Literatura científica selecionada sobre o tema "Troubles du métabolisme des glucides"
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Artigos de revistas sobre o assunto "Troubles du métabolisme des glucides"
de Lonlay, P., e S. Dubois. "Anomalies héréditaires du métabolisme des glucides". EMC - Endocrinologie - Nutrition 8, n.º 1 (janeiro de 2011): 1–10. http://dx.doi.org/10.1016/s1155-1941(11)51210-7.
Texto completo da fonteDamiri, L., M. Alaoui Mhamdi e J. Bahhou. "Dynamique des populations microphytobenthiques couplée à leur composition biochimique au sein du réservoir Allal El Fassi (Maroc)". Revue des sciences de l'eau 15, n.º 1 (12 de abril de 2005): 101–9. http://dx.doi.org/10.7202/705439ar.
Texto completo da fontePANSERAT, S., e S. KAUSHIK. "Régulation nutritionnelle du métabolisme glucidique chez les poissons : exemple de la truite arc-en-ciel (Oncorhynchus mykiss), faible utilisatrice des glucides alimentaires". INRAE Productions Animales 15, n.º 2 (12 de agosto de 2002): 109–17. http://dx.doi.org/10.20870/productions-animales.2002.15.2.3691.
Texto completo da fonteAndreelli, F. "Métabolisme des glucides et méthodes d’exploration chez l’homme". EMC - Endocrinologie - Nutrition 9, n.º 4 (outubro de 2012): 1–13. http://dx.doi.org/10.1016/s1155-1941(12)40468-1.
Texto completo da fontePréau, Sébastien, Alexandre Pierre, Raphael Favory, Benoit Brassart, Arthur Durand, Claire Bourel e Steve Lancel. "Dysfonction énergétique au cours du sepsis". Médecine Intensive Réanimation 33, n.º 1 (29 de março de 2024): 29–46. http://dx.doi.org/10.37051/mir-00200.
Texto completo da fonteJabi, R., e M. Bouziane. "Phéochromocytome et les troubles du métabolisme glucidique". Journal de Chirurgie Viscérale 159, n.º 4 (setembro de 2022): S100. http://dx.doi.org/10.1016/j.jchirv.2022.07.101.
Texto completo da fonteThauvin-Robinet, C., e E. Roze. "Troubles du métabolisme des cobalamines chez l’adulte". Revue Neurologique 163, n.º 10 (outubro de 2007): 911–18. http://dx.doi.org/10.1016/s0035-3787(07)92634-x.
Texto completo da fonteMarcelli, Christian. "Maladies génétiques avec troubles du métabolisme phosphocalcique". Revue du Rhumatisme Monographies 79, n.º 4 (setembro de 2012): 262–68. http://dx.doi.org/10.1016/j.monrhu.2012.09.001.
Texto completo da fonteJabi, R., e M. Bouziane. "Phéochromocytome et les troubles du métabolisme glucidique". Journal de Chirurgie Viscérale 157, n.º 3 (setembro de 2020): S171. http://dx.doi.org/10.1016/j.jchirv.2020.07.094.
Texto completo da fonteBauduer, F. "Anémies par troubles du métabolisme du fer". EMC - Hématologie 4, n.º 1 (janeiro de 2009): 1–11. http://dx.doi.org/10.1016/s1155-1984(09)50262-2.
Texto completo da fonteTeses / dissertações sobre o assunto "Troubles du métabolisme des glucides"
Lieber, Ari Leib. "Macro- et microcirculation au cours des troubles du métabolisme glucidique". Paris 7, 2012. http://www.theses.fr/2012PA077163.
