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Статті в журналах з теми "Métabolisme hépatique des lipides":
Maier. "Seltene, aber wichtige Lebererkrankungen." Praxis 91, no. 48 (November 1, 2002): 2077–85. http://dx.doi.org/10.1024/0369-8394.91.48.2077.
DOUAIRE, M., and S. LAGARRIGUE. "Gènes associés à la lipogenèse chez le poulet." INRAE Productions Animales 13, HS (December 22, 2000): 169–70. http://dx.doi.org/10.20870/productions-animales.2000.13.hs.3832.
ALLEMAN, F., A. BORDAS, J. P. CAFFIN, S. DAVAL, C. DIOT, M. DOUAIRE, J. M. FRASLIN, S. LAGARRIGUE, and B. LECLERCQ. "L’engraissement chez le poulet : aspects métaboliques et génétiques." INRAE Productions Animales 12, no. 4 (September 1, 1999): 257–64. http://dx.doi.org/10.20870/productions-animales.1999.12.4.3886.
KNUDSEN, Christelle, Cécile BONNEFONT, Laurence FORTUN-LAMOTHE, Karine RICAUD, and Xavier FERNANDEZ. "L'engraissement spontané du foie ches les palmipèdes : état des lieux et perspectives de recherche." INRA Productions Animales 31, no. 2 (October 25, 2018): 117–30. http://dx.doi.org/10.20870/productions-animales.2018.31.2.2318.
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.
Sohet, F. M., A. M. Neyrinck, C. Druart, F. C. de Backer, B. D. Pachikian, E. M. Dewulf, L. B. Bindels, P. D. Cani, and N. M. Delzenne. "P234 Impact du traitement thermique des graisses sur le métabolisme hépatique des lipides : importance de la peroxydation lipidique." Diabetes & Metabolism 36 (March 2010): A94. http://dx.doi.org/10.1016/s1262-3636(10)70382-7.
RÉMÉSY, C., Y. CHILLIARD, Y. RAYSSIGUIER, A. MAZUR, and C. DEMIGNÉ. "Le métabolisme hépatique des glucides et des lipides chez les ruminants : principales interactions durant la gestation et la lactation." Reproduction Nutrition Développement 26, no. 1B (1986): 205–26. http://dx.doi.org/10.1051/rnd:19860205.
TESSERAUD, S., and S. TEMIM. "Modifications métaboliques chez le poulet de chair en climat chaud : conséquences nutritionnelles." INRAE Productions Animales 12, no. 5 (December 1, 1999): 353–63. http://dx.doi.org/10.20870/productions-animales.1999.12.5.3894.
Deleye, Yann, Joel Haas, Sarah Hannou, Sandrine Caron-Houde, Emmanuelle Vallez, Bart Staels, and Réjane Paumelle-Lestrelin. "Rôle de CDKN2A/p16Ink4a, un gène suppresseur de tumeur, dans le contrôle du métabolisme hépatique des lipides : impact dans le développement des NAFLD." Diabetes & Metabolism 43, no. 2 (March 2017): A29. http://dx.doi.org/10.1016/s1262-3636(17)30188-x.
Lagarde, M. "Métabolisme des lipides bio-actifs." Pathologie Biologie 51, no. 5 (July 2003): 241–43. http://dx.doi.org/10.1016/s0369-8114(03)00076-2.
Дисертації з теми "Métabolisme hépatique des lipides":
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
Saez, Gladys. "Relation entre l’engraissement intramusculaire chez le canard, la lipogénèse hépatique, la sécrétion hépatique des lipides et la capacité de captage des lipides par les muscles." Pau, 2009. http://www.theses.fr/2009PAUU3007.
