Добірка наукової літератури з теми "Insulines"

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Статті в журналах з теми "Insulines":

1

Faure, Sébastien. "Insulines." Actualités Pharmaceutiques 51, no. 512 (January 2012): 49–54. http://dx.doi.org/10.1016/s0515-3700(12)71130-8.

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de Klaver, P. A. G. "Nieuwe insulines en nieuwe toedieningswegen van insulines." Medisch-Farmaceutische Mededelingen 47, no. 7 (July 2009): 107–8. http://dx.doi.org/10.1007/bf03079996.

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Battu, Valérie. "Les insulines." Actualités Pharmaceutiques 52, no. 530 (November 2013): 55–59. http://dx.doi.org/10.1016/j.actpha.2013.09.013.

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Fougere, Édouard. "Les insulines." Actualités Pharmaceutiques 60, no. 606 (May 2021): 55–57. http://dx.doi.org/10.1016/j.actpha.2021.03.021.

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Messaad, Djamel, Omar Outtas, and Pascal Demoly. "Hypersensibilité aux insulines." La Presse Médicale 33, no. 9 (May 2004): 631–38. http://dx.doi.org/10.1016/s0755-4982(04)98691-5.

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Waton, J., and A. Barbaud. "Comment tester les insulines ?" Revue Française d'Allergologie 52, no. 3 (April 2012): 280. http://dx.doi.org/10.1016/j.reval.2012.02.082.

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Halimi, S., N. Wion, A. L. Coulon, and P. Y. Benhamou. "Les insulines, ultra-rapides, et techniques pour accélérer l’action des insulines rapides." Médecine des Maladies Métaboliques 8, no. 2 (April 2014): 125–32. http://dx.doi.org/10.1016/s1957-2557(14)70724-2.

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M, J. M. "Insulines : après Lantus®, U300." Revue Francophone des Laboratoires 2014, no. 460 (March 2014): 15. http://dx.doi.org/10.1016/s1773-035x(14)72385-8.

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Halimi, S. "Avant-propos: Les insulines, demain." Médecine des Maladies Métaboliques 8, no. 2 (April 2014): 123. http://dx.doi.org/10.1016/s1957-2557(14)70723-0.

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Ekelmans, Nathalie. "Zorgen over preferentiebeleid (biosimilar) insulines." Nederlands Tijdschrift voor Diabetologie 19, no. 1 (March 2021): 18–21. http://dx.doi.org/10.1007/s12467-021-0615-8.

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Дисертації з теми "Insulines":

1

Gilles, Christophe. "Pharmacocinétique des insulines injectées seules ou en mélange : étude par clamp euglycémique et pancréas artificiel." Paris 5, 1988. http://www.theses.fr/1988PA05P029.

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Cohen, Benjamin. "Analyse des profils pharmacocinetiques des insulines porcine et hemi-synthetique humaine a action rapide." Université Louis Pasteur (Strasbourg) (1971-2008), 1985. http://www.theses.fr/1985STR1M060.

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3

Meschi, Eleonora. "Identification de populations neuronales contrôlant la sécrétion des insulines et la croissance en fonction de la nutrition chez Drosophila melanogaster." Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4088/document.

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La taille finale des organismes dépend de la vitesse et de la durée de croissance. Ces paramètres sont contrôlés par différentes hormones. La production d'hormone stéroïdienne détermine la fin de la période de croissance en déclenchant la maturité sexuelle, alors que la vitesse de croissance est régulée par la voie de signalisation de l’insuline/IGF (IIS). La vitesse de croissance des organismes est influencée par la nutrition. En effet, des défauts de croissance sont observés chez les individus souffrant de carence protéique chronique. La nutrition contrôle la croissance grâce à la voie de signalisation de l’insuline/IGF. Cependant, le mécanisme par lequel la nutrition contrôle la voie IIS est complexe et reste à élucider. Afin d’explorer cette régulation, le laboratoire utilise Drosophila melanogaster comme modèle d’étude. Chez la drosophile, il existe 8 insulin-like peptides (Dilps). Parmi eux, Dilp2 est la principale insuline promouvant la croissance systémique. Elle est produite par des neurones spécialisés appelés les Insulin Producing Cells (IPC), homologues des cellules béta du pancréas. La sécrétion de Dilp2 dans l’hémolymphe, équivalent du sang chez les vertébrés, est précisément ajustée en fonction de la nutrition. Cette régulation implique une communication inter-organe avec le corps gras, homologue du foie et du tissu adipeux blanc. Selon les conditions nutritionnelles, plusieurs signaux dérivés du corps gras (FDS) sont sécrétés et contrôlent la sécrétion de Dilp2. Ces FDS agissent directement ou indirectement sur les IPCs, via des relais neuronaux. Mon projet de thèse avait pour but de découvrir et d’étudier de nouvelles cibles neuronales contrôlant l’activité sécrétrice des IPCs, et par conséquent la croissance systémique, en fonction de la nutrition. J’ai identifié une paire de neurones inhibiteurs des IPCs, que l’on a nommé IPC-Connecting Neurons (ICN). Actifs en carence en acides aminés, ils inhibent la sécrétion des Dilps. J’ai montré que la signalisation EGFR réprime l’activité de ces neurones en condition nourrie, ce qui augmente la sécrétion des Dilps et par conséquent la taille des individus. Cette activation est due à un nouveau ligand d’EGFR : Growth Blocking Peptide (GBP). J’ai montré que ce ligand de type EGF possède des propriétés particulières puisqu’il agit de façon endocrinienne. En effet, en condition nourrie, GBP est sécrété par le corps gras dans l’hémolymphe, et atteint les ICN afin d’activer la signalisation EGFR. En conclusion, nous proposons que GBP produit par le corps gras en condition nourrie active la voie EGFR dans les neurones ICN, lève l’inhibition exercée sur les IPCs et stimule la sécrétion des Dilps. Cependant, les mécanismes moléculaires par lequel le couple GBP/EGFR inhibe l’activité neuronale des ICNs reste à élucider. Ce travail a permis d’identifier un nouveau mode de régulation de la sécrétion des insulines et de la croissance des organismes en fonction de la disponibilité et de la qualité nutritionnelle
Body growth is tightly regulated by nutrient availability. Upon nutritional shortage, animals harmoniously reduce their body size by modulating the activity of the insulin/IGF signaling pathway (IIS). To understand how nutrition controls the IIS, we used Drosophila melanogaster as a model. Drosophila has a conserved IIS with 8 insulin-like peptides (Dilps), a unique insulin receptor and a conserved downstream signaling cascade. Among the Dilps, Dilp2 is the main growth-promoting factor. Dilp2 is produced by specialized neurons located in the brain, the Insulin-Producing-Cells (IPCs), functionally related to vertebrate beta cells. Dilp2 secretion is precisely adjusted in response to nutrition: it is released in the hemolymph under normal nutrient condition, but not upon dietary amino acid scarcity. This regulation requires several inter-organ cross-talks between the producing neurons and the fat body, which is the equivalent of the vertebrate white adipose tissue and liver. Depending on diet composition, several fat-derived signals (FDS) are secreted into the hemolymph and control Dilp2 secretion from the IPCs. These FDS act either directly or indirectly through a neuronal relay, to control the IPCs secretory activity. The aim of my PhD project was to better understand these regulations and to discover new neuronal relay controlling the IPCs secretory activity and body growth, according to nutrition. I identified a pair of neurons harboring synaptic connections with the IPCs (IPC-connecting neurons, ICNs). I determined that the ICNs activity is maximal upon amino acids shortage and is required to exert a blockage of the neighbouring IPCs. Moreover, in rich nutrient conditions, EGFR signaling prevents activation of the ICNs, allowing Dilp2 release from the IPCs. GBP1 and 2 are EGF-like peptides produced by the fat body in response to amino acids, and they can modify insulin release. However, the neural circuitries at play are unknown. I demonstrated that GBPs are atypical ligands for the EGF receptor (EGFR), with endocrine function. Using ex-vivo brain culture, I showed that the presence of the fat body-derived GBP1 in the hemolymph activates EGFR signaling in the ICNs and alleviates their inhibitory input on the IPCs, allowing Dilp2 release and therefore body growth. In conclusion, I identified a novel neural circuitry responding to fat-derived EGF-like GBPs, coupling dietary amino acids to the release of insulin-like peptides and systemic growth
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Dumond, François. "Etude de cocktails insuliniques dans le traitement du diabète sucré : étude de l'interaction des insulines ordinaire et NPH après mélange dans une même seringue avant l'injection." Montpellier 1, 1989. http://www.theses.fr/1989MON11086.

