Academic literature on the topic 'Régime pauvre en cholestérol'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Régime pauvre en cholestérol.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Régime pauvre en cholestérol"
FAYE, B., O. ABDELHADI, G. RAIYMBEK, I. KADIM, and J. F. HOCQUETTE. "La production de viande de chameau : état des connaissances, situation actuelle et perspectives." INRAE Productions Animales 26, no. 3 (June 18, 2013): 289–300. http://dx.doi.org/10.20870/productions-animales.2013.26.3.3158.
Full textCOMBES, S. "Valeur nutritionnelle de la viande de lapin." INRAE Productions Animales 17, no. 5 (October 5, 2004): 373–83. http://dx.doi.org/10.20870/productions-animales.2004.17.5.3610.
Full textBouguerra, R., A. Belkadhi, J. Jabrane, J. Hamzaoui, C. Maatki, M. C. Ben Rayana, and C. Ben Slama. "[Metabolic effects of Ramadan fasting on type 2 diabetes]." Eastern Mediterranean Health Journal 9, no. 5-6 (March 31, 2003): 1099–108. http://dx.doi.org/10.26719/2003.9.5-6.1099.
Full textHarouadi, Farid, and Salim Boulahrouz. "Etude et Analyse de la Combustion Turbulente dans un Moteur Alimenté en Gaz Naturel." Journal of Renewable Energies 3, no. 2 (December 31, 2000): 93–103. http://dx.doi.org/10.54966/jreen.v3i2.914.
Full textJouët, Pauline, and Nathalie Morel. "Régime pauvre en FODMAPS, ce que doivent savoir les nutritionnistes." Nutrition Clinique et Métabolisme 33, no. 3 (September 2019): 199–204. http://dx.doi.org/10.1016/j.nupar.2019.05.005.
Full textDescamps, V., C. Fite, C. Cannistra, K. Ezzedine, G. Chaby, H. Maillard, and G. Gabison. "Hidradénite suppurée : intérêt d’un régime pauvre en levure de bière." Annales de Dermatologie et de Vénéréologie 140, no. 12 (December 2013): S557. http://dx.doi.org/10.1016/j.annder.2013.09.440.
Full textDisdier, P., J. R. Harle, Ph Vague, G. Habib, G. Bolla, D. Verrot, and P. J. Weiller. "Un nouveau traitement pour l'amylose portugaise: le régime pauvre en protéines." La Revue de Médecine Interne 14, no. 6 (June 1993): 511. http://dx.doi.org/10.1016/s0248-8663(05)80445-x.
Full textCharlot, Anouk, Ombline Conrad, and Joffrey Zoll. "Le régime cétogène : une stratégie alimentaire efficace en complément des traitements contre le cancer ?" Biologie Aujourd’hui 214, no. 3-4 (2020): 115–23. http://dx.doi.org/10.1051/jbio/2020014.
Full textOloruntola, Olugbenga David, Simeon Olugbenga Ayodele, and Deborah Adebukola Oloruntola. "Effect of pawpaw (Carica papaya) leaf meal and dietary enzymes on broiler performance, digestibility, carcass and blood composition." Revue d’élevage et de médecine vétérinaire des pays tropicaux 71, no. 3 (October 23, 2018): 121. http://dx.doi.org/10.19182/remvt.31640.
Full textKurtz, Maxime, and 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, no. 86 (2023): 26–34. http://dx.doi.org/10.1051/npvcafe/2024017.
Full textDissertations / Theses on the topic "Régime pauvre en cholestérol"
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.
Full textSeveral 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.
Full textSeveral 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.
Full textNutritional 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.
Full textDuranthon, Véronique. "Interactions spécifiques des HDL et des LDL avec la membrane basolaterale des cellules épithéliales intestinales chez le porc : caractérisation et effets d'un régime déficient en acides gras essentiels." Paris 7, 1992. http://www.theses.fr/1992PA077319.
Full textMourot, Jacques. "Contribution à l'étude du rôle des phytostérols sur le métabolisme du cholestérol et des lipides chez le rat." Nancy 1, 1989. http://www.theses.fr/1989NAN10351.
Full textZhu, Tengfei. "Rôle des microARNs dans la régulation du métabolisme du cholestérol chez la truite arc-en-ciel alimentée avec des régimes à base de végétaux." Thesis, Pau, 2018. http://www.theses.fr/2018PAUU3036/document.
