Auswahl der wissenschaftlichen Literatur zum Thema „Régime pauvre en graisses“
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Zeitschriftenartikel zum Thema "Régime pauvre en graisses"
Javalet, Manon. „Régimes pauvres en graisse chez l’enfant“. Perfectionnement en Pédiatrie 5, Nr. 3 (September 2022): 242. http://dx.doi.org/10.1016/j.perped.2022.07.025.
Der volle Inhalt der QuelleHarouadi, Farid, und Salim Boulahrouz. „Etude et Analyse de la Combustion Turbulente dans un Moteur Alimenté en Gaz Naturel“. Journal of Renewable Energies 3, Nr. 2 (31.12.2000): 93–103. http://dx.doi.org/10.54966/jreen.v3i2.914.
Der volle Inhalt der QuelleJouët, Pauline, und Nathalie Morel. „Régime pauvre en FODMAPS, ce que doivent savoir les nutritionnistes“. Nutrition Clinique et Métabolisme 33, Nr. 3 (September 2019): 199–204. http://dx.doi.org/10.1016/j.nupar.2019.05.005.
Der volle Inhalt der QuelleDescamps, V., C. Fite, C. Cannistra, K. Ezzedine, G. Chaby, H. Maillard und G. Gabison. „Hidradénite suppurée : intérêt d’un régime pauvre en levure de bière“. Annales de Dermatologie et de Vénéréologie 140, Nr. 12 (Dezember 2013): S557. http://dx.doi.org/10.1016/j.annder.2013.09.440.
Der volle Inhalt der QuelleDisdier, P., J. R. Harle, Ph Vague, G. Habib, G. Bolla, D. Verrot und P. J. Weiller. „Un nouveau traitement pour l'amylose portugaise: le régime pauvre en protéines“. La Revue de Médecine Interne 14, Nr. 6 (Juni 1993): 511. http://dx.doi.org/10.1016/s0248-8663(05)80445-x.
Der volle Inhalt der QuelleGauze-Gnagne, Chantal, Absalome Monde, Massara Camara-Cisse, Youzan Ferdinand Djohan, Gervais Koffi, Audrey Pellicer, Fabrice Raynaud et al. „Etude de l’effet d’un régime riche en huile de palme sur l’expression génétique des facteurs myogéniques“. International Journal of Biological and Chemical Sciences 15, Nr. 2 (22.06.2021): 461–76. http://dx.doi.org/10.4314/ijbcs.v15i2.8.
Der volle Inhalt der QuelleCharlot, Anouk, Ombline Conrad und Joffrey Zoll. „Le régime cétogène : une stratégie alimentaire efficace en complément des traitements contre le cancer ?“ Biologie Aujourd’hui 214, Nr. 3-4 (2020): 115–23. http://dx.doi.org/10.1051/jbio/2020014.
Der volle Inhalt der QuelleKurtz, Maxime, und Ghita Benchekroun. „Défi thérapeutique du diabète sucré chez le chat : les clés pour obtenir une rémission du diabète“. Le Nouveau Praticien Vétérinaire canine & féline 20, Nr. 86 (2023): 26–34. http://dx.doi.org/10.1051/npvcafe/2024017.
Der volle Inhalt der QuelleBeaupère, Pascale. „Efficacité d’un régime pauvre en sel dans le traitement de l’insuffisance cardiaque : mythe ou réalité ?“ Revue Médicale Suisse 15, Nr. 635 (2019): 228. http://dx.doi.org/10.53738/revmed.2019.15.635.0228.
Der volle Inhalt der QuelleCharlot, Anouk, Alix Lernould, Irène Plus und Joffrey Zoll. „Intérêt du régime cétogène dans la prise en charge de la maladie d’Alzheimer“. Biologie Aujourd’hui 217, Nr. 3-4 (2023): 253–63. http://dx.doi.org/10.1051/jbio/2023031.
Der volle Inhalt der QuelleDissertationen zum Thema "Régime pauvre en graisses"
Bossowski, Józef Piotr. „Induction d’une réponse immunitaire anti-tumorale par un régime pauvre en protéines“. Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4105.
