Auswahl der wissenschaftlichen Literatur zum Thema „Résistance au diabète“
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Zeitschriftenartikel zum Thema "Résistance au diabète"
Nicolau, Julia, Thierry Lequerré, Hélène Bacquet und Olivier Vittecoq. „Polyarthrite rhumatoïde, insulino-résistance et diabète“. Revue du Rhumatisme 84, Nr. 1 (Januar 2017): 17–22. http://dx.doi.org/10.1016/j.rhum.2016.06.004.
Der volle Inhalt der QuelleTan-Chen, Sophie, Olivier Bourron und Éric Hajduch. „Céramides, acteurs cruciaux dans le développement de l’insulino-résistance et du diabète de type 2“. médecine/sciences 36, Nr. 5 (Mai 2020): 497–503. http://dx.doi.org/10.1051/medsci/2020091.
Der volle Inhalt der QuelleAissani, Samia, und Ali Zitouni. „Asthma and diabetes association is not accidental“. Batna Journal of Medical Sciences (BJMS) 7, Nr. 2 (09.11.2020): 159–61. http://dx.doi.org/10.48087/bjmsra.2020.7220.
Der volle Inhalt der QuelleNehar, Z., A. Namouni, A. Behidj, O. Oumeziane, B. Oudjit und M. Caron Debarle. „P164 - Diabète par insulino-résistance extrême de type B, savoir y penser !“ Diabetes & Metabolism 37, Nr. 1 (März 2011): A73. http://dx.doi.org/10.1016/s1262-3636(11)70790-x.
Der volle Inhalt der QuelleRahmoune, R., R. Lounis, L. Ahmed Ali und S. Fedala. „Une résistance aux hormones thyroïdiennes révélée par un diabète sucré : à propos d’un cas“. Annales d'Endocrinologie 78, Nr. 4 (September 2017): 324–25. http://dx.doi.org/10.1016/j.ando.2017.07.348.
Der volle Inhalt der QuelleMutinelli-Szymanski, P., A. Caille, A. Al-Najjar, M. Büchler, C. Barbet, J. F. Marliere, F. Patat, H. Nivet, Y. Lebranchu und J. M. Halimi. „O69 Index de résistance intrarénale comme marqueur de risque de diabète post transplantation (new-onset diabetes after transplantation, NODAT)“. Diabetes & Metabolism 37, Nr. 1 (März 2011): A17. http://dx.doi.org/10.1016/s1262-3636(11)70557-2.
Der volle Inhalt der QuellePatel, S., S. Weber, A. Emser, M. von Eynatten, H. J. Woerle und B. Gibelin. „P285 Linagliptine améliore le contrôle glycémique chez les patients atteints de diabète de type 2 indépendamment de la durée du diabète et de l’insulino-résistance“. Diabetes & Metabolism 38 (März 2012): A97. http://dx.doi.org/10.1016/s1262-3636(12)71387-3.
Der volle Inhalt der QuelleAdatsi, R., F. Pappoe, A. S. Bockarie, L. Derkyi-Kwarteng, P. Nsiah, E. W. Weyori, K. Dankwa, E. Aniakwaa-Bonsu, J. Setorglo und S. Acquah. „<i>Falciparum</i> malaria is associated with risk markers of type 2 diabetes mellitus in individuals with or without COVID-19 exposure“. African Journal of Clinical and Experimental Microbiology 25, Nr. 1 (16.01.2024): 6–16. http://dx.doi.org/10.4314/ajcem.v25i1.2.
Der volle Inhalt der QuelleSahli, N., A. Temessek, H. Tertek, M. Antit, E. Khadraoui, N. Trabelsi und F. Ben Mami. „P155 Le syndrome métabolique et l’insulino-résistance dans le diabète de type 2 et le risque d’ischémie myocardique silencieuse“. Diabetes & Metabolism 38 (März 2012): A68. http://dx.doi.org/10.1016/s1262-3636(12)71257-0.