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5

Bornaque, Florine. "Rôle de l'épitranscriptome dans la physiopathologie de la cellule β pancréatique". Electronic Thesis or Diss., Université de Lille (2018-2021), 2021. https://pepite-depot.univ-lille.fr/ToutIDP/EDBSL/2021/2021LILUS059.pdf.

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La prévalence du diabète dans le monde ne cesse d’augmenter, avec une estimation de 700 millions de malades en 2045. La compréhension des mécanismes impliqués dans le développement de la maladie est devenue un enjeu majeur de santé publique pour limiter la progression du diabète dans le monde.Le diabète de type 2 (DT2) se caractérise par une hyperglycémie chronique causée par une résistance à l’insuline des tissus périphériques et une perte de fonction et/ou de masse des cellules β pancréatiques. Ces cellules, présentes dans les îlots de Langerhans, interviennent dans la régulation de l’homéostasie glucidique en sécrétant de l’insuline, une hormone hypoglycémiante qui agit sur différents tissus, comme le foie, le muscle ou le tissu adipeux. Le dysfonctionnement physiopathologique des cellules β, suite à de nombreux stress cellulaires (stress oxydatif, stress du réticulum endoplasmique, inflammation), est à l’origine du développement du DT2.Outre les facteurs génétiques, l’obésité induite par un régime riche en graisses et en glucides, l’inactivité physique et le vieillissement sont considérés comme des facteurs de risques environnementaux majeurs du développement du DT2. Ces facteurs peuvent induire des modifications épigénétiques sur l’ADN (méthylation des cytosines) ou les histones (acétylation, méthylation, phosphorylation, ubiquitination), altérant l’expression des gènes.D’autres aspects de la régulation de l'expression des gènes sont peu étudiés dans le contexte du diabète de type 2. En effet, les ARN peuvent également être soumis à des modifications chimiques sensibles aux signaux environnementaux, comme pour l'ADN. Ces modifications épitranscriptomiques, correspondent à l’ensemble des modifications chimiques et réversibles de l’ARN, la plus répandue étant la méthylation m6A, en position N6 de l’adénosine. Le groupement méthyle est ajouté par un complexe protéique composé, notamment, des méthyltransférases METTL3 et METTL14 et peut être retiré par les déméthylases ALKBH5 ou FTO. Ces modifications pourront être reconnues par des protéines cytoplasmiques ou nucléaires, qui affecteront la traduction, l’épissage, la stabilité, la structure ou la localisation des ARN.Cette modification intervient dans de nombreux processus physiologiques et physiopathologiques. Toutefois, son rôle au cours du DT2 est encore peu connu, même s’il a été récemment démontré que la méthylation m6A pouvait être altérée dans l’îlot pancréatique et affecter la sécrétion d’insuline.Nous avons émis l'hypothèse que l'environnement, par le biais de variations de la glycémie ou des concentrations d'acides gras libres dans le sang, pourrait induire des changements de la méthylation m6A des ARN et conduire au dysfonctionnement des cellules β pancréatiques au cours du DT2.Les résultats obtenus au cours de cette thèse montrent une diminution significative de la méthylation m6A en présence d'une concentration élevée de glucose, chez la souris et dans des îlots obtenus de donneurs humains, associée à une augmentation d'expression des déméthylases m6A. Le palmitate induit l’effet inverse avec une augmentation de la méthylation m6A et une réduction d’expression des déméthylases. De plus, l'utilisation de siRNA et d'inhibiteurs spécifiques démontre que ces enzymes modulent l'expression de gènes impliqués dans l'identité des cellules β et la sécrétion d'insuline stimulée par le glucose.Ces résultats, associés aux données de la littérature, suggèrent que les variations en glucose régulent la méthylation m6A, qui joue un rôle clé dans le contrôle de l'expression des gènes de l’identité et de la fonction des cellules β pancréatiques. Nos résultats mettent en évidence de nouveaux mécanismes potentiellement impliqués dans la physiopathologie du diabète de type 2 et peuvent donc contribuer à une meilleure compréhension de l'étiologie de cette maladie
The prevalence of diabetes in the world continues to increase, with an estimate of 700 million patients by 2045. Understanding the mechanisms involved in the development of the disease has become a major public health issue to prevent the progression of diabetes in the world.Type 2 diabetes (T2D) is characterized by chronic hyperglycemia (> 1.26 g / L) caused by insulin resistance in peripheral tissues and loss of function and / or mass of pancreatic β cells. These cells, present in the islets of Langerhans, are involved in the regulation of carbohydrate homeostasis by secreting insulin, a hypoglycemic hormone that acts on various tissues sensitive to insulin, such as the liver, muscle or adipose tissue. The pathophysiological dysfunction of β cells, following numerous cellular stresses (oxidative stress, endoplasmic reticulum stress, inflammation, etc.), is at the origin of the development of T2D.In addition to genetic factors, obesity induced by a diet rich in fats and sugars, physical inactivity and aging are considered to be major environmental risk factors for the development of T2DM. These factors modify the environment of the cells and cause chemical modifications of DNA (methylation of cytosines) or histones (acetylation, methylation, phosphorylation, ubiquitination), called epigenetic modifications, thus modulating the expression of many genes and altering, in particular, the identity or function of pancreatic β cells.Other aspects of the regulation of gene expression are little studied in the context of type 2 diabetes. Indeed, RNAs can also be subjected to chemical changes sensitive to environmental signals, such as DNA. These epitranscriptomic modifications correspond to the chemical and reversible modifications of RNA, the most common is m6A methylation, at position N6 of adenosine. The methyl group is added by a protein complex composed in particular of methyltransferases METTL3 and METTL14 and can be removed by demethylases ALKBH5 or FTO. These modifications can be recognized by cytoplasmic or nuclear proteins, which will affect the translation, splicing, stability, structure or localization of RNAs.This modification is involved in many physiological and pathophysiological processes. However, its role in T2D is still poorly understood, although it has recently been shown that m6A methylation may be altered in the pancreatic islet and affect insulin secretion.Thus, in this thesis work, we hypothesized that the environment, through variations in glycemia or free fatty acid concentrations in the blood, could induce changes in the m6A methylation of RNAs and lead to pancreatic β cell dysfunction during T2D.The results obtained during this thesis show a significant decrease in m6A methylation in the presence of a high concentration of glucose, both in mice and in islets obtained from human donors, associated with altered expression levels of m6A demethylases. Palmitate induces the opposite effect with an increase in m6A methylation and a reduction in the expression of demethylases. In addition, the use of siRNA and/or specific inhibitors demonstrates that these enzymes modulate the expression of genes involved in the identity of pancreatic β cells and insulin secretion stimulated by glucose.These results, combined with data from the literature, suggest that changes in glucose concentration regulate m6A methylation, which plays a key role in controlling gene expression for the identity and function of pancreatic β cells. Thus, our results highlight new mechanisms potentially involved in the pathophysiology of type 2 diabetes and may therefore contribute to a better understanding of the etiology of this disease
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Guarilha, Alessandra Lia Gasparetti. "Transdução do sinal da insulina em animais expostos ao frio : o papel do cross-talk entre o receptor 'beta' 3 - adrenergico e o receptor de insulina em tecido adiposo marrom." PublishedVersion, [s.n.], 2004. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310365.