In order to explain the observed difference in intramuscular fatness between Muscovy and Pekin ducks, we compared the lipid metabolism in liver and muscle of these two species. In ad ibitum- fed ducks, we demonstrated that Muscovy duck had a higher ability to synthesise and store lipids in liver than Pekin duck which could partly explain its highest ability to produce fatty liver. Depending on feeding level (ad libitum fed or overfed ducks), the hepatic secretion of lipids under VLDL form was higher in Muscovy duck than in Pekin duck or equivalent for the two species. However, Pekin duck exporting VLDL with higher triglyceride content than those of Muscovy duck could limit the development of hepatic steatosis. This mechanism associated to a highest muscle uptake of circulating lipids, a highest ability for the storage of intramuscular lipids and a more active muscle lipogenesis could explain the highest intramuscular fatness of Pekin duck
Caselli, Claude. "Contribution à l'étude de l'absorption intestinale et du métabolisme cardiaque et hépatique de l'acide erucique chez le rat." Dijon, 1987. http://www.theses.fr/1987DIJOS027.
Cachefo, Pereira de Souza Ana Célia. "Lipogénèse hépatique et synthèse du cholestérol au cours des malabsorptions sévères et de l'hyperthyroïdie humaine." Lyon 1, 2001. http://www.theses.fr/2001LYO1T224.
Coum, Amandine. "Développement de méthodes de SRM à 4,7 T pour l'étude in vivo du métabolisme lipidique chez la souris." Thesis, Rennes 1, 2015. http://www.theses.fr/2015REN1B025/document.
In recent years, there has been an unprecedented increase in the morbidity and mortality associated with diseases such as the steatosis, linked to obesity. In this context, pre-clinical and clinical studies are of interest in the search for new biomarkers allowing the diagnosis of steatosis. Currently, steatosis is diagnosed and graded by histological analyzes from a liver biopsy. On the other hand, it is advantageous to use non-invasive diagnostic modalities, especially in longitudinal studies. In this context, magnetic resonance spectroscopy (MRS), as a non-invasive and non-ionizing approach, is an attractive alternative method for the diagnosis of steatosis by measuring the hepatic fat fraction. Moreover, from the MRS spectrum acquired in the liver, it is possible to quantify the fatty acids (FA) composition of the hepatic lipids, which could be a potential biomarker for the follow-up of steatosis. The work of this thesis has been performed in vitro and in vivo, in the context of pre-clinical (4.7 T) and clinical (3.0 T) studies. An investigation of the optimal MRS acquisition protocol for the quantification of FA was carried out, with particular attention to the role of the water signal suppression module. Different quantification algorithms of the lipid composition were studied and validation of these algorithms was carried out in vitro and in vivo. Finally, still with the objective of determining new biomarkers of steatosis, a method (LOREEDE: LOngitudinal RElaxation time Evaluation from Dynamic Equilibrium) for the measurement in vivo of the T1 of the water resonance and the major lipid resonance, by MRS, was developped and validated in a preliminary study
Delprat, Leslie. "Effets des régimes alimentaires riches en lipides et en fructose sur la performance et le métabolisme de canards Mulard." Master's thesis, Université Laval, 2021. http://hdl.handle.net/20.500.11794/68773.
Different types of dietary carbohydrate and lipids are known to alter feed intake and adiposity in rodents. Long-term feeding of high-fat, high-fructose diets has been shown to alter feed intake and cause fatty liver in mammals. Such diets in combination with the addition of high fructose corn syrup (HFCS) in the drinking water may result in a similar phenotype in ducks destined for the production of foie gras. The aims of these studies were therefore firstly to assess the short-term effects of a diet rich in fat and fructose in mulard ducks and secondly to assess the long-term impact of this type of diet combined with sugar water. Despite its higher energy content, feed intake was not reduced by the FF diet, suggesting a potential alteration of satiety signals, which may impact body liver and weight under longer-term interventions in ducks destined to produce foie gras. However, HFCS in the drinking water reduced voluntary feed intake, whereas overall, FF and C had similar feed intake. In contrast to rodent and human studies, FF diets failed to induce hyperphagia and liver steatosis. In the absence of overfeeding, the long-term feeding of high-fructose, highfat diets, does not promote fatty liver.
