médecine/sciences 15, no. 1 (1999): 56. http://dx.doi.org/10.4267/10608/1196.
Combettes-Souverain, M., F. Milliat, C. Sérougne, J. Férézou, and C. Lutton. "SR-BI et métabolisme du cholestérol." médecine/sciences 15, no. 11 (1999): 1252. http://dx.doi.org/10.4267/10608/1252.
Langhi, Cédric, та Bertrand Cariou. "Métabolisme du cholestérol et function β-cellulaire". médecine/sciences 26, № 4 (квітень 2010): 385–90. http://dx.doi.org/10.1051/medsci/2010264385.
Dereure, O. "Hypotrichose simplex : le métabolisme du cholestérol semble impliqué." Annales de Dermatologie et de Vénéréologie 146, no. 3 (March 2019): 258–59. http://dx.doi.org/10.1016/j.annder.2018.12.003.
Morozova, Svetlana, Isabelle Suc-Royer, and Johan Auwerx. "Modulateurs du métabolisme du cholestérol et avenir du traitement de l’athérosclérose." médecine/sciences 20, no. 6-7 (June 2004): 685–90. http://dx.doi.org/10.1051/medsci/2004206-7685.
Blanchard, C., F. Moreau, F. Borel, A. Ayer, V. Ferchaud, M. Krempf, B. Cariou, and C. Le May. "Effet des chirurgies bariatriques sur le métabolisme du cholestérol chez la souris." Nutrition Clinique et Métabolisme 30, no. 3 (September 2016): 278. http://dx.doi.org/10.1016/j.nupar.2016.09.131.
Feillet, F., C. Feillet, H. J. Parra, J. C. Fruchart, and M. Vidailhet. "Étude du métabolisme du cholestérol dans l'anorexie mentale, effet de la renutrition." Archives de Pédiatrie 3, no. 11 (November 1996): 1167. http://dx.doi.org/10.1016/s0929-693x(96)89563-7.
Caboche, Jocelyne, Radhia Kacher, and Sandrine Betuing. "Rétablir le métabolisme cérébral du cholestérol est neuro-protecteur dans la maladie de Huntington." médecine/sciences 36, no. 1 (January 2020): 12–15. http://dx.doi.org/10.1051/medsci/2019253.
BAUCHART, D., D. DURAND, D. GRUFFAT-MOUTY, C. PIOT, B. GRAULET, Y. CHILLIARD, and J. F. HOCQUETTE. "Transport sanguin et métabolisme tissulaire des lipides chez le veau de boucherie. Effets du remplacement du suif par de l’huile de coprah dans l’aliment d’allaitement." INRAE Productions Animales 12, no. 4 (September 1, 1999): 273–85. http://dx.doi.org/10.20870/productions-animales.1999.12.4.3888.
Roussel, J. P., A. Burger, and C. Hetru. "Etude de l'activité inhibitrice de dérivés alléniques du cholestérol sur la biosynthèse de l'ecdysone." Archives Internationales de Physiologie et de Biochimie 98, no. 2 (January 1990): 253–59. http://dx.doi.org/10.3109/13813459009113985.
Дисертації з теми "Métabolisme des dérivés du cholestérol":
Leclerc, Thierry. "Anomalies du métabolisme lipoprotéique des transplantés cardiaques : mise en évidence d'un déficit du transfert des esters de cholestérol." Paris 5, 1992. http://www.theses.fr/1992PA05P008.
Descat, Amandine. "Développements de méthodes d'analyse des plastifiants de type phtalates et des acides biliaires dans des matrices biologiques : applications dans différents contextes physiopathologiques." Electronic Thesis or Diss., Université de Lille (2022-....), 2023. http://www.theses.fr/2023ULILS054.
