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Relevant bibliographies by topics / Insuline resistance

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Academic literature on the topic 'Insuline resistance'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 April 2022

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Journal articles on the topic "Insuline resistance"

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Onusyko, O. V. "Perinatal consequences in women with the Polycystic Ovarу Syndrome on a background insuline resistance in anamnesis." HEALTH OF WOMAN, no. 10(116) (December 29, 2016): 107–9. http://dx.doi.org/10.15574/hw.2016.116.107.

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In this article features of perinatal consequences in women, pregnancy, which became after the treatment of the Polycystic Ovarу Syndrome on a background of insuline resistance are considered. The clinical and static retrospective analysis of 102 of childbirth histories in women with the Polycystic Ovarу Syndrome in anamnesis is conducted for period from 2009th to 2012th on the base of maternity hospital in Uzhorod. It was found that insuline resistance has negative influence on the state of new-born. The objective: to study the effect of insulin resistance in pregnant women on neonatal status. Patients and methods. Retrospective clinico-statistical analysis of 100 individual cards and stories of labor in patients with polycystic ovary syndrome on the background of insulin resistance and 100 stories of newborns. And the first study group were children of women with PCOS on the background of IR. This is the primary group. And II group (control) took the children of healthy women, whose number was 115. Pregnant women, who were executed in vitro fertilization, the study has not been included. Resalts. The influence of insulin resistance in pregnant women on neonatal status. Established negative its effects on infants, namely an increase in the incidence of perinatal complications. Conclusion. The state of hyperandrogenism and insulin resistance in women with PCOS in history, of course, adversely affects the condition of the newborn: increased risk of asphyxia of the newborn, hypoxic-ischemic encephalopathy, respiratory insufficiency I, II and III degrees, reduced muscle tone. Also increased risk of hypoxic cardiopathy, cardio-respiratory depression and the courts. Key words: pregnancy, polycystic ovary syndrome, insulin resistance, newborn.

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COLINO, E., L. Pe??a, J. C. Ramos, P. Saavedra, and M. Quintana. "P0053 PP INSULINE RESISTANCE SYNDROME IN OBESE CHILDREN." Journal of Pediatric Gastroenterology and Nutrition 39, Supplement 1 (June 2004): S76—S77. http://dx.doi.org/10.1097/00005176-200406001-00177.

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Vigil, L., R. Garcia Carretero, C. Rodriguez Castro, A. Colas, B. Vargas, M. Lopez Jimenez, and M. Varela. "INSULINE RESISTANCE AND CHRONIC RENAL DISEASE IN A HYPERTENSIVE POPULATION." Journal of Hypertension 36, Supplement 1 (June 2018): e274. http://dx.doi.org/10.1097/01.hjh.0000539794.87223.5f.

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ARMASHERNANDEZ, M. "D16 Lacidipine on platelet malondialdehyde production and insuline resistance in hypertensive patients." American Journal of Hypertension 10, no. 4 (April 1997): 108A. http://dx.doi.org/10.1016/s0895-7061(97)89044-9.

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Conterato, Elisabete Vieira, Tania Diniz Machado, Carlos Alberto Nogueira-de-Almeida, and Elza Daniel Mello. "Leptin Levels, Basal Metabolic Rates, and Insulin Resistance in Obese Pubertal Children." International Journal of Nutrology 13, no. 01 (July 2020): 017–23. http://dx.doi.org/10.1055/s-0040-1713796.

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Abstract Introduction Obesity in children and adolescents is considered a serious public health problem. The consequences of overweight can last for life. It is extremely important to have formulas to calculate the basal metabolic rate (BMR) that are truly reliable in relation to the individual caloric expenditure. Objectives To investigate the association of serum levels of leptin, lipid profile, and insulin resistance (insuline resistance by Homeostatic Model Assessment [HOMA] index) with the body mass index (BMI) z-score of pubertal obese children. In addition, to compare the basal metabolic rate (BMR) evaluation carried out using bioimpedance (BIA) with the Food and Agricultural Organization/World Health Organization (FAO/WHO) equation. Methods Cross-sectional study including 37 pubertal obese children (aged 7 to 12 years old) seen for the first time in the outpatient care unit specialized in child obesity between June 2013 and April 2014. The participants were assessed regarding anthropometric data, body composition (fat mass) by BIA 310 bioimpedance analyzer (Biodynamic Body Composition Analyser, model 310 - Biodynamics Corporation, Seattle, EUA), and blood pressure. Blood samples were collected to measure glucose, insulin, lipid profile, triglycerides, and leptin. The stage of sexual maturity was determined by self-assessment according to the Tanner scale. Results Higher leptin levels were found in the severe obesity group (p = 0.007) and, as expected, higher BMI (p < 0.001), and fat mass (p = 0.029). The groups did not differ in relation to insulin, insulin resistance (HOMA-IR), triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), and blood pressure. The BMR measured by bioimpedance was lower as compared to the measure by the FAO/WHO equation (p < 0.001). Conclusions These results suggest that severely obese children may present leptin resistance in this early stage of life, (since this hormone is higher in these children). It is suggested that health professionals prioritize the calculation of BMR by bioimpedance, since the FAO/WHO equation seems to overestimate the caloric values.