Der volle Inhalt der QuelleSeveral arguments from the literature suggested the importance of diets in cancer development and in the efficacy of anti-cancer therapies. Calorie restriction (CR) suppresses cancer growth in various animal models and sensitizes tumor cells to targeted therapies (Meynet & Ricci, 2014). Thus, non-pharmacologic approaches such as CR have a growing interest in the clinic. Considering the nutrient addiction of cancer cells, we wondered which specific macronutrients contribute the most to anti-cancer effects. Therefore, we tested the reduction in specific macronutrient without decrease in general calorie intake on tumor development. We used two diets: reduced in carbohydrates (Low CHO, -25% carbohydrates) and diet reduced in protein (Low PROT, -25% proteins) on the Eµ-Myc transgenic mouse model of B-cell lymphoma. Syngeneic C57BL/6 mice were intravenously injected with primary Eμ-Myc cells. We observed that low PROT-diet, in spite of equal calorie intake among the groups, resulted in increase of the overall survival of Eµ-Myc-bearing C57BL/6 mice. Very importantly, we established that this pro-survival effect is immune system-dependent as both depletion of CD8+ T cells and use of immunodeficient NSG (NOD-SCID il2rγ) mouse model prevented the beneficial effect of the low PROT-diet on the tumor development. We reproduced and further extended our observations using subcutaneous injection of CT26 colorectal cancer cells in syngeneic immunocompetent BALB/c mice and B16 melanoma in C57BL/6 mice. As tumor cells are highly dependent on nutrients, we speculated that low PROT diet could induce ER stress in tumor cells. Indeed, we observed increase in proteins implicated in ER stress signaling – CHOP and sXBP1. Therefore, we treated low PROT-diet fed mice with two ER stress inhibitors, the general inhibitor TUDCA or MKC4485, which targets IRE1 RNAse activity. In both cases, inhibitors significantly prevented the effect of the Low PROT-diet on tumor development and on intratumoral number of CD8+ T cells. To eliminate any side effects of chemical inhibitors, we invalidated IRE1 in CT26 cells and obtained similar results, demonstrating that IRE1 signaling in tumor cells is a central event in the low PROT-diet induced anti-cancer immune response. In addition, we have uncovered RIG-I activation as a downstream event of IRE1 activation and by bioinformatic analysis correlated high-IRE1 signature with high immune infiltration and enhanced immunogenicity of cancer in patients bearing melanoma, glioblastoma and colorectal cancer. Hence, we have shown that the immune system response elicited under a Low PROT diet is a consequence of increased IRE1 activation in cancer cells
Bossowski, Józef Piotr. „Induction d’une réponse immunitaire anti-tumorale par un régime pauvre en protéines“. Thesis, Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4105/document.
Der volle Inhalt der QuelleSeveral arguments from the literature suggested the importance of diets in cancer development and in the efficacy of anti-cancer therapies. Calorie restriction (CR) suppresses cancer growth in various animal models and sensitizes tumor cells to targeted therapies (Meynet & Ricci, 2014). Thus, non-pharmacologic approaches such as CR have a growing interest in the clinic. Considering the nutrient addiction of cancer cells, we wondered which specific macronutrients contribute the most to anti-cancer effects. Therefore, we tested the reduction in specific macronutrient without decrease in general calorie intake on tumor development. We used two diets: reduced in carbohydrates (Low CHO, -25% carbohydrates) and diet reduced in protein (Low PROT, -25% proteins) on the Eµ-Myc transgenic mouse model of B-cell lymphoma. Syngeneic C57BL/6 mice were intravenously injected with primary Eμ-Myc cells. We observed that low PROT-diet, in spite of equal calorie intake among the groups, resulted in increase of the overall survival of Eµ-Myc-bearing C57BL/6 mice. Very importantly, we established that this pro-survival effect is immune system-dependent as both depletion of CD8+ T cells and use of immunodeficient NSG (NOD-SCID il2rγ) mouse model prevented the beneficial effect of the low PROT-diet on the tumor development. We reproduced and further extended our observations using subcutaneous injection of CT26 colorectal cancer cells in syngeneic immunocompetent BALB/c mice and B16 melanoma in C57BL/6 mice. As tumor cells are highly dependent on nutrients, we speculated that low PROT diet could induce ER stress in tumor cells. Indeed, we observed increase in proteins implicated in ER stress signaling – CHOP and sXBP1. Therefore, we treated low PROT-diet fed mice with two ER stress inhibitors, the general inhibitor TUDCA or MKC4485, which targets IRE1 RNAse activity. In both cases, inhibitors significantly prevented the effect of the Low PROT-diet on tumor development and on intratumoral number of CD8+ T cells. To eliminate any side effects of chemical inhibitors, we invalidated IRE1 in CT26 cells and obtained similar results, demonstrating that IRE1 signaling in tumor cells is a central event in the low PROT-diet induced anti-cancer immune response. In addition, we have uncovered RIG-I activation as a downstream event of IRE1 activation and by bioinformatic analysis correlated high-IRE1 signature with high immune infiltration and enhanced immunogenicity of cancer in patients bearing melanoma, glioblastoma and colorectal cancer. Hence, we have shown that the immune system response elicited under a Low PROT diet is a consequence of increased IRE1 activation in cancer cells
Martinez, Turtos Adriana. „Les effets anti-tumoraux d'un régime pauvre en protéines et de la signalisation IRE1α“. Electronic Thesis or Diss., Université Côte d'Azur, 2022. http://www.theses.fr/2022COAZ6012.