Deleye, Yann. "Rôle du gène suppresseur de tumeur p16INK4a dans le métabolisme hépatique des lipides au cours du jeûne." Thesis, Lille 2, 2018. http://www.theses.fr/2018LIL2S002.
P16INK4a is a tumor suppressor protein that is a well described cell cycle regulator. Recently, genome-wide association studies (GWAS) associated the CDKN2A locus, from which p16INK4A is encoded, with increased risk for development of type 2 diabetes. A pathophysiological link between p16INK4a and hepatic glucose homeostasis has been unraveled recently, through the control of gluconeogenesis. Patients with T2D also present with disturbances in fat metabolism, associated with an increased prevalence to Non Alcoholic Fatty liver diseases (NAFLD). In this context, we investigated the role of p16INK4a in hepatic lipid metabolism in vitro using primary hepatocytes, the murin AML12 and human IHH hepatocyte cell line transfected respectively with siRNA-CDKN2A and siRNA-p16 and in vivo using p16+/+ and p16-/- mice.Transcriptomic analyses of p16+/+ and p16-/- primary hepatocytes using microarrays revealed that metabolic and PPARα signaling pathways were among the most modulated in p16 absence. Moreover, in primary hepatocytes and in hepatocyte cell lines, p16 deficiency modulates a subset of PPARα target genes associated to fatty acids oxidation (FAO). These effects were associated with an increased response to GW647, a PPAR945; agonist, and reversed by siRNA targeting PPAR45;. Investigating known PPAR945; activators and transcriptional co-activators in vitro, we found that upregulation of FAO genes expression was linked to SIRT1. AMPK is a known activator of FAO and has been shown to induce SIRT1 activation through increase of NAD/NADH ratio. Interestingly, downregulation of p16 expression in vitro led to increased AMPK phosphorylation and activation.In vitro, p16-/- primary hepatocytes demonstrated enhanced fatty acid oxidation of oleate compared to p16+/+. During fasting, enhanced FAO leads to a shift of acetyl-coA utilization from the TCA cycle to ketogenesis. Interestingly, p16-/- mice showed a tendency to produce more ketone bodies than their control littermate after sodium octanoate injection. These findings describe a new function for p16INK4a in hepatic lipid metabolism through activation of AMPK-SIRT1-PPARα pathway
Allard, Julien. "Mise en évidence de l'implication de différents mécanismes dans la survenue de la stéatose hépatique d'origine médicamenteuse en absence de dysfonction mitochondriale sévère." Thesis, Rennes 1, 2020. http://www.theses.fr/2020REN1B010.
Steatosis is a liver lesion reported with numerous pharmaceuticals. Prior studies showed that severe impairment of mitochondrial fatty acid oxidation (mtFAO) constantly leads to lipid accretion in liver. However, much less is known about the mechanism(s) of drug-induced steatosis in the absence of severe mitochondrial dysfunction, although previous studies suggested the involvement of mild-to-moderate inhibition of mtFAO, increased de novo lipogenesis (DNL) and impairment of very low-density lipoprotein (VLDL) secretion. The objective of our study, mainly carried out in human hepatoma HepaRG cells, was to investigate these 3 mechanisms with 12 drugs able to induce steatosis in human: amiodarone (AMIO, used as positive control), allopurinol (ALLO), D-penicillamine (DPEN), 5-fluorouracil (5FU), indinavir (INDI), indomethacin (INDO), methimazole (METHI), methotrexate (METHO), nifedipine (NIF), rifampicin (RIF), sulindac (SUL) and troglitazone (TRO). Hepatic cells were exposed to drugs for 4 days with concentrations inducing loss of cellular ATP always below 30% of the controls and not exceeding 100xCmax. Among the 12 drugs, AMIO, ALLO, 5FU, INDI, INDO, METHO, RIF, SUL and TRO induced steatosis in HepaRG cells. AMIO, INDO and RIF decreased mtFAO. AMIO, INDO and SUL enhanced DNL. ALLO, 5FU, INDI, INDO, SUL, RIF and TRO impaired VLDL secretion. These 7 drugs reduced the mRNA levels of genes playing a major role in VLDL assembly and also induced endoplasmic reticulum (ER) stress. Thus, in the absence of severe mitochondrial dysfunction, drug-induced steatosis can be triggered by different mechanisms, although impairment of VLDL secretion seems more frequently involved, possibly as a consequence of ER stress
Gjorgjieva, Monika. "Identification des mécanismes moléculaires impliqués dans le développement des pathologies hépatiques et rénales dans des modèles murins de glycogénose de type 1a." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1007/document.