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Анотація:
Orientador: Licio Augusto Velloso
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: A exposição de animais homeotérmicos ao mo é utilizada como um método reprodutível para se obter um modelo animal de hipoinsulinemiaacompanhada por elevada mobilização periférica de glicose. No presente estudo, avaliaram-se as etapas iniciais e intermediárias da via de sinalização da insulina em tecidos periféricos de ratos expostos ao mo. Avaliou-se ainda, a comunicação intracelular entre o receptor (33-adrenérgicoe as vias de sinalização da insulina em tecido adiposo marrom de ratos expostos ao mo e tratados, ou não, com compostos agonista ou antagonista (33-adrenérgicos.A exposição de ratos ao mo promoveu a redução da secreção de insulina, acompanhada de um elevado clearance de glicose e maior captação de glicose por tecido muscular esquelético, adiposo branco e adiposo marrom. Tais fenômenos foram acompanhados por inibição da ativação da maior parte dos componentes da via de sinalização da insulina em tecido muscular esquelético e adiposo branco; por estimulação da maior parte dos componentes da via de sinalização da insulina em tecido adiposo marrom; e por efeitos variados (estímulo, inibição e não-modulação) de componentes da via de sinalização da insulina em figado. Por fim, este estudo demonstrou que a exposição ao mo ativa a sinalização (33-adrenérgicaem tecido adiposo marrom. Tal ativação leva à modulação da atividade de vários componentes da via de sinalização da insulina neste tecido. Entretanto, fatores independentes da sinalização (33-adrenérgica parecem contribuir para a complexa regulação do sinal da insulina obseIVada em tecido adiposo marrom de ratos expostos ao mo. Em conclusão, o presente estudo revelou alguns dos intrincados mecanismos pelos quais a exposição ao mo controla a atividade da insulina em animais homeotérmicos, podendo favorecer a identificação de potenciais alvos para a ação terapêutica em doenças onde a resistência à insulina desempenha papel central
Abstract: Cold exposure provides a reproducible model of improved glucose turnover accompanied by reduced blood levels of insulin. In the present study, the initial and intermediate steps of the insulin-signaling pathway in peripheral tissues of rats exposed to cold environment were evaluated. Also, the intracellular connection between insulin and ~3-adrenergic signaling in brown adipose tissue of cold exposed rats treated, or not, with ~3-adrenergic agonist or antagonist compounds were evaluated. During cold exposure, insulin secretion was significantly impaired, while whole body glucose clearance rates were significantly improved. This was accompanied by an increased glucose uptake by skeletal muscle, white adipose tissue and brown adipose tissue. These phenomena were paralleled by an apparent molecular resistance to insulin in skeletal muscle and white adipose tissue; by improved molecular response to insulin in brown adipose tissue; and by ambiguous effects (stimulation, inhibition and not modulation) of regulation of the insulin-signaling pathway in liver. Finally, cold exposure activated the ~3-adrenergic signaling in brown adipose tissue. It leads to modulation of activity of several components of the insulin signal transduction pathway in this tissue. However, ~3-adrenergic receptor independent mechanisms seem to contribute to the complex regulation of the insulin signaling observed in brown adipose tissue of rats exposed to cold. In conclusion, the present study revealed some of the complex mechanisms that participate in the cold-exposure-induced control of the insulin action in homeothermic animals. These results may favour the identification of novel potential targets for therapeutics in diabetes and related disorders
Doutorado
Medicina Experimental
Doutor em Fisiopatologia Medica
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Lagarrigue, Sylviane. "Implication de la kinase CDK4 dans la biologie de l'adipocyte." Electronic Thesis or Diss., Montpellier 1, 2013. http://www.theses.fr/2013MON1T030.