Der volle Inhalt der QuelleMoreau, F., M. Barthelemy, C. Bellane-Chantelot, L. Kessler, N. Jeandidier und M. Pinget. „P297 - Intérêt de l’exenatide dans le traitement d’un diabète MODY3 avec obésité et insulino-résistance majeure ? A propos d’un cas“. Diabetes & Metabolism 37, Nr. 1 (März 2011): A104. http://dx.doi.org/10.1016/s1262-3636(11)70923-5.
Der volle Inhalt der QuelleDissertationen zum Thema "Résistance au diabète"
Riant, Elodie. „Effets protecteurs des œstrogènes sur l'insulino-résistance et le diabète de type 2“. Toulouse 3, 2009. http://thesesups.ups-tlse.fr/686/.
Der volle Inhalt der QuelleAlthought corroborating data indicate that estrogens protect against insulino-resistance and glucose metabolism throught the activation of the estrogen receptor a (ERa), it has not been established wether this pathway could represent an effective therapeutic target to fight against metabolic disturbances induced by a high-fat diet. Based on the study of animal models in vivo, our experimental approach allowed us to demonstrate that: 1) Activation of the path of ERa in vivo exerts a protective effect in a mouse model subjected to a fat diet, and more precisely, limits the development of adipose tissue, preserves insulin sensitivity of peripheral tissues and prevents also the occurrence of fasting hyperglycemia and glucose intolerance. 2) Furthermore, activation of ERa enhanced inflammatory response characterized by cytokine production in organs sensitive to insulin (liver, fat) and infiltration of macrophages in adipose tissue. This proinflammatory effect results from direct activation of cells derived from bone marrow, but appears dissociated from the metabolic protective effect. Despite its pro-inflammatory effect, selective activation of the path of ERa could be an effective strategy to reduce the deleterious impact of dietary patterns hyperlipidaemia
Hamlat, Nadjiba. „Lipogénèse de la paroi artérielle : régulation de son expression et anomalies dans l'insulino-résistance et le diabète“. Electronic Thesis or Diss., Lyon 1, 2010. http://www.theses.fr/2010LYO10071.
Der volle Inhalt der QuelleWe investigated the expression and regulation of lipogenesis in aortas and VSMC and determined if it is modified during metabolic abnormalities. Zucker obese (ZO), diabetic (ZDF) rats, and the high fat diet fed Psammomys obesus accumulated more triglycerides in their aortas than control rats. However the expression of lipogenic genes, or of genes involved in fatty acids uptake, was not increased. Lipogenesis was not increased in human carotid endarterectomy of diabetic compared to non-diabetic patients. The adipogenic medium (ADM), glucose or insulin stimulated moderately lipogenesis but only in VSMC from control rats. No effect was observed in VSMC from ZO. We showed that the lipogenic effects of TO901317observed in VSMC from Zucker control rats are due solely to the nuclear receptor LXRα, PXR agonist had no effect. Conclusion: Lipogenesis is not increased in arterial wall during insulin-resistance and diabetes
Napolitano, Tiziana. „Confidentiel“. Thesis, Université Côte d'Azur (ComUE), 2017. http://www.theses.fr/2017AZUR4141.
Der volle Inhalt der QuelleLacquemant, Corinne. „Étude génétique de l'insulino-résistance, du diabète et de leurs complications cardio-vasculaires“. Lille 1, 2000. https://pepite-depot.univ-lille.fr/LIBRE/Th_Num/2000/50376-2000-322-323.pdf.
Der volle Inhalt der QuellePar contre, l'incidence des maladies athérosclereuses prématurées a considérablement augmenté ces dernières années a l'île Maurice. Les facteurs de risque généralement associés à cette pathologie sont les anomalies du métabolisme du glucose, des lipides et des facteurs de la coagulation, l'hyperinsulinisme, l'obésité centrale et l'hypertension artérielle. Ce syndrome d'insulinorésistance à une forte composante héréditaire en raison de l'existence d'une forte prévalence de diabète et de maladie coronarienne. L'analyse familiale de liaison dans la population mauricienne nous a permis de détecter des régions liées aux différents facteurs de l'insulinorésistance. D'autres étapes seront nécessaires pour identifier et valider les gènes de prédisposition au développement de ces différentes pathologies
Duquenne, Manon. „Les tanycytes véhiculent la leptine dans le cerveau métabolique : mécanismes moléculaires et rôle dans la physiopathologie de la résistance hormonale et l'obésité/diabète“. Thesis, Lille, 2019. https://pepite-depot.univ-lille.fr/RESTREINT/EDBSL/2019/2019LILUS054.pdf.