This thesis has two main focuses:1/ Plasticizers, including phthalates, have been identified as category 1b carcinogenic, mutagenic and reprotoxic (CMR) and as endocrine disruptors. Di-2-ethylhexyl phthalate (DEHP) is one of the most common plasticizers and is generally associated with polyvinyl chloride (PVC) in medical devices. As DEHP is not covalently bound to PVC, it can easily migrate into lipophilic matrices and then reach the bloodstream. It is metabolized by the liver into mono-2-ethylhexyl phthalate (MEHP), which is just as toxic. In recent years, alternative plasticizers to DEHP have been developed, notably di-2-ethylhexyl terephthalate (DEHT), which is metabolized in vivo to mono-2-ethylhexyl terephthalate (MEHT).The first part of this thesis involved developing methods for measuring plasticizers and their metabolites in various biological matrices, such as plasma. Two LC-MS/MS methods were developed for the determination of DEHP and MEHP as well as DEHT metabolites. As the ionization in mass spectrometry of DEHT is very low, a LC-UV method was developed to quantify this terephthalate. These methods have made it possible to estimate the release of DEHP and DEHT from blood bags and to measure their primary metabolites in blood products.2/ Bile acids (BA) are a large family of steroids made up of numerous species. They are synthesized in the liver and intestine and represent the main route of cholesterol catabolism. 7a-hydroxy-4-cholesten-3-one (C4) is the precursor of BA. BA play an essential role in lipid absorption but also in cell signaling, as they are ligands for the nuclear receptor 'Farnesoid X receptor' (FXR) and/or the G protein-coupled membrane receptor, TGR5. These receptors, and hence their ligands, are involved in glucose homeostasis, lipid homeostasis and energy expenditure. Any modulation of the BA profile can therefore lead to changes in metabolic homeostasis. The second part of this thesis involved developing two LC-MS/MS assay methods for 31 BA species and C4 in different biological matrices, including plasma. A specific method for the determination of recently described BA derived from LCA in caecal contents is currently being optimized. These methods have made it possible to analyze variations in the BA profile in various cardiometabolic disease contexts (obesity, insulin resistance, type 2 diabetes, NAFLD).In conclusion, the analytical methods developed for quantifying plasticizers and BA have been validated and applied in preclinical and clinical studies. Interestingly, data from the literature and preliminary transient transfection assays have shown that phthalates and their metabolites modulate the activity of the peroxisome proliferator-activated receptor alpha (PPARa), a key regulator of metabolic homeostasis and expression of CYP7A1 (a major enzyme in hepatic BA synthesis). The analytical tools developed in this thesis open up original perspectives for studying the effects of phthalates on metabolic homeostasis via the regulation of BA metabolism. All of this work has made it possible to link analytical developments and applications in the field of biology and health
Paillasse, Michaël. "Métabolisme du cholestérol et cancer." Toulouse 3, 2009. http://thesesups.ups-tlse.fr/766/.
This manuscript describes the study of deregulations of the metabolism of cholesterol occuring in cancerous processes. This includes first the importance of esters of cholesterol to the proliferation of cancer cells. Evidence is given the effects of cancer drugs such as Tamoxifen are concurrent to inhibition of the Cholesterol Epoxyde Hydrolase and potentially to the accumulation of 5, 6a-epoxycholestanol in the tissues. We postulated the existence of a new metabolism around this epoxyde, consisting in its aminolysis by biogenic amines and have shown that such products, the Dendrogenines, promote differenciation in different cell lines resulting in either anticancerous (Dendrogenine A) or neuroprotective (Dendrogénine B) activities. Finally we could explain the difference of reactivity toward nucleophiles between 5,6a- and 5,6beta- epoxycholestanol and could vouch for the stereospecificity of aminolysis reaction
Chériti, Abdelkrim. "Hémisynthèses de saponosides dérivés du cholestérol et des acides oléanolique et ursolique." Aix-Marseille 3, 1992. http://www.theses.fr/1992AIX30053.
Lauressergues, Emilie. "Antipsychotiques et métabolisme hépatique des lipides et du cholestérol." Lille 2, 2010. http://www.theses.fr/2010LIL2S020.
Schizophrenia is a psychiatric disorder that heavily impacts the mental functions and social relations of the patients concerned. More than 1 % of the world population suffers from this disease that is characterized by different kinds of symptoms which are commonly subclassified as either positive (hallucinations, illusions) or negative (loss of affect and motivation, social withdrawal). These symptoms can be controlled by treatment with antipsychotic drugs (APDs) which act primarily through the modulation of dopamine and serotonin receptors. Unfortunately, some of these drugs induce important metabolic side effects such as weight gain (as much as 10 kg the first year with clozapine for example), dyslipemia, alterations of glucose homeostasis and development of diabetes. The consequences of these disturbances are treatment disruption and an increase of cardiovascular risks which contributes to a death rate twice as high for schizophrenic patients versus the general population, associated with a reduction in the average life expectancy by 10 years. The mechanisms underlying the side effects by APDs are not completely understood. At the level of the central nervous system (CNS), actions on serotoninergic, dopaminergic or histaminergic receptors are believed to be implicated in metabolic side effects (particularly by modifying appetite or energy homeostasis). In the periphery, certain APDs perturb essential physiological functions such as insulin secretion by pancreatic b cells, glucose transport into skeletal muscle and lipogenesis at the adipose tissue level, as well as physiological parameters like the sensitivity of various tissues to insulin. Althoug the liver is an essential organ for maintaining the nutrients homeostasis, few