Der volle Inhalt der QuelleNutritional interventions are investigated in the context of non-communicable diseases such as cancer. Dietary regimens such as caloric restriction, fasting, ketogenic and protein-restricted diets have shown benefits to control tumor progression. Indeed, we have previously reported the protective effect of an isocaloric diet partially reduced in protein in several cancer mouse models. Beyond a stronger anticancer immunosurveillance dependent on cytotoxic T cells, the low protein diet limited tumor growth in an IRE1α-dependent manner.Inositol-requiring enzyme 1α (IRE1α) is the most evolutionally conserved ER (endoplasmic reticulum) stress sensor induced as part of the Unfolded Protein Response (UPR). The UPR is activated by accumulation of misfolded proteins in the ER, lipidic disturbances in the ER membrane, hypoxia and nutrient deprivation. IRE1α activates downstream targets via its endoribonuclease activity resulting in XBP1 splicing as well as degradation of RNAs by a process known as the Regulated IRE1-Dependent Decay (RIDD). While XBP1 splicing recovers cellular homeostasis, massive RIDD induction leads to apoptosis under chronic ER stress.The IRE1α signaling has been described to play dual roles in most hallmarks of cancer. While the IRE1α-XBP1 axis in tumor cells supports tumor progression in several solid and liquid oncogenic malignancies, the IRE1α-RIDD branch has been suggested as tumor-suppressive in glioblastoma. Since our previous findings showed that IRE1 is implicated in the tumor-protective effects of a low protein diet, we investigated the effect of the exogenous expression of IRE1 in tumor cells implanted in immunocompetent mice.We found that overexpression of IRE1 and self-induction of its full RNAse activity was detrimental for subcutaneous tumor growth of colorectal and Lewis lung carcinomas. Tumors with higher IRE1 activity were characterized by active IRE1α-XBP1 and IRE1α-RIDD branches, a higher anticancer immunosurveillance and tumor cells undergoing apoptosis. The enhanced anti-cancer immune response elicits upon IRE1α overexpression was mainly dependent on T cell-mediated-cytotoxicity. In conclusion, our findings support the notion that IRE1α with a full RNAse activity can have tumor-suppressive roles
Baillet-Blanco, Laurence. „Étude de la dépense énergétique chez 10 patients insuffisants rénaux chroniques avant et après 3 mois de régime très pauvre en protides“. Bordeaux 2, 1999. http://www.theses.fr/1999BOR23040.
Der volle Inhalt der QuelleEl, Khayat El Sabbouri Hiba. „Impacts d'un pesticide, le chlorpyriphos (CPF), et d'un régime riche en graisses "High Fat Diet" sur l'activité contractile du muscle lisse digestif et strié diaphragmatique“. Thesis, Amiens, 2019. http://www.theses.fr/2019AMIE0040.
