Academic literature on the topic 'Insulines'
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Journal articles on the topic "Insulines":
Faure, Sébastien. "Insulines." Actualités Pharmaceutiques 51, no. 512 (January 2012): 49–54. http://dx.doi.org/10.1016/s0515-3700(12)71130-8.
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.
Battu, Valérie. "Les insulines." Actualités Pharmaceutiques 52, no. 530 (November 2013): 55–59. http://dx.doi.org/10.1016/j.actpha.2013.09.013.
Fougere, Édouard. "Les insulines." Actualités Pharmaceutiques 60, no. 606 (May 2021): 55–57. http://dx.doi.org/10.1016/j.actpha.2021.03.021.
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.
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.
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.
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.
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.
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.
Dissertations / Theses on the topic "Insulines":
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.
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.
Meschi, Eleonora. "Identification de populations neuronales contrôlant la sécrétion des insulines et la croissance en fonction de la nutrition chez Drosophila melanogaster." Thesis, Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4088/document.
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
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.
Bornaque, Florine. "Rôle de l'épitranscriptome dans la physiopathologie de la cellule β pancréatique." Thesis, Université de Lille (2018-2021), 2021. https://pepite-depot.univ-lille.fr/ToutIDP/EDBSL/2021/2021LILUS059.pdf.
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
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." [s.n.], 2004. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310365.
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
Lagarrigue, Sylviane. "Implication de la kinase CDK4 dans la biologie de l'adipocyte." Thesis, Montpellier 1, 2013. http://www.theses.fr/2013MON1T030.
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
Rollin, Bénédicte. "Les stylos injecteurs d'insuline : enquête auprès des diabétiques utilisateurs." Paris 5, 1990. http://www.theses.fr/1990PA05P237.
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." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313949.
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
Moraes, Keila Aziz Chehoud de [UNESP]. "Efeitos decorrentes da ingestão do fluoreto na sensibilidade à insulina e transdução do sinal insulínico." Universidade Estadual Paulista (UNESP), 2006. http://hdl.handle.net/11449/95423.
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.
Books on the topic "Insulines":
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.
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.
Obermayer, Merapi. Insulinde's dochter. Amsterdam: B. Bakker, 2001.
Kartodiwirio, Sudarsono Katam. Insulinde Park. Bandung: Kiblat, 2014.
Cuatrecasas, Pedro, and Steven Jacobs, eds. Insulin. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5.
Brian, Kahn. Insulin. Cambridge: Cambridge Micro Software, 1987.
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.
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.
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.
Krentz, Andrew J., ed. Insulin Resistance. Oxford, UK: Blackwell Science Ltd, 2002. http://dx.doi.org/10.1002/9780470698921.
Book chapters on the topic "Insulines":
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Conference papers on the topic "Insulines":
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Reports on the topic "Insulines":
Anthony Di Franco, Anthony Di Franco. Open Insulin. Experiment, July 2015. http://dx.doi.org/10.18258/5755.
Muti, Paola. Insulin and Breast Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada395852.
Muti, Paola. Insulin and Breast Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, June 2000. http://dx.doi.org/10.21236/ada383382.
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.
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.
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.
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.
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.
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.
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.