studies show an interest for the direct impact of these molecules on this tissue. The main goal of this thesis is to characterise the impact of APDs on hepatic lipid and cholesterol metabolism using various markers from appropriate hepatocyte cellular models, such as de novo synthesis of lipids and cholesterol, the quantification of the mature transcription factors SREBP-1 and -2 (sterol regulatory element binding protein) as well as the evaluation of the expression of several genes of interest. In the first part, we selected hepatocyte cellular models (cells isolated from rat liver and the human IHH cell line) and showed their relevance for the study of the “potential adverse effects” of different compounds on lipid and cholesterol metabolism. For this, the physiological and sensitive character of these cultures was shown through their response to nutritional (or hormonal) changes and to pharmacological treatments. In the second part, we highlighted three profiles of APD molecules :-molecules strongly inducting de novo lipogenesis and cholesterogenesis (clozapine, olanzapine, risperidone and NDMC), -molecules with more moderate effects (haloperidol and paliperidone), -molecules with little or no effect(s) (aripiprazole, quetiapine, bifeprunox and chlorpromazine). Induction of de novo lipogenesis and cholesterogenesis by certain APDs is associated to the stimulation of the SREBP pathway (transcription factors and SREBP target genes) and correlate relatively well with the metabolic disturbances of schizophrenia patients under APD treatment. We therefore suggest that certain unfavourable effects of these APD molecules are due to a direct action on the liver. Furthermore we stated that those APDs that present the most unfavourable profiles in our in vitro models, activate the PERK pathway (protein kinase RNA-like ER kinase) of the UPR (unfolding protein response), illustrating the presence of endoplasmic reticulum (ER) stress. However, the ER stress is known to activate the SREBP pathways and to cause, in chronic, diseases such as steatosis, dyslipidemia and diabetes. This discovery opens new perspectives regarding the research for the action mechanisms of these molecules. More precisely, in our human hepatocyte model we show that the treatment with thapsigargine (inductive of ER stress by calcium depletion) stimulates the SREBP pathways. Whereas no detectable modification of the cytosolic calcium concentrations was observed following APD treatment, the use of calcium chelating agents reverses the effects of clozapine on the SREBP-1 and -2 pathways. We therefore presume that clozapine, by disturbing calcium homeostasis, generates ER stress which would activate the SREBPs pathways and lipogenesis and cholesterogenesis in consequence. To corroborate these findings, two experimental studies in rat and mouse were conducted that support our in vitro results. In the rat, a study employing acute drug administration confirms that clozapine, olanzapine and risperidone, at an early stage (1h, 3h), cause transcriptional deregulations of hepatic lipogenic, cholesterogenic and UPR genes. In the mouse, a study with chronic administration of risperidone indicates significant inductions of weight gain in relation to the activation of the SREBP-1c pathway and of FAS (fatty acid synthase). Altogether these data suggest that independent of their specific effects at the CNS level, APDs can modulate hepatic lipid metabolism. In conclusion, rat primary hepatocyte cultures and IHH cells are models of interest for the detection of potential unfavourable effects of molecules on hepatic lipid and cholesterol metabolism. Moreover, the SREBP pathways (proteins and target genes associated) are appropriate indicators of cellular metabolic disturbances and thus can be considered as pertinent markers of the respective processes. These models could therefore be integrated in the research process and in the selection of new chemical compounds destined to become APDs. With respect to the clinic, our results support the strategy to associate hypolipemic or hypocholesterolemic (statines) treatments to patients treated with clozapine, olanzapine and risperidone
Harmancey, Romain. "Caractérisation des propriétés de deux protéines associes à l'obésité : une nouvelle apolipoprotéine et l'adrénomedulline." Toulouse 3, 2006. http://www.theses.fr/2006TOU30195.
White adipose tissue is known to secrete a number of proteins named adipokines, whose dysregulations are suspected to play major roles in the development of several diseases commonly associated to obesity. Moreover, excess fat deposition in cardiomyocytes is believed to contribute to heart diseases through lipotoxicity and lipoapoptosis processes. The present data aimed to define the physiological functions of two secreted proteins up-regulated in obese patients. We demonstrate that one of these proteins, whose cardiac expression is increased with obesity, is a novel apolipoprotein (named Apo O) originally linked to a chondroitine sulfate chain, found mainly associated to HDL particles. Recombinant Apo O strongly stimulates cholesterol efflux from cells. Thus, Apo O could contribute to heart protection by preventing lipid accumulation in cardiomyocytes. The second protein studied, adrenomedullin (AM), is a multifunctional regulatory factor known for its natriuretic and vasodilating properties. Our results demonstrate that AM is a new adipokine that acts locally to modulate fat mass metabolism and development. First, we reported that AM inhibits isoproterenol-induced lipolysis through the nitric oxide-dependent oxidation of the beta-agonist. This reaction generates aminochromes, which is the product of catecholamines' oxidation and known to be cardiotoxic. Second, the molecular modulation of AM synthesis in a murine preadipocyte cell line showed that the peptide has anti-adipogenic properties. This last finding could be related to insulin proadipogenic effects since we found AM to be down-regulated by insulin at the transcriptional level through insulin-responsive elements
Viallard, Viviane. "Aspects du métabolisme énergétique et du métabolisme du cholestérol dans la cellule néoplasique du côlon." Toulouse 3, 1991. http://www.theses.fr/1991TOU30247.