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Afandi, Muhammad Rafli, and Ferdy Royland Marpaung. "CORRELATION BETWEEN APOPROTEIN B/APOPROTEIN A-I RATIO WITH HOMA IR VALUE (HOMEOSTATIC MODEL ASSESMENT INSULIN RESISTANCE) IN TYPE 2 DIABETES MELLITUS." Journal of Vocational Health Studies 3, no. 2 (December 21, 2019): 78. http://dx.doi.org/10.20473/jvhs.v3.i2.2019.78-82.

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Background: Diabetes mellitus (DM) is the seventh leading cause of death in the world (the occuring rate has reached 400 million people). Type2 DM is caused by the body cells’ inability to respond normally to insulin (insulin resistance). Homeostatic Model Assessment-Insuline Resistance (HOMA-IR) is a calculation method which function is to measure the body insulin resistance. Diabetes mellitus can cause lipid metabolism disorders (dyslipidemia) resulting in an increased level of LDL cholesterol and decreased HDL cholesterol. The apoprotein B/apoprotein A-I ratio is the result of comparisons of apoprotein B (LDL protein constituent) and apoprotein A-I (HDL protein constituent). The apo B/apo A-I ratio represents a balance between LDL cholesterol (atherogenic) and HDL (anti-atherogenic). It is astrong signifier in predicting heart disease. Purpose: This study aim to determine the correlation between the apoprotein B/apoprotein A-I ratio with HOMA-IR in patients with type 2 diabetes mellitus. Methods: Observasional, consecutive, 100 people with type 2 diabetes mellitus who is examined in apoprotein B, apoprotein A-I test that calculating the ratio in which ratio are calculated, as well as HOMA-IR in Parahita Clinical Laboratory Surabaya. This study uses Pearson correlation test method with SPSS 22.0 for Windows program. Results: The result of Pearson correlation test between apoprotein B/apoprotein A-I ratio with HOMA-IR in 100 samples is a strong and significant correlation value (r=0,610, p<0,05).Conclusion: There is a strong correlation between the apoprotein B/apoprotein A-I ratio with HOMA-IR in patients with type 2 diabetes mellitus.

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Mouly, S., J. F. Bergmann, and P. J. Guillausseau. "Psychological Insuline Resistance. Descriptive Observational Study in 123 Patients with Type 2 Diabetes Mellitus Not Taking Insulin in Paris Area, France." Clinical Therapeutics 39, no. 8 (August 2017): e16. http://dx.doi.org/10.1016/j.clinthera.2017.05.050.

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A.Taher, Mohammed, Waleed R. Sulaiman, and Hillal Y. Al-Khairi. "Rosiglitazone , Metformin or both for Treatment of Polycystic Ovary Syndrome." Iraqi Journal of Pharmaceutical Sciences ( P-ISSN: 1683 - 3597 , E-ISSN : 2521 - 3512) 17, no. 2 (March 30, 2017): 80–86. http://dx.doi.org/10.31351/vol17iss2pp80-86.

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This study was designed to show the advantages of using the combination of metformin and rosiglitazone over using each drug alone in treatment of women with polycystic ovary syndrome (PCOS).Forty four women with PCOS were classified into 3 groups , group 1 received rosiglitazone (4mg/day) for 3 months , group Î™Î™ received metformin ( 1500 mg/day)for three months and groupÎ™Î™Î™ received the combination ( rosiglitazone 4mg/day + metformin 1500 mg/day) for the same period of treatment . The blood samples were drawn before treatment and after 3 months of treatment . The fasting serum glucose , insulin , progesterone , testosterone , leutinizing hormone were measured before and after treatment. The reduction of serum insulin , glucose ,homostasis model assessment of insuline resistance ( HOMA-IR) , LH and testosterone levels were greater in the group received the combination of rosiglitazone with metformin than that those taken each one alone. Testosterone levels decreased significantly (P<0.05) from baseline level 1Â±0.04ng/ml to 0.073Â±0.32ng/ml after treatment with combination.The rate of ovulation is 29.4%,36.4% , 62.5% in rosiglitazone , metformin and combination of both, respectively.The combination of rosiglitazone with metformin has more beneficial effect on ovulation rate. Key words: polycystic ovary syndrome, rosiglitazone, metformin, ovulation rate .

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Kumar, Sinha Ritesh, and Chandra Satish. "Insulin resistance." Asian Pacific Journal of Health Sciences, Supplimentary 2014 (2014): 71–78. http://dx.doi.org/10.21276/apjhs.2014.1.1s.15.

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Wiedemann, Jean Yves, Laurent Jacquemin, Olivier Roth, Ronan Le Bouar, Mahmoud Moussaoui, Jacques Levy, and Jean Pierre Monassier. "048 Unlike hyperglycemia, insulin deficiency and insuline resistance index are not associated with ST-segment resolution after primary percutaneous coronary intervention for acute myocardial infarction." Archives of Cardiovascular Diseases Supplements 3, no. 1 (January 2011): 15–16. http://dx.doi.org/10.1016/s1878-6480(11)70050-7.