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CDK4 est une sérine/thréonine kinase qui est largement décrite pour son implication dans le contrôle du cycle cellulaire. Notre laboratoire et d'autres ont montré qu'elle jouait également un rôle majeur dans le contrôle de l'homéostasie du glucose (croissance des cellules β du pancréas et sécrétion d'insuline) et des lipides (adipogenèse). Nous avons montré au cours de cette thèse, par le biais de deux modèles de souris, invalidés pour CDK4 (Cdk4-/- ;cre/cre) ou exprimant un mutant hyperactif de la kinase (Cdk4R24C/R24C), qu'elle est un médiateur important de la voie de l'insuline et régule la lipogenèse et la lipolyse. Les souris Cdk4-/- ;cre/cre ont une diminution significative de la taille des adipocytes et du poids du WAT ou l'inverse est observé sur les souris Cdk4R24C/R24C. CDK4 est activée par l'insuline et va ainsi promouvoir le transport de glucose, la synthèse des lipides de novo et réprimer la lipolyse dans les adipocytes. De plus, nous avons démontré que dans l'adipocyte, cellule non proliférative, CDK4 et son partenaire la cycline D3 sont préférentiellement localisés dans le cytoplasme suggérant un rôle indépendant de leurs fonctions nucléaires. Nous avons identifié deux nouveaux substrats de CDK4 : IRS1 et IRS2. CDK4 phosphoryle IRS1 et IRS2 activant un rétrocontrôle positif permettant le maintien de l'action de l'insuline sur les adipocytes. Nos résultats prouvent un nouveau rôle de CDK4 sur la signalisation de l'insuline et sa fonction dans l'adipocyte. Par conséquent, la modulation de son activité pourrait avoir des conséquences majeures sur le mécanisme de résistance à l'insuline, une complication fréquente dans le développement de pathologies comme le diabète et l'obésité
CDK4 is a serine/threonine kinase mainly known by its involvement in the control of cell cycle progression. Our laboratory and other laboratories have previously shown a major role for CDK4 in the control of glucose homeostasis (pancreatic β-cell growth) and lipid homeostasis (adipogenesis). In this thesis, we showed that CDK4 is an insulin effector that controls lipogenesis and lipolysis in mature adipocytes. We used Cdk4-/- ;cre/cre mice and Cdk4R24C/R24C mice, carrying a hyperactive mutant Cdk4 allele, for this study. Cdk4-/ - ;cre/cre mice have a manifest adipose tissue phenotype with a significant decrease in body weight and WAT mass. On the other hand, Cdk4R24C/R24C mice show increased body weight and increased adiposity. Furthermore, we demonstrate that CDK4 is activated by insulin to promote glucose transport, lipogenesis and repress lipolysis in adipocytes. Interestingly, we showed that in mature quiescent adipocytes CDK4 and its partner, Cyclin D3, are preferentially localized in the cytoplasm, suggesting a role independent from their nuclear functions. We identified two novel substrates of CDK4: IRS1 and IRS2. CDK4 phosphorylates both IRS1 and IRS2 in order to sustain insulin signaling in adipocytes via a positive feed-back loop. To sum up, our results identify a new function of CDK4 on insulin signaling in adipocyte metabolism. Thus, the modulation of its activity could have consequences on insulin resistance, a common complication of obesity and diabetes
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Rollin, Bénédicte. "Les stylos injecteurs d'insuline : enquête auprès des diabétiques utilisateurs." Paris 5, 1990. http://www.theses.fr/1990PA05P237.

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Protzek, André Otavio Peres 1984. "Increased insulin secretion and decreased insulin clearance contributes to the hyperinsulinemia in rats and mice treated with glucocorticoid = Aumento da secreção e redução do clearance de insulina contribuem para a hiperinsulinemia compensatória em ratos e camundongos tratados com glicocorticoide." PublishedVersion, [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313949.