Blanchard-Louis, Claire. "Effets de la chirurgie bariatrique sur le métabolisme du cholestérol." Thesis, Nantes, 2016. http://www.theses.fr/2016NANT1020/document.
Obesity is a major public health issue, with increasing prevalence. Metabolic complications such as type 2 diabetes, hypertension and dyslipidemia are frequently associated with morbid obesity. Bariatric surgery represents the therapeutic alternative of choice for these patients. Clinical studies show thatplasma cholesterol is clearly improved after surgery. Interestingly, the magnitude of reduction depends on the surgical techniques used suggesting that cellular and molecular mechanisms involved are different. Using mouse models,we demonstrated that Roux en Y Gastric Bypass (RYGB) strongly lowers plasma cholesterol compared to sleeve gastrectomy. RYGB increases fecal cholesterol excretion via the stimulation of trans intestinal cholesterol excretion (TICE) and a reduction of intestinal cholesterol absorption. In this context, and expanding in the management of hypercholesterolemia, TICE seems to be an interesting therapeutic target.In parallel with this work, we assessed, in collaboration with members of INSERM unit 913 (Dr Neunlist), the short-term effect of sleeve gastrectomy on intestinal barrier. We show that sleeve gastrectomy induces significant modifications of intestinal para and transcellular permeability by altering the expression of proteins involved in tight junctions. These changes favor plasma LPS translocation promoting a low grade pro-inflammatory state in adipose tissue. These effects of sleeve gastrectomy on intestinal permeability remain to be assessed after a longer post-surgical period
Kreit, Joseph. "Catabolisme microbien des stérols : caractérisation de la cholestérol oxydase, de la cholestérol ester hydrolase et d'une alcool secondaire deshydrogénase chez Rhodococcus Sp. CIP 105 335." Vandoeuvre-les-Nancy, INPL, 1999. http://www.theses.fr/1999INPL044N.
Jenty, Marion. "Rôle de la signalisation LRP1/Wnt5a dans le métabolisme du cholestérol." Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ025/document.
Protects against intracellular cholesterol accumulation and we identified the secreted protein Wnt5a as a partner of this inhibitory effect of LRP1. The aim of this thesis is to determine the molecular mechanisms by which the LRP1/Wnt5a signaling pathway prevents cholesterol accumulation in cells and to study the antiatherogenic potential of Wnt5a. We first showed in vitro and in vivo that Wnt5a decreases cellular cholesterol content by stimulating its efflux through the induction of cholesterol transporters expression and by down-regulating the expression of HMGCoA-reductase. Then we used mice deleted for Wnt5a specifically in smooth muscle cells, which present more atherosclerotic lesions than control mice after a high cholesterol diet. This confirms that Wnt5a protects against atherosclerosis and could be an interesting therapeutic target in the treatment of the disease
Книги з теми "Métabolisme des dérivés du cholestérol":
Robert, Bittman, ed. Cholesterol: Its functions and metabolism in biology and medicine. New York: Plenum Press, 1997.
Robert, Bittman, ed. Subcellular biochemistry. New York: Plenum Press, 1997.
Riadh, Jazrawi, Northfield Tim, and Zentler-Munro Patrick, eds. Bile acids in health and disease: Update on cholesterol gallstones and bile acid diarrhoea. Dordrecht: Kluwer Academic, 1988.
Myant, N. B. Cholesterol metabolism, LDL, and the LDL receptor. San Diego: Academic Press, 1990.
Bittman, Robert. Cholesterol (Subcellular Biochemistry). Springer, 1997.
Dupont, Jacqueline. Cholesterol Systems in Insects and Animals. Taylor & Francis Group, 2018.
Dupont, Jacqueline. Cholesterol Systems in Insects and Animals. Taylor & Francis Group, 2018.
Dupont, Jacqueline. Cholesterol Systems in Insects and Animals. Taylor & Francis Group, 2018.
Dupont, Jacqueline. Cholesterol Systems in Insects and Animals. Taylor & Francis Group, 2018.
Dupont, Jacqueline. Cholesterol Systems in Insects and Animals. Taylor & Francis Group, 2017.