Der volle Inhalt der QuelleChlorpyrifos (CPF) is an acetylcholinesterase (AChE)-inhibiting organophosphorus insecticide. CPF exposure is harmful during the perinatal period and adulthood. Such developmental perturbations are linked to disorders in adults. Maternal obesity associated to pesticides exposure can program children’s metabolism and promote obesity onset. The first model assessed the effects of CPF exposure for 6 weeks in adult rats on diaphragm function. The second examined the impacts of perigestational exposure of dams to CPF and/or high-fat diet (HFD) during 4 months before gestation till the end of the lactation. Respiratory and intestinal functions were studied in young adult pups at postnatal day 60. We showed that CPF exposure to adults increased diaphragm contractility and fatigability associated with lower AChE activity and altered hormonal regulation and myosin heavy chain (MHC) isoforms composition. Perigestational exposure to CPF and/or HFD increased the sleep apnea index and diaphragm contractility. These changes can be ascribed to prolonged cholinergic transmission, altered sarcoplasmic reticulum calcium release/uptake function, and elevated expression of MHC isoforms mRNA. Perigestational CPF exposure increased ileal muscles contractility through cholinergic and non-cholinergic mechanisms involving muscarinic m2 acetylcholine receptor and substance P. Exposure to CPF and/or HFD reduced ileal AChE activity. Despite the lack of direct exposure, perigestational exposure to CPF and/or HFD programs the risks for altered respiratory and intestinal functions in young adult offspring. Besides, CPF exposure in adults affects diaphragm physiological function
Lambert, Delphine. „Influence d’un régime riche en graisses sur un modèle de vieillissement « accéléré » : étude de la fonction et de la morphologie cardiaque, la fonction artérielle, le métabolisme et l’inflammation“. Thesis, Université de Lorraine, 2016. http://www.theses.fr/2016LORR0266/document.
Der volle Inhalt der QuelleObesity and being overweight have been described as a global pandemic. Both obesity and aging will lead to cardiovascular complications. In addition, it has been highlighted that obesity promotes premature cardiac aging in young adults. The hypothesis of this work is that a high fat diet begun before adulthood, pursued over a long period of time, could lead to “accelerated” cardiovascular and metabolic aging. We have demonstrated, in an aging mouse model, that an early high fat diet leads to metabolic disorders and to an increase in fat mass and a deterioration in metabolism of white adipose tissue. These disorders are associated with alterations in cardiac morphology and function, despite an absence of changes in blood pressure and heart rate. Ageing, in obese mice, leads to ventricular remodeling accompanied by systolic dysfunction. In cardiac tissue, aging and early diet lead to an increased expression of fibrosis genes confirming the hypertrophic phenotype. Aging associated with an early high fat diet led also to an up-regulation of GDF11. GDF11 may then be considered as a marker of accelerated cardiac aging. These results may suggest therapeutic or preventive pathways, where inhibition of GDF11 improves prognosis and survival in obese subjects with cardiovascular disease. The study of this model has allowed us to demonstrate that a high fat diet leads to accelerated aging at the level of the heart
Cardinal, Pierre. „Rôle du récepteur aux cannabinoïdes de type 1 (CB1) hypothalamique dans la régulation de la balance énergétique et de l’homéostasie du glucose“. Thesis, Bordeaux 2, 2013. http://www.theses.fr/2012BOR22029/document.
Der volle Inhalt der QuelleThe endocannabinoid system is a major player in energy balance regulation. However, a complete understanding of its role within the hypothalamus, a region critically involved in energy balance regulation, is still missing. The general aim of this PhD work was to dissect the specific role of the cannabinoid type 1 receptor (CB1) expressed on different hypothalamic neuronal populations in energy balance regulation and glucose homeostasis by characterizing three new mouse mutant lines with a conditional deletion of CB1. On standard diet, CB1 deletion within the hypothalamus induced an increase in energy expenditure and a decrease in body weight gain without modifying food intake, while CB1 deletion within the ventromedial nucleus of the hypothalamus (VMN-CB1-KO) decreased fat mass, increased fatty acid oxidation in vivo and sympathetic nervous system (SNS) activity, and improved peripheral glucose metabolism. CB1 deletion within the paraventricular nucleus of the hypothalamus (PVN-CB1-KO) decreased body weight gain without affecting food intake or body composition. When exposed to a high-fat diet, VMN-CB1-KO mice gained significantly more weight and fat mass than their WT, while PVN-CB1-KO mice were partly protected from diet-induced obesity thanks to increased energy expenditure. These results overall suggest that CB1 expressed on different hypothalamic neuronal populations have distinct roles in energy balance regulation, which in turn also depend on the diet consumed
Vial, Guillaume. „Métabolisme hépatocytaire et insulinorésistance : effets d'un régime enrichi en graisse et d'un nouvel antidiabétique "E008"“. Phd thesis, Grenoble 1, 2009. http://www.theses.fr/2009GRE10269.