Der volle Inhalt der QuelleThe control of energy balance that allows for the maintenance of body mass requires a continued dialogue between the periphery and the hypothalamus in the brain. The access of peripheral hormones to that structure is essential to the proper functioning of neural circuits that regulate energy balance. However, little is known about the transport mechanisms of circulating metabolic signals into the hypothalamus. The median eminence, a hypothalamic structure forming the floor of the 3rd ventricle, contains specialized ependymoglial cells called tanycytes. Tanycytes have been shown to shuttle metabolic signals such as leptin into the cerebrospinal fluid, via transcytosis. Identifying the molecular mechanisms involved in this transport is essential to our understanding of the phenomenon of central hormone resistance found in obese and type 2 diabetes patients. During my thesis, after an infusion of a recombinant fusion protein (TAT-Cre) into the 3rd ventricle of leptin receptor gene-floxed mouse model (LepR(loxP/loxP)), we investigated the role of the LepR in tanycytes on the central control of energy homeostasis in mice. Our results show that selectively impairing LepR expression in tanycytes increases body weight, adiposity, cholesterolemia, triglyceridemia and decreases noradrenaline serum concentration. It’s associated with an increase of food intake, peripheral but not central leptin anorectic effect and glucose intolerance. Pancreas and adipose tissue activity of our model is also affected. In parallel, we studied the mechanisms underlying the anorexigenic action of endozepines. Our results show that endozepines induce ERK activation necessary for leptin transport into the brain in primary culture of tanycytes and require tanycytic LepR expression to promote STAT3 phosphorylation in the hypothalamus. Finally, we also investigated the effect of the expression of the type B botulinum neurotoxin BoNTB, in tanycytes on the central control of energy homeostasis in mice. BoNTB inactivates synaptobrevins 1-3 by proteolytic cleavage and thus alters synaptobrevin-mediated exocytosis. Our results show that selectively impairing synaptobrevin function in tanycytes affects as in the previous model the basal food intake, leptin sensitivity and glucose tolerance in mice. However, we noticed some differences in pancreas activity compared to the model in which we selectively impaired LepR expression in tanycytes. Altogether, these data demonstrate for the first time the key role of tanycytes in the central control of energy regulation in-vivo and the involvement of LepR expression in tanycytes for circulating leptin and endozepines action in the metabolic brain
Hamlat, Nadjiba. „Lipogénèse de la paroi artérielle : régulation de son expression et anomalies dans l'insulino-résistance et le diabète“. Thesis, Lyon 1, 2010. http://www.theses.fr/2010LYO10071.
Der volle Inhalt der QuelleWe investigated the expression and regulation of lipogenesis in aortas and VSMC and determined if it is modified during metabolic abnormalities. Zucker obese (ZO), diabetic (ZDF) rats, and the high fat diet fed Psammomys obesus accumulated more triglycerides in their aortas than control rats. However the expression of lipogenic genes, or of genes involved in fatty acids uptake, was not increased. Lipogenesis was not increased in human carotid endarterectomy of diabetic compared to non-diabetic patients. The adipogenic medium (ADM), glucose or insulin stimulated moderately lipogenesis but only in VSMC from control rats. No effect was observed in VSMC from ZO. We showed that the lipogenic effects of TO901317observed in VSMC from Zucker control rats are due solely to the nuclear receptor LXRα, PXR agonist had no effect. Conclusion: Lipogenesis is not increased in arterial wall during insulin-resistance and diabetes
Napolitano, Tiziana. „Gfi1 : une nouvelle cible pour la thérapie du diabète“. Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2017. http://www.theses.fr/2017AZUR4141.