Glycogen storage disease type I (GSDI) is a rare genetic disease, due to a deficiency in glucose-6 phosphatase (G6Pase), a key enzyme in the endogenous glucose production. Besides severe hypoglycemia, the loss of G6Pase leads to the accumulation of glycogen and lipids in the liver and kidneys. On the long term, most patients develop hepatic tumors and chronic kidney disease (CKD).The goal of this thesis was to characterize the molecular mechanisms involved in hepatic carcinogenesis and CKD, thanks to viable and unique mouse models with specific deletion of G6Pase in the liver or kidneys, which exhibit all hallmarks of hepatic and renal pathologies, respectively.On a hepatic level, our study allowed us to highlight a « Warburg-like » metabolic reprogramming, very similar to what is observed in cancer cells, associated with a loss of cellular defenses and tumor suppressors. Furthermore, we showed that formation of hepatocellular adenoma, which transform later in carcinoma, occurs in the absence of liver fibrosis, due to the fact that pro-fibrotic pathways are not activated. In the kidneys, the study of CKD highlighted the development of renal cysts in mice with GSDI, as well as in the patients presenting an advanced stage of CKD. Finally, the last study on the activation of the oxidation of lipids, by treating the mice with fenofibrate, allowed us to suggest a deleterious role of lipid accumulation in the development of the hepatic and renal pathologies
Leplaix-Charlat, Laurence. "Effets des acides gras et du cholestérol alimentaires sur le métabolisme des lipides et des lipoprotéines aux niveaux plasmatique et hépatique chez le veau préruminant : conséquences sur la composition lipidique des tissus." Aix-Marseille 3, 1995. http://www.theses.fr/1995AIX30085.
Книги з теми "Métabolisme hépatique des lipides":
Nicolaou, Anna, and George Kokotos. Bioactive lipids. Bridgwater: The Oily Press, 2004.
Marinetti, Guido V. Disorders of lipid metabolism. New York: Plenum Press, 1990.
Vance, Dennis E. Biochemistry of lipids, lipoproteins and membranes. 5th ed. Amsterdam: Elsevier, 2008.
Meyerhof, Wolfgang. Sensory and Metabolic Control of Energy Balance. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.
1944-, Grimaldi André, ed. Dyslipidémie et athérogenèse. Paris: Elsevier, 2004.
Hilderson, Herwig J. Intracellular Transfer of Lipid Molecules (Subcellular Biochemistry). Springer, 1990.
Foundation, Novartis. Fatty Acid and Lipotoxicity in Obesity and Diabetes (Novartis Foundation Symposia). Wiley, 2008.
F, Keane William, ed. Lipids and renal disease. New York: Churchill Livingstone, 1991.
1932-, Podmore J., Padley F. B. 1936-, and Society of Chemical Industry (Great Britain), eds. The Role of fats in human nutrition. Weinheim, Federal Republic of Germany: VCH, 1985.
(Editor), D. E. Vance, and J. E. Vance (Editor), eds. Biochemistry of Lipids, Lipoproteins and Membranes, Fifth Edition. 5th ed. Elsevier Science, 2008.