Der volle Inhalt der QuelleWith a steadily increasing prevalence, type II diabetes is becoming a major public health issue. This pathology is characterized by an increase of the hepatic glucose production, reflecting a raise of gluconeogenesis, which evolves into chronic hyperglycemia. Liver is thus a privileged target to fight against imbalances of glucose metabolism. A new drug derived from the Metformin and devoid of side effects, the E008, was synthesized by Merck-Santé to normalize blood glucose levels in diabetic patients. The dual objective of our work consisted in (i) studying liver metabolic fluxes in a nutritional rat model which exhibits a metabolic syndrome, and (ii) analysing the effects of this new compound while elucidating its mechanisms of action. Animals fed a high-fat diet have an increased gluconeogenesis, associated with disturbances of the mitochondrial function: increase of ROS production, inhibition of oxygen consumption and changes in redox potential. A common denominator in these events could be a mutual alteration of the composition of membrane lipids and quinones. On rats fed with a high-fat diet, E008 treatment decreases the hepatic glucose output by modifying metabolic control. Furthermore, it induces a subtle inhibition of cellular respiration while acting, at the same time, on the respiratory chain activity and phosphorylating system. (Inhibition of complex I and ANT reduced expression). Its action is also related to an activation of AMP-activated protein kinase (AMPK), by modification of adenine nucleotides ratios
Ramadan, Wiâm. „Étude des répercussions d'un régime enrichi en graisses, du diabète de type 2 et de la metformine sur la fonction respiratoire à l'éveil et au cours du sommeil chez le rat mâle adulte“. Amiens, 2005. http://www.theses.fr/2005AMIED004.
Der volle Inhalt der QuelleTo day, it is difficult to distinguish the respective role of obesity and metabolic disorders as insulin resistance and/or type 2 diabetes mellitus in the occurrence of respiratory disorders and notably sleep apneas since these disorders are typically diagnosed late in their course. Data from literature suggest that, although increase morbidity and mortality from this syndrome, the mechanisms underlying this pathology remain poorly understood. This lack of knowledge stems in part from a paucity of animal models to study naturally occurring apnea during sleep. The aim of this work was to study insulin resistance and type 2 diabetes mellitus repercussions on energetic metabolism, ventilation, apneas occurrence in absence of obesity and diaphragmatic contractility by using the rat model fed high fat diet developed by Reed et al (metabolism, 2000). Our study was also designed to assess whether the use of metformin, one of the most common drugs used in the treatment of insulin resistance, could reverse or suppress the possible ventilation impairments and apnea occurrence. This study demonstrates that insulin resistance increases apneas score during sleep in absence of obesity. This increase was reversed by metformin treatment reinforcing the idea that insulin resistance could induce ventilatory disorders during sleep independently of obesity. This study also demonstrated that metformin treatment in parallel with high fat fed diet prevent the development of sleep apnea syndrome. The decrease, in vitro, of the force of diaphragm, the principal inspiratory muscle, could be linked to an increase of apnea during sleep. Indeed, morphological modifications in diaphragmatic fibres had been shown with an increase of type IIb fibres and a decrease of type I and IIa fibres in diabetic rats
Porta, Natacha. „Acides gras poly-insaturés, activation des récepteurs nucléaires PPAR-alpha, régime cétogène : effet anticonvulsivant chez le rongeur“. Phd thesis, Université du Droit et de la Santé - Lille II, 2008. http://tel.archives-ouvertes.fr/tel-00343236.