Der volle Inhalt der QuelleThe mature pancreas consists of two main tissue types: the exocrine tissue, including acinar cells and a ductal tree, and the endocrine tissue. Acinar cells are dedicated to the synthesis of digestive enzymes, which are collected and conveyed to the duodenum by a ductal network running through the entire organ. Endocrine cells are organized into highly vascularized cell clusters, termed islets of Langerhans, which contain five cell subtypes, α-, β-, δ-, PP- and ε-cells secreting glucagon, insulin, somatostatin, pancreatic polypeptide and ghrelin, respectively. Classical genetic approaches have revealed much about individual factors regulating pancreatic development, however, we have yet to understand the regulatory network underlying pancreas formation and all the factors involved. Some of these factors are well known and studied but increasing researches revealed new and unknown factors involved in pancreas development and maturation. Among these, through in silico studies, we accumulated evidences suggesting a role of Gfi1 in pancreas cell development and specification. This protein, a zinc finger transcription factor, had previously been implicated in hematopoiesis, inner ear cell development, and in the maintenance of intestinal cell phenotypes. Here, we investigated the role of Gfi1 in the pancreas. Towards this goal, we generated a transgenic mouse line allowing Gfi1 inactivation exclusively in the pancreas. Altogether, our observations suggest that Gfi1 is required for the full maturation of pancreatic acinar cells. Importantly, we demonstrated that the sole loss of Gfi1 in the pancreas is sufficient to protect mice against two models of diabetes induction
Lacroix, Marilyn. „Implication de l'adiponectine dans la physiopathologie du diabète gestationnel“. Mémoire, Université de Sherbrooke, 2013. http://hdl.handle.net/11143/6321.
Der volle Inhalt der QuelleMunkonda, Mercedes Nancy. „Le rôle de l'ASP dans la résistance à l'insuline et le diabète de type 2“. Thesis, Université Laval, 2012. http://www.theses.ulaval.ca/2012/29282/29282.pdf.
Der volle Inhalt der QuelleDray, Cédric. „Rôle et régulation de l'Apeline au cours de la résistance à l'insuline associée à l'obésité“. Toulouse 3, 2009. http://thesesups.ups-tlse.fr/552/.
Der volle Inhalt der QuelleApeline is a peptide synthesized by adipocytes and present in plasma under different forms such as 36, 17 and 13 aminoacids forms. During this doctoral, I have studied the apelin regulation and role during insulin resistance and type II diabetes. At first, we showed that TNFalpha, an inflammatory cytokine involved in insulin resistance, increased adipocyte apelin expression and secretion in mouse and human. Another study allows us to show a wide-range expression of apelin and APJ during type II diabetes development stages. In mouse and human, adipose tissue apelin and APJ expression is insulin sensible during insulin resistance but fails to be sensible during type II diabetes. In striated skeletal muscle, this kind of regulation is not clear and has to be more studied. At the same time, we also considered the metabolic role of apelin in mouse model. Ex vivo and in vivo experiences realised in mouse highlighted that apelin increased glucose uptake in muscle and adipose tissue. Furthermore, apelin-induced signalling pathways studies in isolated soleus muscle showed AMPK, eNOS and Akt activation. Interestingly, in high fat diet induced obese and insulin-resistant mice, we showed that apelin effect was still effective to ameliorate glucose tolerance (OGTT) and, as observed in healthy mouse, increased skeletal muscle and white adipose tissue glucose utilization. Surprisingly, glucose utilization was also increased in hearts of apelin-infused mice. Even if supplemental data are necessary, apelin seems to behave as a new anti-diabetic hormone and could be considered as a new potential target to fight metabolic diseases
Buchteile zum Thema "Résistance au diabète"
Dr. Tanima Paul (Das). „Adiponectin: The Wonder Hormone in Therapy of Obesity“. In CONTEMPORARY SOCIAL RESEARCH: PEOPLE, SOCIETY AND ENVIRONMENT: [VOLUME 1]. REDSHINE London, 2019. http://dx.doi.org/10.25215/1387453440.012.
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