نمایش مختصر رکورد

dc.contributor.authorJuárez-Vázquez, Clara Ien_US
dc.contributor.authorGurrola-Díaz, Carmen Men_US
dc.contributor.authorVargas-Guerrero, Belindaen_US
dc.contributor.authorDomínguez-Rosales, José Aen_US
dc.contributor.authorRodriguez-Ortiz, Jessicaen_US
dc.contributor.authorBarros-Núñez, Patricioen_US
dc.contributor.authorFlores-Martínez, Silvia Een_US
dc.contributor.authorSánchez-Corona, Joséen_US
dc.contributor.authorRosales-Reynoso, Mónica Aen_US
dc.date.accessioned1399-07-09T08:22:38Zfa_IR
dc.date.accessioned2020-09-30T08:22:38Z
dc.date.available1399-07-09T08:22:38Zfa_IR
dc.date.available2020-09-30T08:22:38Z
dc.date.issued2018-05-01en_US
dc.date.issued1397-02-11fa_IR
dc.date.submitted2017-07-12en_US
dc.date.submitted1396-04-21fa_IR
dc.identifier.citationJuárez-Vázquez, Clara I, Gurrola-Díaz, Carmen M, Vargas-Guerrero, Belinda, Domínguez-Rosales, José A, Rodriguez-Ortiz, Jessica, Barros-Núñez, Patricio, Flores-Martínez, Silvia E, Sánchez-Corona, José, Rosales-Reynoso, Mónica A. (2018). Insulin glargine affects the expression of Igf-1r, Insr, and Igf-1 genes in colon and liver of diabetic rats. Iranian Journal of Basic Medical Sciences, 21(5), 489-494. doi: 10.22038/ijbms.2018.24867.6185en_US
dc.identifier.issn2008-3866
dc.identifier.issn2008-3874
dc.identifier.urihttps://dx.doi.org/10.22038/ijbms.2018.24867.6185
dc.identifier.urihttp://ijbms.mums.ac.ir/article_10542.html
dc.identifier.urihttps://iranjournals.nlai.ir/handle/123456789/340260
dc.description.abstract<em><strong>Objective(s):</strong></em> The mitogenic effect of the analogous insulin glargine is currently under debate since several clinical studies have raised the possibility that insulin glargine treatment has a carcinogenic potential in different tissues. This study aimed to evaluate the Igf-1r, Insr, and Igf-1 gene expression in colon and liver of streptozotocin-induced diabetic rats in response to insulin glargine, neutral protamine Hagedorn (NPH) insulin, and metformin treatments. <br /><em><strong>Materials and Methods:</strong> </em>Male Wistar rats were induced during one week with streptozotocin to develop Type 2 Diabetes (T2D) and then randomly distributed into four groups. T2D rats included in the first group received insulin glargine, the second group received NPH insulin, the third group received metformin; finally, untreated T2D rats were included as the control group. All groups were treated for seven days; after the treatment, tissue samples of liver and colon were obtained. Quantitative PCR (qPCR) was performed to analyze the Igf-1r, Insr and Igf-1 gene expression in each tissue sample. <br /><em><strong>Results:</strong></em> The liver tissue showed overexpression of the Insr and Igf-1r genes (P>0.001) in rats treated with insulin glargine in comparison with the control group. Similar results were observed for the Insr gene (P>0.011) in colonic tissue of rats treated with insulin glargine. <br /><em><strong>Conclusion:</strong></em> These observations demonstrate that insulin glargine promote an excess of insulin and IGF-1 receptors in STZ-induced diabetic rats, which could overstimulate the mitogenic signaling pathways.en_US
dc.format.extent522
dc.format.mimetypeapplication/pdf
dc.languageEnglish
dc.language.isoen_US
dc.publisherMashhad University of Medical Sciencesen_US
dc.relation.ispartofIranian Journal of Basic Medical Sciencesen_US
dc.relation.isversionofhttps://dx.doi.org/10.22038/ijbms.2018.24867.6185
dc.subjectColonen_US
dc.subjectDiabetesen_US
dc.subjectInsulin glargineen_US
dc.subjectLiveren_US
dc.subjectMetforminen_US
dc.subjectNPH insulinen_US
dc.subjectRatsen_US
dc.subjectGeneticsen_US
dc.titleInsulin glargine affects the expression of Igf-1r, Insr, and Igf-1 genes in colon and liver of diabetic ratsen_US
dc.typeTexten_US
dc.typeOriginal Articleen_US
dc.contributor.departmentDivisión de Medicina Molecular, Centro de Investigación Biomédica de Occidente. Instituto Mexicano del Seguro Social. Guadalajara, Jalisco, Méxicoen_US
dc.contributor.departmentInstituto de Enfermedades Crónico Degenerativas, Departamento de Biología Molecular y Genómica, C.U.C.S, Universidad de Guadalajara. Guadalajara, Jalisco, Méxicoen_US
dc.contributor.departmentInstituto de Enfermedades Crónico Degenerativas, Departamento de Biología Molecular y Genómica, C.U.C.S, Universidad de Guadalajara. Guadalajara, Jalisco, Méxicoen_US
dc.contributor.departmentInstituto de Enfermedades Crónico Degenerativas, Departamento de Biología Molecular y Genómica, C.U.C.S, Universidad de Guadalajara. Guadalajara, Jalisco, Méxicoen_US
dc.contributor.departmentDivisi&oacute;n de Gen&eacute;tica, Centro de Investigaci&oacute;n Biom&eacute;dica de Occidente. Instituto Mexicano del Seguro Social. Guadalajara, Jalisco, M&eacute;xico.en_US
dc.contributor.departmentDivisión de Genética, Centro de Investigación Biomédica de Occidente. Instituto Mexicano del Seguro Social. Guadalajara, Jalisco, Méxicoen_US
dc.contributor.departmentDivisión de Medicina Molecular, Centro de Investigación Biomédica de Occidente. Instituto Mexicano del Seguro Social. Guadalajara, Jalisco, Méxicoen_US
dc.contributor.departmentDivisión de Medicina Molecular, Centro de Investigación Biomédica de Occidente. Instituto Mexicano del Seguro Social. Guadalajara, Jalisco, Méxicoen_US
dc.contributor.departmentDivisión de Medicina Molecular, Centro de Investigación Biomédica de Occidente. Instituto Mexicano del Seguro Social. Guadalajara, Jalisco, Méxicoen_US
dc.citation.volume21
dc.citation.issue5
dc.citation.spage489
dc.citation.epage494
nlai.contributor.orcid0000-0002-9851-8961


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