Texto completo da fonteHigh blood pressure and glucose metabolism disorders share common comorbidities that originate from a common ground : the vessel and its annexes. Epidemiological analysis of predictors of cardiovascular risk is based on the analysis of the macrocirculation with arterial stiffness, wave reflections, pulse pressure, and of the microcirculation due to structural changes of arterioles with target organ damage. We observed in this work that arterial stiffness was present in hypertensive diabetics. Among diabetics, those on insulin had a lower augmentation index, perhaps due to the vasodilatory effects of insulin on a ground where the mitogenic effects of long-term hyperinsulinism have stiffened the arterial wall. The criterion of disorder of glucose metabolism is probably responsible for the arterial stiffness in patients with metabolic syndrome. This study found that patients receiving ACE inhibitors and insulin patients had a higher PWV and PP, probably because they had the most advanced disease. Finally the question of wave reflection was assessed by measuring its speed and magnitude and the hypothesis of increased pressure made us think that thewave reflection does not return faster, but sooner and this had been added to the systolic peak systolic because the reflection sites were closer due to the small size in women or the microcirculatory damage
Gilleron, Martine. "Structure et propriétés immunologiques de nouveaux glycolipides isolés de Mycobacterium kansasii et Mycobacterium gastri". Toulouse 3, 1991. http://www.theses.fr/1991TOU30221.
Texto completo da fonteCartault, François. "Psychotropes et troubles de la régulation glycémique". Montpellier 1, 1992. http://www.theses.fr/1992MON11203.
Texto completo da fonteElferchichi-Ben, Rhouma Miryam. "Effet du champ magnétique statique sur le métabolisme du rat". Montpellier 1, 2009. http://www.theses.fr/2009MON1T002.
Texto completo da fonteBrun, Antoine. "Troubles du métabolisme glucidique chez le cirrhotique avec shunt porto cave spontané". Montpellier 1, 1991. http://www.theses.fr/1991MON11212.
Texto completo da fonteDeloumeaux-Tyndal, Jacqueline. "Aspects épidémiologiques des anomalies du métabolisme glucidique et du diabète de type 2 en Guadeloupe". Bordeaux 2, 2006. http://www.theses.fr/2006BOR21376.
Texto completo da fonteType 2 diabetes is now qualified as a worldwide epidemic by the World Health Organization (WHO). The links of type 2 diabetes with co morbidities such as hypertension and dyslipidemia, focuse on the need of primary health care in the next decades. Guadeloupe is a French Carobbean archipelago with more than 422 000 inhabitants including people of Indian and African descents and Caucasians. Prevalence of type 2 diabetes reaches 6,6 % in general population compared to 22,5 % in subjects of Indian descents which are respectively 2 and 7 fold higher than in mainland France. Diabetic subjects represent about 30 % of patients on hemodialysis with a mortality rate 3 fold higher than non diabetic subjects. Our works are presented in four studies preceded by a review of the literature. The association between anthropometric parameters (WHO criteria) and type 2 diabetes was studied for potential use in clinical practice in a population with a mean age over 50 years old. The distribution of metabolic syndrome, involved in type 2 diabetes and cardiovascular complications, was studied by comparing subjects of Indian descents with subjects of the general population. We report in a third study, the association of arterial pulse pressure, a non-traditional risk factor, with cardiovascular complications in type 2 diabetic patients undergoing haemodialysis. We finally study, glucose metabolism abnormalities, dyslipidemia and proinflammatory cytokines (adiponectin and leptin), as risk factors for insulin resistance in an HIV infected cohort of patients
Taveau, Christopher. "Rôle de la vasopressine dans les troubles du métabolisme glucidique : possible impact dans le développement du diabète". Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066211/document.