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Dissertations / Theses on the topic "Insuline resistance"

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Napolitano, Tiziana. "Confidentiel." Thesis, Université Côte d'Azur (ComUE), 2017. http://www.theses.fr/2017AZUR4141.

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CARTOTTO, DENIS. "Syndrome d'alstrom et insulinoresistance : a propos de trois observations." Aix-Marseille 2, 1988. http://www.theses.fr/1988AIX20367.

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FIMBEL, SYLVIE. "Les troubles endocriniens lies a l'acanthosis nigricans : insulinoresistance et hyperandrogenie ; implications cliniques et physiopathologiques ; a propos de 13 observations." Lyon 1, 1992. http://www.theses.fr/1992LYO1M075.

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Morzyglod, Lucille. "L’adaptateur moléculaire Grb14 contrôle les actions métaboliques et mitogéniques de l’insuline dans le foie." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015PA05T041.

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L'insuline, hormone clé du contrôle de l'homéostasie métabolique, exerce également des effets trophiques sur la croissance et la prolifération cellulaire. Des études épidémiologiques ont récemment montré que les individus obèses ou diabétiques de type 2 ont un risque plus élevé de développer des cancers et elles ont également suggéré que l’insuline jouerait un rôle dans ce développement tumoral. Ainsi, une signalisation adéquate en aval du récepteur de l’insuline est indispensable pour éviter des processus physiopathologiques. La signalisation de l’insuline est contrôlée par des mécanismes de rétrocontrôle, dont l’adaptateur moléculaire Grb14 qui agit comme un inhibiteur endogène de l’activité catalytique du RI. L’objectif de ma thèse a été d’étudier les conséquences métaboliques et mitogéniques de l’inhibition de Grb14 in#vivo spécifiquement dans le foie de souris. Dans une première étude, nous montrons que sept jours après l’invalidation de Grb14, les souris présentent une activation des voies de signalisation de l’insuline, qui s’accompagne d’une amélioration de la tolérance au glucose et de la production hépatique de glucose. Cependant, de façon paradoxale, la voie de la lipogenèse est très fortement diminuée. En décryptant le mécanisme moléculaire impliqué, nous montrons que l’inhibition de Grb14 permet la libération de la protéine p62/sqstm1 qui active le facteur de transcription Nrf2, ce qui entraine une inhibition du récepteur nucléaire pro-lipogénique LXR. De façon intéressante, l’invalidation de Grb14 chez des souris ob/ob permet de restaurer la glycémie et la stéatose hépatiques à des valeurs comparables aux témoins. Cette étude a ainsi permis de mettre en évidence une nouvelle voie de régulation de la lipogenèse hépatique. Dans une deuxième étude, nous nous sommes intéressés à l'action mitogénique de l'insuline. Nous montrons que 48 heures après l'inhibition de Grb14, les hépatocytes, qui sont des cellules quiescentes, entrent massivement dans le cycle cellulaire. Ce processus est dépendant de l’expression du RI et est médié par la signalisation PI3K/Akt/mTORC1 et la voie Rb/E2F1. Ces données révèlent ainsi que l'insuline est un puissant facteur mitogène dans le foie et que son action est étroitement contrôlée par l’adaptateur Grb14. D’un point de vue physiopathologique, nous avons pu mettre en évidence une diminution de significative de 58% de l’expression de Grb14 dans une collection de 70 CHC humains, apportant ainsi une explication moléculaire à une action pro-tumorigène de l’insuline dans le foie. L’ensemble de ces deux études permet de placer Grb14 au centre de la régulation des actions métaboliques et mitogéniques de l’insuline dans le foie
Insulin is a key hormone controling metabolic homeostasis which also exerts having trophic effects on cell growth and proliferation. Epidemiological studies have recently shown that obese and type 2 diabetes patients are at higher risk of developing cancers, suggesting that insulin could be involved in tumor development. Proper signaling downstream the insulin receptor is thus essential to prevent pathophysiological processes. Insulin signaling is controlled by feedback mechanisms including the molecular adapter Grb14 which acts as an endogenous inhibitor of the IR catalytic activity. The aim of my PhD was to investigate the metabolic and mitogenic consequences of liver specific Grb14 inhibition in mouse. In the first study, we showed that after seven days of Grb14 invalidation, liver insulin signaling is enhanced, resulting in improved glucose tolerance and diminished hepatic glucose production. However, paradoxically, lipogenesis was greatly decreased. Deciphering the molecular mechanism, we show that Grb14 inhibition leads to the release of its partner p62/SQSTM1, inducing the activation of the Nrf2 transcription factor, which ultimatly inhibited the pro-lipogenic LXR nuclear receptor. Interestingly, Grb14 invalidation in ob/ob mice can restore blood glucose and hepatic steatosis comparable to control values. The study thus highlighted a new pathway controlling lipogenesis that could be targetted to improve metabolic diseases. In the second study, we were interested in insulin mitogenic action. We showed that 48 hours after Grb14 inhibition, hepatocytes that are quiescent cells, massively go through one cell cycle. This process depend on IR expression and is mediated by the PI3K/Akt/mTORC1 pathway and the Rb/E2F1 complex. Our data thus suggest that insulin is a potent mitogenic factor in the liver whose action is closely controlled by the Grb14 adapter in physiological conditions. Importantly, Grb14 expression is significantly decreased in a collection of human HCC, hence bringing out a molecular basis for a pro-tumorigenic action of hyperinsulinemia. Together these two studies reveal that Grb14 is a crucial gatekeeper of insulin metabolic and mitogenic actions in the liver