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Анотація:
Orientadores: Antonio Carlos Boschiero, Alex Rafacho
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Os glicocorticoides (GC) são amplamente utilizados devido aos seus efeitos anti-inflamatórios. Porém, o tratamento com GC pode induzir efeitos deletérios sobre a homeostase glicêmica como a resistência à insulina (RI), intolerância à glicose e, dependendo do tempo e dose, pode levar a instalação do Diabetes mellitus tipo 2 (DM2). Neste sentido, ratos têm sido vastamente utilizados como modelo animal para elucidar as compensações pancreáticas envolvidas na hiperinsulinemia induzida por GC e, poucos estudos enfocando os efeitos do tratamento com GC foram realizados em camundongos. Além disso, não é completamente elucidado se a hiperinsulinemia compensatória induzida pelo tratamento com GC esta associada com alteração do clearance de insulina. Assim, nossos objetivos foram avaliar se: as compensações do pâncreas endócrino em resposta ao tratamento com GC são similares entre camundongos e ratos e, identificar possíveis mecanismos que as expliquem; e se a hiperinsulinemia compensatória induzida pelo tratamento com GC em camundongos e ratos esta associada com alterações do clearance de insulina e a expressão da proteína insuling degrading enzyme (IDE) no fígado. Para isto, camundongos Swiss e ratos Wistar machos foram tratados com o glicocorticoide sintético dexametasona (1 mg/kg p.c.; 5 dias consecutivos). O tratamento com GC induziu RI, hiperinsulinemia e dislipidemia em ambas as espécies, embora mais pronunciado em ratos, que também apresentaram intolerância à glicose e hiperglicemia no jejum. Ambas as espécies tratadas com GC apresentaram incremento da secreção de insulina ex vivo estimulada com glicose, massa e proliferação de células ?, que foram associados com aumento da sinalização da via Ir-?/AKT/mTOR e redução da via AMPK/ACC/AS160 em ilhotas isoladas. O clearance de insulina reduziu em camundongos e ratos tratados com GC, o que foi associado com redução da expressão de IDE no fígado. Desta forma, nossos resultados indicam que camundongos são menos sensíveis aos efeitos deletérios do tratamento com GC sobre a homeostase glicêmica, quando comparado com ratos. Ainda, camundongos e ratos apresentam compensações pancreáticas semelhantes (incremento da função e massa de células ?) em resposta ao tratamento com GC, que foi associado com aumento da sinalização da via canônica de insulina e redução da via não canônica em ilhotas isoladas. Além disso, a redução do clearance de insulina foi, ao menos em parte, devido a redução da expressão de IDE no fígado, o que contribuiu para a hiperinsulinemia compensatória em ambas as espécies tratadas com GC. Em conclusão, estes resultados corroboram a hipótese de que fármacos que inibam a expressão ou atividade da IDE no fígado podem ser uma intervenção anti-diabetogênica que auxilie na manutenção da homeostase glicêmica sem sobrecarregar as células ?
Abstract: Glucocorticoids (GCs) are widely used as anti-inflammatory agent, but they may induce adverse metabolic effects such as insulin resistance (IR), glucose intolerance, and occasionally, diabetes mellitus type 2. Healthy rats have been used as animal models to elucidate the islet compensatory mechanisms involved in these metabolic disturbances, and only a few studies, which have focused on the in vivo effects of GCs, have been conducted in mice models. Yet, whether the reduced insulin clearance also contributes to the compensatory hyperinsulinemia in GC-treated rodents is not fully understood. Here, we aimed to elucidate whether mice and rats share the pancreatic compensations that result in response to dexamethasone (DEX) treatment and also to identify the possible mechanisms that can explain its effects. Yet, we investigated whether the hyperinsulinemia induced by GC treatment in mice and rats is associated with altered hepatic insulin degrading enzyme (IDE) expression and insulin clearance. For this, male Swiss mice and Wistar rats were treated with the synthetic GC dexamethasone (1 mg/kg b.w.; 5 days). DEX treatment induced IR, hyperinsulinemia and dyslipidemia in both species (there was a higher magnitude in rats), but treatment had a greater effect in rats that had glucose intolerance and increased basal blood glucose compared to the control group. Ex vivo insulin secretion at different glucose concentrations was higher in both groups of DEX-treated rodents compared to their controls. Mice and rats showed a significant increase in ?-cell mass due to increased ?-cell proliferation, which was associated with upregulation of the Ir-?/AKT/mTOR and downregulation of AMPK/ACC/AS160 signaling. Insulin clearance reduced in GC-treated mice and rats, which were associated with reduced hepatic IDE expression. Thus, mice are less vulnerable than rats to the deleterious effect of GCs on glucose homeostasis. In addition, rats and mice share common islet compensations (increased ?-cell function and mass) in response to GC treatment, which were associated with increased canonical and decreased non-canonical insulin signaling. Farther, the reduced insulin clearance in GC-treated rodents was, at least in part, due to reduced hepatic IDE expression, which contributed to the compensatory hyperinsulinemia. These findings corroborate the idea that pharmacological interventions that inhibit hepatic IDE may be an alternative anti-diabetic agent that helps to maintain glucose homeostasis due to hyperinsulinemia instead of hypoglycemic agent, which increase the overload in the ?-cells and may lead to ?-cell failure and DM2
Doutorado
Fisiologia
Doutor em Biologia Funcional e Molecular
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Moraes, Keila Aziz Chehoud de [UNESP]. "Efeitos decorrentes da ingestão do fluoreto na sensibilidade à insulina e transdução do sinal insulínico." PublishedVersion, Universidade Estadual Paulista (UNESP), 2006. http://hdl.handle.net/11449/95423.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Nos últimos anos tem ocorrido uma redução acentuada nos índices de cárie dentária em diversas regiões do planeta, fato que tem se atribuído ao consumo de produtos fluoretados. Entretanto, o flúor, quando ingerido em excesso, causa intoxicação crônica ou aguda, como a fluorose dentária e distúrbios na homeostase da glicose. As crianças se tornam foco de preocupação, principalmente às portadoras de diabetes mellitus (DM), pois geralmente ingerem grandes quantidades de dentifrício fluoretado durante a escovação, ultrapassando a dose preconizada como limite de ingestão diária de flúor de 0,05 a 0,07mg/F/kg de peso corpóreo. Este trabalho, que foi dividido em duas partes, pretende realizar uma breve revisão de literatura sobre os efeitos decorrentes da ingestão de NaF no metabolismo de carboidratos e avaliar os efeitos da ingestão do fluoreto na sensibilidade à insulina e na transdução do sinal insulínico. A primeira parte, baseada em artigos científicos publicados, procura discorrer sobre os efeitos da ingestão de flúor no metabolismo de carboidratos, na tolerância à glicose e no sinal insulínico, e algumas considerações sobre o diabetes mellitus e sobre as possíveis complicações que a ingestão de NaF pode ocasionar às crianças portadoras desta doença. Estes trabalhos demonstraram que o tratamento agudo ou prolongado com altas doses de fluoreto de sódio interfere na homeostase da glicose. Convém salientar que esta alteração é similar à observada em casos de diabetes mellitus. Além do mais, o flúor quando ingerido em excesso, também ocasiona diminuição da secreção de insulina, inibição da glicólise e depleção de glicogênio. Muitas dessas respostas sugerem que o NaF pode promover resistência à insulina. Portanto, a ingestão em excesso de NaF pode prejudicar a saúde, principalmente de crianças portadora de DM.
Over the last few years there has been a significant reduction in the incidence of dental caries in several regions of the world. This has been attributed to the consumption of fluoridated products. However, excess of fluoride intake can cause chronic or acute intoxication, such as dental fluorosis and impaired glucose homeostasis. Concern is focused on children, especially those with diabetes mellitus, because children usually swallow large amounts of fluoridated dentifrice during tooth brushing, in excess of the maximum recommended daily fluoride dose of 0.05 to 0.07 mg/F/kg of body weight. This report, divided into two parts, intends to make a brief literature review about effects of NAF intake on glucose metabolism, and to determine the effects of this intake on insulin sensitivity and insulin signal transduction. The first part, based on published scientific articles, endeavors to describe the effects of NaF intake on glucose metabolism, glucose tolerance and insulin signal, and put forward considerations concerning diabetes mellitus (DM), and the possible complications that NaF intake could cause in children with DM. These reports demonstrated that the acute or chronic treatment with high sodium fluoride dose interferes in glucose homeostasis, resulting in conditions such as hyperglycemia. This alteration is similar to that observed in DM. Furthermore, NaF ingestion in high doses can produce abnormalities in insulin secretion, glycolysis inhibition, and glycogen depletion. Many of these evidences suggest that NaF can induce insulin resistance. Thus, excessive fluoride consumption could worsen health, particularly of diabetic children. Based on that fluoride can interfere in the glucose metabolism, it is important for the second part of this report to determine the acute effect of fluoride on insulin sensitivity and pp185 (IRS-1/IRS-2) phosphorylation in insulin sensitive tissues.