Full textAquaculture has been subjected to a huge development during the last decades. Due to limiting availabilities, fishmeal and fish oil, the traditional ingredients of fish feed, have been widely replaced with vegetable ingredients in order to support the sustainable development of aquaculture. This evolution of aquafeeds has resulted in a reduction of the cholesterol content of the diets. In this context, the major objective of the thesis was to decipher the physiological changes related to cholesterol metabolism occurring in fish fed the plant-based diet. We furthermore analyzed the mechanisms underlying the regulation of cholesterol metabolism, focusing on transcription factors and microRNAs. Additionally, the possibility of utilizing miRNA as potential noninvasive biomarker was also investigated in the thesis. Our studies have shown that utilization of plant-based diet resulted in hypocholesterolemia and modified the expression of genes involved in cholesterol synthesis and efflux as well as that of their corresponding transcriptional factors SREBP-2 and LXRα. We also observed a lower expression of miR-223 in the liver of trout fed the plant-based diet suggesting the involvement of posttranscriptional mechanisms in the regulation of cholesterol synthesis. We then carried out another experiment using a line of rainbow trout selected for better growth performance on plant-based diet. We found that the hepatic expression of miR-33a increased in trout fed the plant-based diet, while the expression of miR-122 and miR-128 was much higher in the selected line regardless of the diet. By analyzing the expression of putative target genes of miR-33a, 122 and 128, we noticed consistent regulations between miR-33a and 128 and their respective putative targets, which were caspase 6 apoptosis-related cysteine peptidase like 2 (casp612) and cAMP-specific phosphodiesterase 4B a (pde4ba). These results highlighted two new molecular pathways affected by the plant-based diet. Through the combination in vivo and in vitro approaches, we demonstrated that the expression of the genes involved in cholesterol synthesis and that of the transcription factor SREBP-2 and the miR-33a increased in trout fed plant-based diet devoid of cholesterol while conversely decreased in rainbow trout primary cell culture of hepatocytes stimulated by 25-hydroxycholesterol. These data indicate that SREBP-2 and miR-33a act synergistically to control cholesterol synthesis. Finally, we successfully detected miR-1, miR-33a, miR-122, miR-128 and miR-223 in trout plasma. We observed similar postprandial changes between plasma levels of miR-128 and miR-223 and their hepatic counterparts. Significant correlations were observed between hepatic and plasma levels of miR-128 and miR-223. Other correlations appeared between miR-122, 128 and 223 and the expression of genes related to synthesis and efflux of cholesterol. Altogether, these results indicate that plasma microRNAs 122, 128 and 223 are potential non-invasive biomarkers of cholesterol metabolism in rainbow trout
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.
Full textDans 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
Baron, Stéphanie. "Insulino-résistance et vieillissement cardiovasculaire : un traitement chronique par le resvératrol peut-il les améliorer ?" Phd thesis, Université René Descartes - Paris V, 2013. http://tel.archives-ouvertes.fr/tel-01002731.
Full textDesmarchelier, Charles. "Effets de régimes hyperlipidique et cafeteria sur le développement de l'obésité et ses désordres associés chez la souris." Phd thesis, AgroParisTech, 2010. http://pastel.archives-ouvertes.fr/pastel-00601961.
Full textBooks on the topic "Régime pauvre en cholestérol"
Tiano, Myrette. Le régime anti-cholestérol. [Montréal]: Primeur/Sand, 1986.
Find full textTurner, Roger Newman. Votre régime pour contrôler le cholestérol. [Montréal]: Éditions de l'Homme, 1991.
Find full textIlies, Angelika. 200 recettes pour réduire le cholestérol. Montréal: Modus Vivendi, 2006.
Find full textDubuc, Micheline Brault. Le compte-cholestérol. [Montréal]: Éditions de l'Homme, 1989.
Find full textStarenkyj, Danièle. Le mal du gras. Richmond, Québec: Orion, 1997.
Find full textShriver, Brenda J. No red meat. Tucson, AZ: Fisher Books, 1989.
Find full textMcCann, Anne Lindsay Greer. Low-cholesterol cuisine. New York: Wings Books, 1996.
Find full textTalbot, Lise Giroux. Votre assiette santé. Montréal: Éditions Trustar, 1997.
Find full textC, Atkins Robert. Le nouveau régime Atkins. Montréal: Modus Vivendi, 2004.
Find full textAssociation, American Heart, ed. The new American Heart Association cookbook. 7th ed. New York: Clarkson Potter/Publishers, 2004.
Find full textBook chapters on the topic "Régime pauvre en cholestérol"
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.
Full text