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Izard-Sudres, Hélène. "Evaluation de la sensibilité à l'insuline et de l'insulinosécrétion selon la méthode du Minimal Model de Bergman dans une population de sujets obèses." Montpellier 1, 1996. http://www.theses.fr/1996MON11031.

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Papazoglou, Ioannis. "Cross-talk between insulin and serotonin signaling in the brain : Involvement of the PI3K/Akt pathway and behavioral consequences in models of insulin resistance." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T039/document.

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L’insuline et la sérotonine (5-HT) sont deux acteurs majeurs du maintien de l’homéostasie énergétique, fonction placée sous le contrôle de l’hypothalamus. En ciblant cette région, l’insuline remplit de nombreuses fonctions métaboliques via l’activation de la voie PI3K/Akt. La 5-HT exercent des effets biologiques similaires mais les voies de signalisation impliquées dans ces processus étaient jusqu’alors mal connues. De plus, il avait été démontré que la 5-HT est capable d’activer la voie PI3K/Akt/GSK3β dans l’hippocampe, mécanisme sous-tendant potentiellement les effets antidépresseurs du neurotransmetteur. Les principaux objectifs de cette thèse étaient d’étudier 1/ l’activation de la voie PI3K/Akt par la 5-HT dans l’hypothalamus de rats diabétiques (modèle Goto-Kakizaki) et chercher un potentiel dialogue avec l’insuline and 2/ les mécanismes sous-tendant l’induction de la dépression par une alimentation hyperlipidique, par l’analyse de la phosphorylation d’Akt et GSK3β sous l’action de l’insuline, de la leptine et de la 5-HT dans l’hippocampe de rat.Ici on montre que 1/ la 5-HT stimule la voie PI3K/Akt dans l’hypothalamus et que la phosphorylation d’Akt induite par la 5-HT est atténuée dans des conditions d’insulino-résistance, suggérant l’existence d’un dialogue entre les voies de signalisation de l’insuline et de la 5-HT. Par ailleurs, nos résultats indiquent qu’une alimentation hyperlipidique induit un comportement dépressif réversible chez le rat, qui pourrait impliquer la voie PI3K/Akt/GSK3β dans les neurones subgranulaires du gyrus denté. La mise en évidence d’un dialogue entre les voies de signalisation de la 5-HT, de la leptine et de l’insuline au niveau central enrichit nos connaissances sur le rôle de ces facteurs dans la régulation de l’homéostasie énergétique et de l’humeur, et propose un lien moléculaire entre diabète de type 2, obésité et dépression
Insulin and serotonin (5-HT) are two key players in the maintenance of energy homeostasis which is controlled by the hypothalamus. In this brain region, insulin mediates numerous metabolic effects via the activation of the PI3K/Akt signaling pathway. 5-HT exerts similar biological properties by acting in the hypothalamus but the signaling pathways accountable for these effects are still unclear. Moreover, it has been reported that 5-HT induces the activation of the PI3K/Akt pathway in the hippocampus and the inhibition of GSK3β, suggesting this action as a potential mechanism for the antidepressant effects of this neurotransmitter.The main objectives of this thesis were to study 1/ the serotonin-induced activation of the PI3K/Akt in the hypothalamus of wild type and diabetic rats (Goto-Kakizaki model) and search a potential cross-talk with insulin and, 2/ the mechanisms underlying the high-fat diet induced depression by investigating the role of the phosphorylation of Akt and GSK3β by 5-HT, insulin and leptin in the hippocampus of rats.Here, we show that 5-HT triggers the PI3K/Akt signaling pathway in the rat hypothalamus, and that this activation is attenuated in insulin-resistant conditions, suggesting a cross-talk between insulin and 5-HT. Moreover, we reported that high-fat diet feeding induces a reversible depressive-like behavior, which may involve the PI3K/Akt/GSK3β pathway in subgranular neurons of the dentate gyrus. In conclusion, the activation of the PI3K/Akt pathway and its target GSK3β by 5-HT in the hypothalamus and in the dentate gyrus, respectively, can be impaired in insulin-/leptin-resistant states, which may underlie a link between metabolic diseases and depression

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Boisvilliers, Fabienne de. "L'insulinorésistance dans le syndrome des ovaires polykystiques avec acanthosis nigricans : étude clinique et biologique de cinq cas." Montpellier 1, 1992. http://www.theses.fr/1992MON11050.