Книги з теми "Insulines":

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Hoogenberg, K., and M. G. J. Willink. Het Insuline formularium. Houten: Bohn Stafleu van Loghum, 2006. http://dx.doi.org/10.1007/978-90-313-6343-8.

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Hoogenberg, K., and M. G. J. Willink. Het Insuline formularium. Houten: Bohn Stafleu van Loghum, 2010. http://dx.doi.org/10.1007/978-90-313-7599-8.

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Obermayer, Merapi. Insulinde's dochter. Amsterdam: B. Bakker, 2001.

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Kartodiwirio, Sudarsono Katam. Insulinde Park. Bandung: Kiblat, 2014.

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Cuatrecasas, Pedro, and Steven Jacobs, eds. Insulin. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5.

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Kahn, Brian. Insulin. Cambridge: Cambridge Micro Software, 1987.

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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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Strachan, Mark W. J., and Brian M. Frier. Insulin Therapy. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4760-2.

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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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Частини книг з теми "Insulines":

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Titchener, Janet. "Insulins and insulin management." In Diabetes Management, 25–37. First edition. | Boca Raton: CRC Press, 2020.: CRC Press, 2020. http://dx.doi.org/10.4324/9780429326196-6.

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Titchener, Janet. "Insulins and insulin management." In Diabetes Management, 25–37. First edition. | Boca Raton: CRC Press, 2020.: CRC Press, 2020. http://dx.doi.org/10.1201/9780429326196-6.

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Danne, Thomas, and Jan Bolinder. "New Insulins and Insulin Therapy." In ATTD 2011 Yearbook, 83–95. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118321508.ch5.

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Tager, H. S. "Mutant Human Insulins and Insulin Structure-Function Relationships." In Insulin, 41–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_3.

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Dirks, Burkhard. "Insuline." In Pharmaka in der Intensiv- und Notfallmedizin, 332–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-09266-8_11.

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Brandenburg, D. "Insulin Chemistry." In Insulin, 3–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_1.

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Hollenberg, M. D. "Insulin Receptor-Mediated Transmembrane Signalling." In Insulin, 183–207. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_10.

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Rothenberg, P., M. F. White, and C. R. Kahn. "The Insulin Receptor Tyrosine Kinase." In Insulin, 209–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_11.

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Levy, J. R., and J. M. Olefsky. "Receptor-Mediated Internalization and Turnover." In Insulin, 237–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_12.

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Jacobs, S. "Insulin-like Growth Factor I Receptors." In Insulin, 267–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_13.

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Тези доповідей конференцій з теми "Insulines":

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Duarte, Gabriela Alves Carvalho, Vanessa Bridi, Dhullya Eduarda Resende Santos, and Hanstter Hallison Alves Rezende. "TECNOLOGIA DO DNA RECOMBINANTE NA PRODUÇÃO DE INSULINA." In I Congresso de Engenharia de Biotecnologia. Revista Multidisciplinar de Educação e Meio Ambiente, 2021. http://dx.doi.org/10.51189/rema/1377.

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Introdução: A diabetes mellitus (DM) é uma doença metabólica, que gera hiperglicemia. Decorre devido à uma deficiência nas células beta pancreáticas, responsável por produzir o hormônio da insulina, ou a uma resistência à insulina, sendo classificadas como DM tipo 1 e DM tipo 2. Tanto tipo 1, quanto tipo 2 severa, são tratadas com reposição de insulina. O avanço da engenharia genética, especialmente a tecnologia do DNA recombinante, possibilitou a criação de novas terapias gênicas, baseadas na programação de células, principalmente bacterianas, como Escherichia coli, utilizando fragmentos do plasmídeo bacteriano, recombinados à fragmentos do DNA humano, com a característica desejada. Ao introduzir esse DNA recombinado na célula hospedeira ocorrerá multiplicação do plasmídeo recombinante e divisão das bactérias. Objetivo: Descrever como a tecnologia do DNA recombinante foi aplicada na produção de insulina, e consequentemente no aprimoramento do tratamento de diabetes mellitus. Materiais e métodos: Refere-se à uma revisão bibliográfica, no qual foram utilizados os bancos de dados, PUBMED, SciELO e Google Acadêmico, utilizando os descritores: diabetes mellitus, tecnologia do DNA recombinante e tratamento de diabetes mellitus com DNA recombinante. Restringiu-se a busca a partir do ano 2000, selecionando 4 textos científicos. Resultados: A insulina é utilizada no tratamento da diabetes, tornando necessário a ampliação da produção, simultaneamente que diminuam a rejeição e possuam baixo custo. A princípio utilizavam-se insulina animal, porém haviam suprimentos limitados, comparado à demanda. Posteriormente, fabricaram a insulina humana semissintética, onde purificavam a insulina animal, assim, amenizando as reações imunes. Com a criação da tecnologia do DNA recombinante, foram produzidas as insulinas humanas recombinantes, elevando os benefícios devido sua pureza e melhor qualidade. Subsequente desenvolveram análogos da insulina que possui maior eficiência, pois, reduz casos de hipoglicemia, contudo, a insulina recombinante até então, é utilizada devido ao custo-benefício. Conclusão: Constata-se que a criação dessa biotecnologia foi um marco para o tratamento da diabetes, visto que possibilitou a fabricação de insulina com DNA humano em larga escala, com valor acessível e redução de rejeições, porém é mostrado obstáculos nesse tratamento, tendo potencial na combinação dessa tecnologia a outras, gerando inovações no tratamento da DM e de outras doenças.
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Pfützner, A., R. Nagar, J. Spatz, and W. Reeh. "Eine wiederverwendbare Kappe für Insulinpens schützt das Insulin vor der Degradation bei hoher Umgebungstemperatur." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641942.