Texto completo da fonteIt is well established that vasopressin (AVP) level is high in both human and experimental diabetes. In humans, several recent studies have shown an association between copeptin (biomarker of AVP secretion) and the occurrence of diabetes mellitus or hyperglycemia, metabolic syndrome and obesity. Our team has shown a reverse association between water consumption (decrease AVP secretion) and the risk of hyperglycemia in the general population (D.E.S.I.R cohort). The aim of my thesis was to determine the role of AVP and fluid intake in glucose homeostasis in healthy rats and in a rat model of metabolic syndrome. AVP, administered acutely or chronically in healthy rats, increases glycaemia and this effect is reversed by a V1a receptor antagonist. V1b receptor activation does not influence insulin secretion but stimulates moderately basal glucagon production by the pancreas. These effects were observed in two different healthy strains of rats. In obese Zucker rats, a high AVP level worsens fasting hyperinsulinaemia and glucose intolerance whereas hydration does not affect glucose tolerance but drastically reduces hepatic steatosis, the content of cholesterol and triglycerides in liver and expression of genes involved in hepatic lipogenesis. In conclusion, these studies show for the first time, that AVP aggravates glucose tolerance whereas a highly hydrated diet is protective. These results, in agreement with our epidemiological data, demonstrate a causal link between vasopressin and/or hydration and glucose metabolism disorders
Clément, Laurence. "Effets des lipides sur le contrôle nerveux de l'homéostasie glucidique chez le rat : aspects cellulaires et moléculaires". Paris 11, 2002. http://www.theses.fr/2002PA11T025.
Texto completo da fonteType 2 diabetes represents 90 to 95% of all cases of diabetes and is characterised by insulinresistance along with an alteration pancreatic β-cell insulin secretion, resulting in chronic hyperglycemia. The mechanisms responsible for such alterations are not fully understood. In a preliminary study, we found that β-cell dysfunction partly results from a deleterious effect of free fatty acids (FFA) on the sympathetic nervous system. The aim of this work was to determine the molecular and cellular mechanisms implicated in the alteration of nervous regulation of glucose homeostasis by lipids. In Wistar rats infused intracerebroventricularly with a triglyceride emulsion and heparin, we found that lipids may act on the central nervous system (CNS) to induce an increase in glucose-induced insulinsecretion (GIIS). As shown by the pancreatic turnover of norepinephrine, the effect of lipids is probably mediated by a decrease in the sympathetic output to the pancreas. We also found a decreased liver insulin sensitivity in these rats, associated with a hypercorticosteronernia. Consequently, our aim was to determine the molecular mechanisms les mécanismes cellulaires implicated in the action of lipids on the CNS. Microarray studies of the hypothalamic RNA of these rats showed that lipids induce transcriptional changes of specifie genes, which could account for the metabolic alterations, such as the leptine receptor. We then focused on the binding characteristics of pancreatic β-cell α2A adrenergic receptors in response to elevated circulating FFA levels. These receptors have been shown to mediate inhibition of GIIS by norepinephrine. We found a decreased number and an increased affinity of these receptors. We also found that FFA induce changes in islet membrane phospholipidic composition, which may account for the increased affinity of the receptors. We conclude that these data suggest that the diabetogenic effect of FFA may not only result from changes in glucose metabolisme, but also from alterations in the sympathetic nervous output to the pancreas, and to neurophysiologie modifications, probably mediated by changes in hypothalamic activity
Rezki, Amel. "Le petit déjeuner standardisé. Un outil diagnostique du statut glycémique et des modifications cardiovasculaires postprandiales ? : Comparaison vs la charge en glucose ; et explorations cardiovasculaires sous saxagliptine vs placebo chez des patients intolérants au glucose". Thesis, Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCD029.