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Jaecker, Pierre. "Exploration, par le clamp euglycemique hyper-insulinique, de l'insulino-resistance et des consequences de l'hyperinsulinemie sur le metabolisme azote dans la cirrhose." Université Louis Pasteur (Strasbourg) (1971-2008), 1989. http://www.theses.fr/1989STR1M151.

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Guillot, Alexandre. "Couplage "complexe récepteur de l'élastine / récepteur de l'insuline" : la désialylation des glycanes comme facteur d'insulino résistance." Thesis, Reims, 2017. http://www.theses.fr/2017REIMS031/document.

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Longtemps considérée comme un simple support mécanique, la matrice extracellulaire (MEC) est un élément majeur dans le maintien de l’homéostasie. Ainsi l’élastine, principal constituant de la MEC des gros vaisseaux élastiques, est dégradée au cours du vieillissement, produisant ainsi des peptides d’élastine bioactifs (PE). Plusieurs études ont démontré l'implication des PE en physiopathologies tels que l’invasion tumorale, l’athérosclérose ou l’insulino-résistance (IRes). Ces effets s’expliquent par l’activation du complexe récepteur de l’élastine (CRE), composé par : une sous-unité extracellulaire liant les PE (EBP, elastin binding protein), la cathepsine A (dont le rôle reste inconnu), et la neuraminidase 1 (induisant la signalisation intracellulaire). L'IRes décrite, pourrait être associée à l’activité de désialylation de la neuraminidase-1 sur les chaines de N-glycosylation (Ng-c) du récepteur de l’insuline (RI). Sur la base de cette hypothèse, notre objectif a donc été de confirmer ce mécanisme et ses conséquences in silico (sur le RI), in vitro (pré-adipocytes 3T3-L1) et in vivo (aorte de souris). Nous montrons ainsi in vitro que les PE provoquent un dysfonctionnement de l’autophosphorylation du RI se répercutant sur plusieurs processus cellulaires comme l’entrée du glucose ou encore la différenciation adipocytaire. In silico, nous montrons pour la première fois le rôle des acides sialiques sur le comportement des Ng-c d'une part et sur le RI d'autre part. Enfin, in vivo, cette interaction CRE / IR engendre une hypertension artérielle par une diminution de la vasorelaxation des cellules endothéliales
Often considered as a simple mechanical support, the extracellular matrix (ECM) is a major element of homeostasis regulation. Thus, elastin, the main constituent of large elastic vessels, is degraded during aging, producing bioactive elastin-derived-peptides (EDP). Several studies have demonstrated the EDP effects in physiopathologies such as tumor invasion, atherosclerosis, or insulin resistance (IRes) development. Those effects are explained by the activation of the elastin receptor complex (CRE), composed of: an extracellular subunit binding EDP (EBP, elastin binding protein), cathepsin A (its role is still unknown) and the sialidase neuraminidase-1 (Neu-1, involved in signaling pathway induction). Interestingly, the lab suggested that IRes may be induced by the desialylation of the N-glycan chains (Ng-c) on the insulin receptor (IR). The aim of this study was to confirm this hypothesis by demonstrating the consequence of desialylation on the IR in silico, on a 3T3-L1 pre-adipocyte cell in vitro, and on vascular complications in vivo. We show that EDP induce in vitro an impairment of IR autophosphorylation, affecting glucose uptake and adipocyte differentiation. In silico approach demonstrates the role of sialic acids on the behavior of Ng-c in the one hand and in other hand of IR. Finally, the IRes induced by ERC-IR interaction increase the vascular complication such as arterial hypertension by endothelial cell impairment. To conclude, Ng-c alteration would likely be responsible for structural changes in the IR at the origin of insulin resistance

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Guhmann, Pauline. "Délivrance orale d'insuline par double encapsulation : développement et évaluation de l'efficacité et de la sécurité des systèmes entériques et nanoparticulaires." Phd thesis, Université de Strasbourg, 2013. http://tel.archives-ouvertes.fr/tel-01071851.