Der volle Inhalt der QuelleDans un premier temps, nous avons administré per-os, pendant 4 semaines un mélange d'AGPI contenant 70% d'oméga-3 et 25% d'oméga-6 à des rats Wistar. Les animaux ayant reçu la complémentation alimentaire par des AGPI présentaient une augmentation du seuil au PTZ comparable à celle obtenue chez les animaux ayant reçu un régime cétogène. Les animaux supplémentés par les AGPI ou ayant reçu le régime cétogène présentaient des variations plasmatiques en AGPI concernant l'acide arachidonique, l'acide alpha linolénique et l'acide eicosapentaenoïque. Aucune modification du statut nutritionnel ou des phospholipides cérébraux membranaires n'était retrouvée. Dans un second temps, nous avons administré pendant 14 jours de la nourriture contenant 0,2% de fénofibrate (agoniste des récepteurs PPAR-alpha) à des rats Wistar. Le traitement par 0,2% de fénofibrate conduisait à augmenter le seuil au PTZ et retarder le début de l'état de mal épileptique dans le modèle lithium-pilocarpine. Ces résultats étaient comparables à ceux obtenus avec le régime cétogène. En revanche le traitement associant le régime cétogène et le fénofibrate ne conduisait pas à moduler le seuil au PTZ chez les animaux.
Ces travaux ont permis de montrer que les AGPI ont des propriétés anticonvulsivantes, comparables à celles du régime cétogène. Ces propriétés anticonvulsivantes ont également été retrouvées suite à l'activation des récepteurs nucléaires PPAR-alpha par le fénofibrate. Les propriétés anticonvulsivantes portées par les AGPI ne sont pas liées à une variation de la composition des membranes cellulaires cérébrales en phospholipides. Les récepteurs nucléaires PPAR-alpha modulent quant à eux de nombreuses voies (métaboliques, inflammatoires, stress oxydant) via des variations d'expression génique et peuvent être activés par les AGPI. L'implication de ces différentes voies dans l'efficacité anticonvulsivante du fénofibrate, reste à explorer. Ces résultats, s'ils sont confirmés par des études complémentaires dans d'autres modèles, laissent penser qu'une simplification du régime cétogène pourrait être envisagée via l'utilisation des AGPI et/ou via l'activation des récepteurs nucléaires PPAR-alpha
Bücher zum Thema "Régime pauvre en graisses"
C, Atkins Robert. Le nouveau régime Atkins. Montréal: Modus Vivendi, 2004.
Den vollen Inhalt der Quelle findenGrillparzer, Marion. Brûleurs de graisses: Pour retrouver la forme et la garder : les aliments qui font fondre les graisses : amincisseurs, nutriments essentiels, protéines et enzymes : supplément, régime bio, 5 kilos perdus en 10 jours. Paris: Vigot, 2001.
Den vollen Inhalt der Quelle findenAssociation des hypoglycémiques du Québec, Hrsg. Bien se nourrir sans mauvais sucres. Outremont, Québec: Quebecor, 2004.
Den vollen Inhalt der Quelle findenKeith, Lierre. The vegetarian myth: Food, justice and sustainability. Crescent City, Ca: Flashpoint Press, 2009.
Den vollen Inhalt der Quelle findenFrappier, Renée. Le guide des bons gras. 2. Aufl. [Longueuil, Québec]: Éditions Maxam, 1999.
Den vollen Inhalt der Quelle findenLaurent, Thibault. Formules Cétogènes Pour Stimuler la Perte de Poids: Plan de Perte de Poids Sain Basé Sur un Régime Pauvre en Glucides et Riche en Graisses. Independently Published, 2022.
Den vollen Inhalt der Quelle findenPinson, Claire. Le régime brûle-graisse. Marabout, 2001.
Den vollen Inhalt der Quelle findenLe Régime brûle-graisse : Maigrissez grâce aux aliments brûleurs de graisses ! Marabout, 2002.
Den vollen Inhalt der Quelle findenGuide Complet de RÉgime CÉtogÈne: Brûler les Graisses en Excès Sans Mourir de Faim. Independently Published, 2021.
Den vollen Inhalt der Quelle findenComment Augmenter Votre MÉtabolisme et BrÛlez les Graisses: Recettes étonnantes Pour un Régime KETO Facile. Independently Published, 2021.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "Régime pauvre en graisses"
Chevallier, Laurent. „Digestif : régime d’épargne digestive (pauvre en fibres)“. In 65 Ordonnances Alimentaires, 165–69. Elsevier, 2021. http://dx.doi.org/10.1016/b978-2-294-76804-0.00027-1.
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