Texto completo da fontePostprandial metabolic changes are essential both to characterize glycemic status (normal, prediabetes or diabetes, best diagnosed by oral 75g glucose tolerance test of (OGTT)) but also because of cardiovascular changes induced by food intake. A standardized breakfast with 75g carbohydrates (SB) could be an alternative. The continuous glucose monitoring allowed us to show a great concordance of the amplitude / kinetics of the metabolic response (glycemia, insulin resistance indexes, glucose variability) after OGTT vs after SB in obese subjects without known diabetes. The SB also offered good diagnostic performance. We also used the SB to explore fasting and postprandial metabolic and cardiovascular changes (endothelial function, microcirculation, autonomic nervous system, arterial stiffness, myocardial function) in obese patients with impaired glucose tolerance (ACCES study), according to randomiziation to a 12-week treatment with Saxagliptin, a dipeptidyl 4 inhibitor (iDPP4), or its placebo. We showed that this treatment allowed the regression of glucose intolerance for 9 patients out of 10 in the saxagliptin arm against 4 out of 9 in the placebo arm. We did not observe any change in our cardiovascular parameters according to iDPP4 vs placebo, both at fasting and after the SB, after a single dose and after 12 weeks of treatment. Only the decrease in postprandial vagal activity was more sustained in the saxagliptin group.These results support the cardiovascular safety of saxagliptin.To conclude, the SB appears to be a promising diagnostic test for dysglycemia, as it is simple and well tolerated. It can also be used to explore cardiovascular changes after a mixed meal,with more physiological modifications than after OGTT
Mellouk, Namya. "Etude de trois adipocytokines, adiponectine, visfatine et chémérine au niveau plasmatique et dans plusieurs tissus métaboliques et reproducteurs de différentes espèces". Thesis, Tours, 2018. http://www.theses.fr/2018TOUR4007.
Texto completo da fonteThis thesis is focused on the study of three adipokines (adiponectin, visfatin and chemerin) in species that develop abnormalities of energy metabolism associated with reproductive disorders. Our results have shown some diet effects on the lipid and carbohydrate metabolisms and in a less extend, on the reproductive functions in dairy cows and broiler hens. These effects were partly associated with the expression profiles of adiponectin, visfatin and chemerin. In addition, we have demonstrated overexpression of the chemerin/CMKLR1 system in follicular fluid and in ovarian cells of patients with polycystic ovarian syndrome, with or without obesity. First, these findings reveal the possibility of considering these adipokines as potential biomarkers for evaluating growth, fattening status and fertility in agricultural farms. On the other hand, they suggest a potential involvement of chemerin in the regulation of ovarian functions in women
Livros sobre o assunto "Troubles du métabolisme des glucides"
1945-, Fukuda Minoru, e Hindsgaul Ole, eds. Molecular and cellular glycobiology. Oxford: Oxford University Press, 2000.
Encontre o texto completo da fonteBorg, Jacques. Biochimie métabolique: Metabolisme des glucides. Paris: Ellipses, 2004.
Encontre o texto completo da fonte1939-, Beitner Rivka, ed. Regulation of carbohydrate metabolism. Boca Raton, Fla: CRC Press, 1985.
Encontre o texto completo da fonteJ, Favus Murray, e American Society for Bone and Mineral Research., eds. Primer on the metabolic bone diseases and disorders of mineral metabolism. 6a ed. Washington, DC: American Society for Bone and Mineral Research, 2006.
Encontre o texto completo da fontePerlemuter, Léon. Diabète et maladies métaboliques. 4a ed. Paris: Masson, 2003.
Encontre o texto completo da fonte1944-, Grimaldi André, ed. Dyslipidémie et athérogenèse. Paris: Elsevier, 2004.
Encontre o texto completo da fontePerlemuter, Léon. Diabète et maladies métaboliques. Paris: Masson, 1987.
Encontre o texto completo da fonteMundy, Gregory R. Calcium homeostasis: Hypercalcemia and hypocalcemia. London: Dunitz, 1989.
Encontre o texto completo da fonte1900-1978, Harrison Tinsley Randolph, e Jameson J. Larry, eds. Harrison's endocrinology. New York: McGraw-Hill Medical Pub. Division, 2006.
Encontre o texto completo da fonteInternational Magnesium Symposium. (11th 2006 Osaka, Japan). New perspectives in magnesium research: Nutrition and research. London: Springer, 2007.
Encontre o texto completo da fonteCapítulos de livros sobre o assunto "Troubles du métabolisme des glucides"
Bourrillon, A. "Métabolisme – Troubles nutritionnels". In Pédiatrie, 567–97. Elsevier, 2011. http://dx.doi.org/10.1016/b978-2-294-71375-0.50020-9.
Texto completo da fonte