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Actuellement, l'injection sous-cutanée d'insuline est le seul moyen pour les diabétiques de type 1 d'équilibrer leur glycémie. Les travaux de thèse entrent dans le cadre du projet ORAIL qui vise à développer un système de délivrance orale d'insuline basé sur la double encapsulation, et à valider l'efficacité et la sécurité de ce système in vitro dans des modèles d'épithélium intestinal, et in vivo chez le rat. Le vecteur pharmaceutique développé est composé d'une gélule contenant des nanoparticules (NPs) d'insuline formulées à partir d'acide (lactique-co-glycolique) par la méthode de double émulsion eau/huile/eau. Un premier objectif de la thèse a été d'évaluer chez le rat la gastrorésistance et l'entérosolubilité de la gélule sélectionnée pour l'encapsulation des NPs, par tomodensitométrie aux rayons X et par l'étude de la biodisponibilité de l'ibuprofène et de l'acétaminophène. Les résultats de ces travaux ont montré que la gélule est résistante en conditions gastriques et se dégrade au niveau de l'intestin. Un deuxième objectif a été de synthétiser des NPs d'insuline de taille croissante (100 à 800 nm), et d'évaluer l'internalisation de ces NPs et leur sécurité dans des cultures de cellules Caco-2, et dans des co-cultures de cellules Caco-2 et HT29-MTX. Les résultats de ces travaux ont montré que les NPs sont internalisées de manière dose et temps-dépendante, et que la taille de NPs permettant une internalisation optimale est de 400 nm après 4h d'incubation. Des études mécanistiques ont suggéré l'implication de mécanismes cavéoline-dépendants dans l'internalisation des NPs. Aucune toxicité des NPs n'a été observée quels que soient les paramètres étudiés (viabilité et mort cellulaire, augmentation de perméabilité, production de mucus, sécrétion de cytokines pro-inflammatoires). Dans une dernière partie de notre travail, nous avons montré que l'administration intraduodénale de NPs d'insuline de 200 et 400 nm à des rats diabétiques permettait une diminution significative de leur glycémie sans altération morphologique de leur paroi intestinale, données confortant nos résultats in vitro. Notre vecteur basé sur la double encapsulation semble donc être un système prometteur pour l'administration orale d'insuline. Le vecteur complet doit cependant être évalué in vivo chez le rat.

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Books on the topic "Insuline resistance"

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Reaven, Gerald M., and Ami Laws, eds. Insulin Resistance. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1.

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Zeitler, Philip Scott, and Kristen J. Nadeau, eds. Insulin Resistance. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-192-5.

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Krentz, Andrew J., ed. Insulin Resistance. Oxford, UK: Blackwell Science Ltd, 2002. http://dx.doi.org/10.1002/9780470698921.

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Kumar, Sudhesh, and Stephen O'Rahilly, eds. Insulin Resistance. Chichester, UK: John Wiley & Sons, Ltd, 2004. http://dx.doi.org/10.1002/0470011327.

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Zeitler, Philip S., and Kristen J. Nadeau, eds. Insulin Resistance. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-25057-7.

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Heller, Richard F. Vaincre la dépendance aux glucides: Programme pour un coeur en santé : triomphez du rapport glucides-insuline à l'origine des maladies coronariennes. Varennes, Québec: Éditions AdA, 2002.

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Ulf, Smith, ed. Hypertension as an insulin-resistant disorder: Genetic factors and cellular mechanisms : proceedings of the 5th Novo Nordisk Foundation Symposium "Hypertension as an insulin-resistant disorder--genetic factors and cellular mechanisms," Copenhagen, Denmark, 1-3 July 1991. Amsterdam: Excerpta Medica, 1991.

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Fantus, I. George, ed. Insulin Resistance and Cancer. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9911-5.

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Swan, Jonathan William. Insulin resistance and heart disease. Manchester: University of Manchester, 1994.

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Krentz, Andrew J. Metabolic studies in insulin resistance. Birmingham: University of Birmingham, 1991.

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Book chapters on the topic "Insuline resistance"

1

Stern, Michael P., and Braxton D. Mitchell. "Genetics of Insulin Resistance." In Insulin Resistance, 3–18. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1_1.

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Mandarino, Lawrence J. "Skeletal Muscle Insulin Resistance in Humans: Cellular Mechanisms." In Insulin Resistance, 179–95. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1_10.

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Radziuk, Jerry, and Susan Pye. "The Role of the Liver in Insulin Action and Resistance." In Insulin Resistance, 197–231. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1_11.

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Reaven, Gerald M. "The Pathophysiological Consequences of Adipose Tissue Insulin Resistance." In Insulin Resistance, 233–46. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1_12.

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Baron, Alain D., and Michael J. Quon. "Insulin Action and Endothelial Function." In Insulin Resistance, 247–63. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1_13.

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Laws, Ami. "Insulin Resistance and Dyslipidemia: Implications for Coronary Heart Disease Risk." In Insulin Resistance, 267–80. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1_14.

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Ferrannini, Ele. "Insulin Resistance and Blood Pressure." In Insulin Resistance, 281–308. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1_15.

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Yip, Jeannie, and Roberto Trevisan. "Microalbuminuria and Insulin Resistance." In Insulin Resistance, 309–16. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1_16.

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Juhan-Vague, Irène, Marie-Christine Alessi, and Pierre E. Morange. "PAI-1, Obesity, and Insulin Resistance." In Insulin Resistance, 317–32. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1_17.

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Folsom, Aaron R. "Insulin Resistance and Cardiovascular Disease." In Insulin Resistance, 333–46. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1_18.

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Conference papers on the topic "Insuline resistance"

1

Al-Jaber, Hend Sultan, Layla Jadea Al-Mansoori, and Mohamed Aghar Elrayess. "The Role of GATA3 in Adipogenesis & Insulin Resistance." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0143.