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Araujo, Anna Júlia Papa De, Joanna D'arc Luciana De Souza Almeida De Oliveira, and Soraya Solon. "ESTÁGIO EM SAÚDE PÚBLICA: ASSISTÊNCIA FARMACÊUTICA NO TRATAMENTO DE DIABETES." In III Congresso Brasileiro de Ciências Farmacêuticas On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbracif/26.

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Introdução: O estágio obrigatório durante a graduação em farmácia possibilita a vivência da prática profissional em um ambiente supervisionado. A formação para atuação no SUS conta com estágios nos diferentes serviços de saúde pública, incluindo a atenção básica. Nesse campo, o tratamento e monitoramento da diabetes é rotineiro do farmacêutico e dos agentes comunitários de saúde (ACS´s), os quais estão próximos aos pacientes em uma área com diversidade no tratamento, visto que alguns utilizam a caneta Novo Nordisk, enquanto outros utilizam seringas com ampolas de insulina. Objetivo: Esse trabalho objetiva relatar a experiência do estágio em uma Unidade de Saúde da Família (USF) e propor uma reflexão sobre as intervenções relacionadas à distribuição e uso das canetas de insulina oferecidas no sistema de saúde público. Metodologia: O estágio ocorreu no segundo semestre e teve como requisito a disciplina Saúde da Comunidade, correlacionando a prática com a Política Nacional da Atenção Básica. As atividades foram desenvolvidas em 96 h, em uma USF, da periferia de Campo Grande-MS. O trabalho envolveu o diagnóstico do cenário, território de prática e intervenções individuais e coletivas. Realizaram-se visitas domiciliares com ACS’s e atividades na USF nos setores de acolhimento, triagem, gerência, farmácia, vacinas e testes rápidos. As visitas foram direcionadas a pacientes que necessitavam de intervenção farmacêutica de acordo com a percepção dos ACS´s e da farmacêutica preceptora. Resultados: A maioria dos pacientes era idosos, analfabetos ou com dificuldade de leitura, acometidos por diabetes, porém, com problemas na aplicação e armazenamento das canetas de insulina. Em uma visita, foram recolhidas canetas vencidas que ainda eram usadas pelo paciente e que as intercalava com a aplicação das seringas. Para cada paciente, foi realizada abordagem educativa e orientadora sobre o uso e armazenamento do dispositivo. Conclusão: Apesar do programa governamental Caneta da Saúde disponibilizar canetas de insulinas em substituição às seringas para otimizar o tratamento do diabetes, alguns idosos apresentam dificuldade para manuseá-la. Portanto, a prescrição e dispensação do referido medicamento no SUS pelos médicos e farmacêuticos devem obedecer critérios individuais considerando o caso clínico, as condições familiares além de somente a faixa etária do indivíduo.
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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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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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Wang, Bin, Hui Hu, Ayodeji Demuren, and Eric Gyurcsko. "Experimental and Theoretical Studies of Pulsed Micro Flows Pertinent to Continuous Subcutaneous Insulin Infusion (CSII) Therapy." In ASME 2010 3rd Joint US-European Fluids Engineering Summer Meeting collocated with 8th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2010. http://dx.doi.org/10.1115/fedsm-icnmm2010-30303.

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Continuous subcutaneous insulin infusion (CSII) therapy, also known as insulin pump therapy, has become an important advancement in diabetes therapy to improve the quality of life for millions of diabetes patients. Insulin delivery failures caused by the precipitations of insulin within micro-sized CSII tubing systems have been reported in recent years. It has also been conjectured that the flow of insulin through an insulin infusion set may be reduced or inhibited by air bubbles entrained into the capillary CSII tubing system during the typical three- to five-day operation between refills. Currently, most solutions to insulin occlusion related problems are based on clinical trials. In the present study, an experimental and theoretic study was conducted to investigate the pulsed flows inside the micro-sized CSII tubing system. A micro-PIV system was used to provide detailed flow velocity field measurements inside the capillary CSII tubing system to characterize the transient behavior of the micro-flows upon the pulsed actuation of the insulin pump used in CSII therapy. It was found that the microflow inside the CSII tubing system is highly unsteady, which is much more interesting than the creeping flow that the nominal averaged flow rates would suggest. A theoretic frame work was also performed to model the pulsed micro-flows driven by the insulin pump to predict the transient behavior of the microflows and velocity distributions inside the micro-sized CSII tubing system. The measurement results and the theoretic predictions were compared quantitatively to elucidate underlying physics for a better understanding of the microphysical process associated with the insulin delivery in order to provide a better guidance for troubleshooting of insulin occlusion in CSII therapy.
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Islami, Dian Dini, Didik Gunawan Tamtomo, and Hanung Prasetya. "The Effect of Insulin Provision on the Risk Reduction of Type 2 Diabetes Mellitus: Meta-Analysis." In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.05.49.

