Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/348754
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampAnhê, Gabriel Forato-
dc.typeArtigopt_BR
dc.titleIntensive insulin treatment induces insulin resistance in diabetic rats by impairing glucose metabolism-related mechanisms in muscle and liverpt_BR
dc.contributor.authorOkamoto, Maristela Mitiko-
dc.contributor.authorAnhê, Gabriel Forato-
dc.contributor.authorSabino-Silva, Robinson-
dc.contributor.authorMarques, Milano Felipe dos Santos Ferreira-
dc.contributor.authorFreitas, Helayne Soares-
dc.contributor.authorMori, Rosana Cristina Tieko-
dc.contributor.authorMelo, Karla Fabiana S-
dc.contributor.authorMachado, Ubiratan Fabres-
dc.subjectInsulinapt_BR
dc.subjectGlicosept_BR
dc.subject.otherlanguageInsulinpt_BR
dc.subject.otherlanguageGlucosept_BR
dc.description.abstractInsulin replacement is the only effective therapy to manage hyperglycemia in type 1 diabetes mellitus (T1DM). Nevertheless, intensive insulin therapy has inadvertently led to insulin resistance. This study investigates mechanisms involved in the insulin resistance induced by hyperinsulinization. Wistar rats were rendered diabetic by alloxan injection, and 2 weeks later received saline or different doses of neutral protamine Hagedorn insulin (1.5, 3, 6, and 9 U/day) over 7 days. Insulinopenic-untreated rats and 6U- and 9U-treated rats developed insulin resistance, whereas 3U-treated rats revealed the highest grade of insulin sensitivity, but did not achieve good glycemic control as 6U- and 9U-treated rats did. This insulin sensitivity profile was in agreement with glucose transporter 4 expression and translocation in skeletal muscle, and insulin signaling, phosphoenolpyruvate carboxykinase/glucose-6-phosphatase expression and glycogen storage in the liver. Under the expectation that insulin resistance develops in hyperinsulinized diabetic patients, we believe insulin sensitizer approaches should be considered in treating T1DMpt_BR
dc.relation.ispartofJournal of endocrinologypt_BR
dc.relation.ispartofabbreviationJ. endocrinol.pt_BR
dc.publisher.cityBristolpt_BR
dc.publisher.countryReino Unidopt_BR
dc.publisherBioScientificapt_BR
dc.date.issued2011-
dc.language.isoengpt_BR
dc.description.volume211pt_BR
dc.description.issuenumber1pt_BR
dc.description.firstpage55pt_BR
dc.description.lastpage64pt_BR
dc.rightsFechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn0022-0795pt_BR
dc.identifier.eissn1479-6805pt_BR
dc.identifier.doi10.1530/JOE-11-0105pt_BR
dc.identifier.urlhttps://joe.bioscientifica.com/view/journals/joe/211/1/55.xmlpt_BR
dc.description.sponsorshipFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPpt_BR
dc.description.sponsordocumentnumber2006/60101-1pt_BR
dc.date.available2020-09-04T17:52:34Z-
dc.date.accessioned2020-09-04T17:52:34Z-
dc.description.provenanceSubmitted by Susilene Barbosa da Silva (susilene@unicamp.br) on 2020-09-04T17:52:34Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-01-04T15:12:43Z : No. of bitstreams: 1 000295000500007.pdf: 418673 bytes, checksum: d9e4f3d9c40528c3fb0142355aa333c4 (MD5)en
dc.description.provenanceMade available in DSpace on 2020-09-04T17:52:34Z (GMT). No. of bitstreams: 0 Previous issue date: 2011en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/348754-
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.subject.keywordDiabeticpt_BR
dc.identifier.source000295000500007pt_BR
dc.creator.orcid0000-0002-7694-8397pt_BR
dc.type.formArtigopt_BR
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