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Background: Impaired adipogenesis plays an important role in the development of obesityassociated insulin resistance and type 2 diabetes. Adipose tissue inflammation is a crucial mediator of this process. In hyperglycemia, immune system is activated partially through upregulation of GATA3, causing exacerbation of the inflammatory state associated with obesity. GATA3 also plays a role as a gatekeeper of terminal adipocyte differentiation. Here we are examining the impact of GATA3 inhibition in adipose tissue on restoring adipogenesis, reversing insulin resistance and potentially lowering the risk of type 2 diabetes. Results: GATA-3 expression was higher in insulin resistant obese individuals compared to their insulin sensitive counterparts. Targeting GATA-3 with GATA-3 specific inhibitors reversed impaired adipogenesis and induced changes in the expression of a number insulin signaling-related genes, including up-regulation of insulin sensitivity-related gene and down-regulation of insulin resistance-related genes. Conclusion: GATA3 expression is higher in differentiating adipocytes from obese insulin resistant. Inhibiting GATA3 improves adipocytes differentiation and rescues insulin sensitivity in insulin resistant cells

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Goodwin, P. "Obesity, Insulin Resistance and Insulin." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-ms2-1.

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Aldali, Sara Haitham, and Sownd Sankaralingam. "Induction of Glyoxalase 1 to prevent Methylglyoxal-Induced Insulin Resistance in Cardiomyocytes." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0230.

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Background: Type 2 Diabetes mellitus is characterized by hyperglycemia and insulin resistance. Methylglyoxal (MG) a highly reactive dicarbonyl compound is also increased in diabetes. MG is detoxified by glyoxalase 1 (Glo-1) enzyme using reduced glutathione (GSH) as a co-factor. MG has been shown to have deleterious effects on cardiovascular cells and impairs insulin signaling. Insulin resistance is associated with diabetic cardiomyopathy. Trans-resveratrol (tRES) and Hesperetin (HES) combination has been shown to increase Glo-1 and improve insulin signaling in obese patients. Aim(s): The aim of this study is to investigate whether tRES-HES combination prevents MG-induced cardiac insulin resistance and the underlying mechanisms in cardiomyocytes in culture. Methodology: (H9C2) rat cardiomyocytes were treated with MG (100 µM) for 24 hours in the presence or absence of tRES-HES (10 µM). Glo-1 activity was determined by the formation of S-D lactoylglutathione; protein expression of P-Akt and P-GSK3b was determined using Western blot. In some experiments, cells were stimulated with insulin (100 nM) for 10 minutes to test insulin sensitivity. Results: MG reduced Glo-1 activity by ~25%, blunted insulin-induced phosphorylation of Akt and Gsk3b and increased the expression of beta-myosin heavy chain by ~50% (a marker of cardiac dysfunction) significantly (P˂0.05) compared to untreated control group of cells. Co-administration of tRES-HES combination restored Glo1 activity, maintained insulin-induced phosphorylation of Akt and GSK3b and prevented the increase in beta myosin heavy chain significantly (P<0.05). Conclusion: Induction of Glo1 prevents MG-induced cardiac insulin resistance and the increase in marker of cardiac dysfunction. This strategy could be helpful in preventing cardiovascular complications associated with diabetes.

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Senhorinha, Gláucia Maria, Arlys Emanuel Mendes da Silva Santos, and Douglas Daniel Dophine. "The role of metabolic syndrome in Alzheimer’s disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.319.

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Background: Metabolic syndrome (MS) leads to the deposits formation of insoluble protein aggregates, neuroinflammation, oxidative stress, neuronal insulin resistance, progressive insulin resistance, desensitization and β-amyloid amyloidosis in the brain, besides direct ischemic effects which are closely associated with Alzheimer’s disease (AD).1 Objectives: The present study seeks to understand the role of the metabolic syndrome in the pathophysiology of Alzheimer’s disease and to describe preventive and therapeutic interventions. Methods: PUBMED and Web of Science were the databases used, the following descriptors were used to search the articles: “Alzheimer Disease” OR “Alzheimer Dementia” AND “Metabolic Syndrome”. Results: The studies in general have shown that MS is related to AD through brain insulin resistance, triggered by oxidative stress and neuroinflammation. It is related to the progressive atrophy of brain regions involved in the progression of AD. Insulin resistance in the brain is related to the progressive atrophy of the brain regions from initial progression of AD. These regions are cingulate cortices, medial temporal lobe, prefrontal gyri and other regions.³ Thus, there is an inhibition of the mechanisms of beta-amyloid removal, leading to its accumulation, which generates neuroinflammation, that in turn potentiates insulin resistance in the central nervous system, contributing to the genesis and progression of cognitive damage.2,3 Conclusions: Insulin resistance plays a major role in the initiation and perpetuation of cognitive impairment in AD. Furthermore, the components of the MS associated with AD, when treated with preventive and therapeutic measures, break this association by promoting rebalancing of the metabolism.

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Christopher, Pretty,. "Corticosteroids and Insulin Resistance in the ICU." In Modeling and Control in Biomedical Systems, edited by Rees, Stephen, chair Andreassen, Steen and Andreassen, Steen. Elsevier, 2009. http://dx.doi.org/10.3182/20090812-3-dk-2006.00005.

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"Genetic Variations in Women with Insulin Resistance." In International Institute of Chemical, Biological & Environmental Engineering. International Institute of Chemical, Biological & Environmental Engineering, 2015. http://dx.doi.org/10.15242/iicbe.c0615079.