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ABSTRACT Background: Insulin is the pivotal hormone regulating cellular energy supply and macronutrient balance, directing anabolic processes of the fed state. Insulin is essential for the intra-cellular transport of glucose into insulin-dependent tissues such as muscle and adipose tissue. The purpose of this study was to examine the effect of insulin provision on the risk reduction of type 2 diabetes mellitus. Subjects and Method: This was meta-analysis and systematic review. The study was conducted by collecting articles from PubMed, Google Scholar, and Springer Link databases, from 2010-2020. Keywords used “effect insulin” OR “giving insulin” AND “diabetes mellitus” OR “diabetes” AND “cross sectional” AND “adjusted odd ratio”. The inclusion criteria were full text, using English or Indonesia language, and using crosssectional study design. The articles were selected by PRISMA flow chart. The quantitative data were analyzed by RevMan 5.3. Results: A meta-analysis from 5 studies in Ethiopia, Northeast Ethiopia, Taiwan, African American, and South Korea, reported that insulin provision reduced the risk of diabetes mellitus (aOR= 1.89; 95% CI= 1.82 to 3.57; p= 0.05) with I2= 84%. Conclusion: Insulin provision reduced the risk of diabetes mellitus. Keywords: insulin, type 2 diabetes mellitus Correspondence: Dian Dini Islami. Masters Program in Public Health, Universitas Sebelas Maret. Jl. Ir. Sutami 36A, Surakarta 57126, Central Java. Email: dian.dinii94@gmail.com. Mobile: 085729483960. DOI: https://doi.org/10.26911/the7thicph.05.49
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Pfliegler, G., J. Arnout, J. Kienast, K. Wittevrongel, and J. Vermylen. "INSULIN RECEPTORS ARE NOT COUPLED TO THE PHOSPHOINOSITIDE OR ADENYLCYCLASE MESSENGER SYSTEMS IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644523.

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Insulin receptors have been found not only on its “target Cells” but also on several other cell-types, including human platelets. From studies on adipocytes and liver cells it seems that they are coupled both to the adenylate cyclase-cyclic AMP and the polyphosphoinositide messenger systems. Circulating blood cells might faithfully reflect the insulin receptor state of target organ tissues. Impaired platelet function has an important role in the pathogenesis of vascular and thrombotic complications in diabetes mellitus, and insulin seems to act directly on platelets. A reduction in the number and binding capacity of platelet insulin receptors in diabetic patients (Udvardy et al. 1986) suggested a (patho)physiological role for these receptors. In our studies, insulin (1 × 10-9 - 1 × 10-6 M) did not affect basal platelet cyclic AMP levels, as measured following incorporation of [3H] adenine. Insulin did not prevent PGI2 (25-75 nmol/L) induced cyclic AMP formation in platelets. Insulin did not modify the basal levels of inositol phosphate (IP), IP2 or IP3 in platelets, as measured following incorporation of [3H] inositol. Insulin did not affect formation of IP, IP2 or IP3 by thrombin. No changes in cytosolic free Ca2+ (Quin 2 method) were detected in the presence of insulin. Sodium nitroprusside on the other hand, which is known to mimic several effects of insulin on adipocytes, inhibited IP formation induced by threshold concentrations of thrombin.On the basis of our results the insulin receptors in human platelets seem to be “non-functional” insofar as their occupancy is not accompanied by the stimulation or inhibition of phospho-inositide breakdown or cyclic AMP formation. Similarly, “silent” muscarinic-cholinergic receptors have recently been reported in human erythrocytes (Sehar et al. 1986).
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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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Zedelmair, Michael M., and Abhijit Mukherjee. "Numerical Simulation of Insulin Depot Formation in Subcutaneous Tissue." In ASME 2016 Fluids Engineering Division Summer Meeting collocated with the ASME 2016 Heat Transfer Summer Conference and the ASME 2016 14th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/fedsm2016-7719.

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In this study a numerical model of the insulin depot formation and absorption in the subcutaneous adipose tissue is developed using the commercial Computational Fluid Dynamics (CFD) software ANSYS Fluent. A better understanding of these mechanisms can be helpful in the development of new devices and cannula geometries as well as predicting the concentration of insulin in the blood. The injection method considered in this simulation is by the use of an insulin pump using a rapid acting U100 insulin analogue. The insulin is injected into the subcutaneous tissue in the abdominal region. The main composition of the subcutaneous tissue is blood vessels and adipose cells surrounded by interstitial fluid. The numerical simulation is conducted in a 2D-axisymmetric domain where the tissue is modeled as a fluid saturated porous media. Due to the presence of channel formation in lateral direction in the tissue, an anisotropic approach to define the permeability is studied having an impact on the viscous resistance to the flow. This configuration is resulting in a rather disk shaped depot following recent experimental findings. The depot formation is analyzed running Bolus injections ranging from 5–15 Units of insulin corresponding to 50–150μl. The depot formation model has been extended implementing the process of absorption of insulin from the depot to be able to run the simulation over longer timeframes where absorption starts playing an important role.

Звіти організацій з теми "Insulines":

1

Anthony Di Franco, Anthony Di Franco. Open Insulin. Experiment, July 2015. http://dx.doi.org/10.18258/5755.

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2

Muti, Paola. Insulin and Breast Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada395852.

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3

Muti, Paola. Insulin and Breast Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, June 2000. http://dx.doi.org/10.21236/ada383382.

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4

González-rivas, Juan Pablo, Juan Pablo González Rivas, Mariela Paoli, Raul García Santiago, María Verónica Avendaño, Merlys Lobo, and Andrea Avendaño. La resistencia psicológica al uso de insulina en Venezuela. Buenos Aires: siicsalud.com, June 2018. http://dx.doi.org/10.21840/siic/157480.

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5

ZHU, Dongshan. The lifestyle changes after initiating basal insulin in insulin naive patients with type 2 diabetes: Results from the ORBIT study. Science Repository, June 2019. http://dx.doi.org/10.31487/j.jicoa.2019.02.04.

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6

Shi, Jinping, Feng L, Liting X, Jing L, and Xing L. Meta analysis of efficacy and safety of insulin aspart and biosynthetic human insulin in the treatment of gestational diabetes mellitus. Xi'an International Medical Center Hospital, July 2021. http://dx.doi.org/10.37766/inplasy2021.7.0047.

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7

Cleveland, Rebecca J., Marilie D. Gammon, and Ralph S. Baric. Insulin-Like Growth Factor I Polymorphisms in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada412654.

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8

Smith, Nadine, Michael Pishko, Robert Gabbay, and Jacob Werner. Closed-Loop Noninvasive Ultrasound Glucose Sensing and Insulin Delivery. Fort Belvoir, VA: Defense Technical Information Center, September 2006. http://dx.doi.org/10.21236/ada458974.

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9

Gross, Jennifer M. Insulin-Like Growth Factor Binding Protein-1 Interacts with Integrins to Inhibit Insulin-Like Growth Factor-Induced Breast Cancer Growth and Migration. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada420347.

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10

Byron, Sara A. Differential Roles of Insulin Receptor Substrate-1 and -2 (IRS-1, IRS-2) in Insulin-Like Growth Factor Signaling in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada418361.

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