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SM ISO690:2012 CONDREA, Cătălina, SARDARI, Veronica. Biochemical mechanisms of insulin resistance. In: Cercetarea în biomedicină și sănătate: calitate, excelență și performanță, Ed. 1, 20-22 octombrie 2021, Chişinău. Chișinău, Republica Moldova: 2021, p. 45. ISBN 978-9975-82-223-7 (PDF).. |
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Cercetarea în biomedicină și sănătate: calitate, excelență și performanță 2021 | ||||||
Conferința "Cercetarea în biomedicină și sănătate: calitate, excelență și performanță" 1, Chişinău, Moldova, 20-22 octombrie 2021 | ||||||
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Pag. 45-45 | ||||||
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Background. The mutation of the Insulin Receptor Substrate-1 gene is a cause for insulin resistance. The mutations is due to the replacement of Gly with Arg at codon 972, which leads to the formation of a defective protein and that causes the translocation of the GLUT-4 protein. Objective of the study. To elucidate and describe the biochemical mechanisms of insulin resistance (IR) underlying the development of effective treatment for type 2 diabetes. Material and Methods. In order to achieve the proposed goal, a bibliographic search was performed using the Medical Scientific Library of USMF „NicolaeTestemitanu” and the following platforms: Medscape, PubMed and American Physiological Society Journal. Articles that were published between 2010 and 2020 were selected. Results. In obesity adipocytes become hypertrophied and they are the source of proinflammatory cytokines, such as TNF-α, IL-6, resistin and Monocyte Chemoattractant Protein-1 (MCP-1), which have a direct action on the Insulin Receptor Substrate-1 (IRS-1) proteins phosphorylation, there is a interruption of the enzyme cascade of reactions that are necessary for the GLUT-4 translocation. Elevated endothelin-1 levels contribute to the IR installing by deteriorating the insulin signaling pathway at the receptor level. Nicotine also leads to IR, by activating serine kinases, which will cause an increased level of IRS-1 Ser 636 and, therefore, will impede the translocation of GLUT-4. Conclusion. With the exception of the mutation in the Insulin Receptor Substrate-1 gene, all other pathogenic mechanisms of IR are essential for the development of an effective treatment, which may interrupt the pathogenetic chain of IR in patients with type 2 diabetes. |
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Cuvinte-cheie insulinresistance, proinflammatorycytokines, IRS-1, GLUT-4., insulinorezistenţă, citokine proinflamatorii, IRS-1, GLUT-4 |
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