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Altuve, Miguel, Erika Severeyn, and Sara Wong. "Unsupervised subjects classification using insulin and glucose data for insulin resistance assessment." In 2015 20th Symposium on Signal Processing, Images and Computer Vision (STSIVA). IEEE, 2015. http://dx.doi.org/10.1109/stsiva.2015.7330444.

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Nogueira, Fábio Dias, Ana Klara Rodrigues Alves, Barbara Beatriz Lira da Silva, Ana Kamila Rodrigues Alves, Marlilia Moura Coelho Sousa, Ana Karla Rodrigues Alves, Wanderson da Silva Nery, Breno Carvalho de Almeida, Flávia Dias Nogueira, and Leiz Maria Costa Véras. "The relationship of diabetes mellitus with Alzheimer’s disease: a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.280.

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Introduction: Alzheimer’s disease (AD) is closely related to diabetes mellitus (DM), and AD is also considered to be type 3 diabetes (T3D). Glycogen synthase kinase-3β (GSK-3β) may be the potential link between DM and AD. GSK-3β is one of the main factors that lead to insulin deficiency and insulin resistance, and insulin resistance is a characteristic of the development of DM. In AD, GSK-3β plays an important role in hyperphosphorylation of the tau protein (tau) associated with microtubules, which is one of the pathological features in AD. Objective: To analyze DM as a factor for the development of AD. METHODOLOGY: This is an integrative review of the literature, which is a construction of a comprehensive analysis of the literature with pre-defined steps, carried out through PubMed, 1.501 articles were found, of which 10 were selected, through the simultaneous crossing between the descriptors “Diabetes mellitus”, “Alzheimer “. Articles written in Portuguese and English published between 2016 and 2021 were inserted. Results: DM associated with insulin resistance affects psychomotor efficiency, attention, learning memory, mental flexibility, speed and executive function of the brain, thus being an independent risk factor for cognitive impairment and damage to the central nervous system, hyperglycemia, which can cause increased oxidative stress leading to progressive functional and structural abnormalities in the brain. Conclusion:The risk of dementia in patients with DM is higher than in nondiabetic patients and it is also well known that DM2 / insulin resistance is involved in AD.

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Abogamal, A., E. Mahmoud, S. Abdulhakiem, S. Abdelatif, and A. Abdelaziz. "FRI0482 Insulin resistance in patients with psoriatic arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5165.

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Forstner, Thomas, Christiane Dienhart, Ludmilla Kedenko, Gernot Wolkersdörfer, and Bernhard Paulweber. "Models for Predicting the Development of Insulin Resistance." In 6th International Conference on Data Science, Technology and Applications. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0006344801210125.

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Reports on the topic "Insuline resistance"

1

Malin, Alecia, Wei Zheng, and Herbert Yu. Insulin Resistance, IGFs and Energy Balance on the Risk of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada406834.

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Olefsky, Jerrold. Role of Inflammation and Insulin Resistance in Mouse Models of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada580520.

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Gao, Hui, Dan Chen, and Miao Zang. Association between phthalate exposure and insulin resistance: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2021. http://dx.doi.org/10.37766/inplasy2021.4.0026.

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Cai, Wangyu, and Jian Xu. Insulin resistance in women with recurrent miscarriage: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2021. http://dx.doi.org/10.37766/inplasy2021.11.0055.

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Zhao, Junyu, Qianping Zhang, Yupeng Yang, Jinming Yao, Lin Liao, and Jianjun Dong. High Prevalence of Thyroid Carcinoma in Patients with Insulin Resistance: A Meta-analysis of Case-control Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0043.

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Miao, Chenyun, Qingge Guo, Xiaojie Fang, Yun Chen, Ying Zhao, and Qin Zhang. Effects of Probiotics and Synbiotics Supplementation on Insulin Resistance in Women with Polycystic Ovary Syndrome: A Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2021. http://dx.doi.org/10.37766/inplasy2021.5.0112.

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Podgorski, Izabela. Biochemical and Genetic Markers in Aggressiveness and Recurrence of Prostate Cancer: Race-Specific Links to Inflammation and Insulin Resistance. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada566642.

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HE, QINGQING, and CHANGQIANG LI. The effect of isotretinoin in the treatment of acne vulgaris on insulin resistance: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2021. http://dx.doi.org/10.37766/inplasy2021.9.0065.

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Fagan, Dedra. Type-I Insulin-Like Growth Factor Receptor (IGF1R)-Estrogen Receptor (ER) Crosstalk Contributes to Antiestrogen Therapy Resistance in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, February 2013. http://dx.doi.org/10.21236/ada575846.

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Yao, Jia, Jia Zhao, Zhaojun Yang, Yuping Lin, Qiyun Lu, Wenwen Xie, Jianxuan Wen, and Guanjie Fan. Flavonoids on insulin resistance in overweight and obesity subjects: protocol for a systematic review and meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2022. http://dx.doi.org/10.37766/inplasy2022.2.0011.

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