Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/342769
Full metadata record
DC FieldValueLanguage
dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampMoreira, Ricardo Pereira-
dc.contributor.authorunicampBerardi, Elza Olga Ana Muscelli-
dc.typeArtigopt_BR
dc.titleEffect of insulin on proximal tubules handling of glucose : a systematic reviewpt_BR
dc.contributor.authorPereira-Moreira, Ricardo-
dc.contributor.authorMuscelli, Elza-
dc.subjectInsulinapt_BR
dc.subjectGlicosept_BR
dc.subject.otherlanguageInsulinpt_BR
dc.subject.otherlanguageGlucosept_BR
dc.description.abstractRenal proximal tubules reabsorb glucose from the glomerular filtrate and release it back into the circulation. Modulation of glomerular filtration and renal glucose disposal are some of the insulin actions, but little is known about a possible insulin effect on tubular glucose reabsorption. This review is aimed at synthesizing the current knowledge about insulin action on glucose handling by proximal tubules. Method. A systematic article selection from Medline (PubMed) and Embase between 2008 and 2019. 180 selected articles were clustered into topics (renal insulin handling, proximal tubule glucose transport, renal gluconeogenesis, and renal insulin resistance). Summary of Results. Insulin upregulates its renal uptake and degradation, and there is probably a renal site-specific insulin action and resistance; studies in diabetic animal models suggest that insulin increases renal SGLT2 protein content; in vivo human studies on glucose transport are few, and results of glucose transporter protein and mRNA contents are conflicting in human kidney biopsies; maximum renal glucose reabsorptive capacity is higher in diabetic patients than in healthy subjects; glucose stimulates SGLT1, SGLT2, and GLUT2 in renal cell cultures while insulin raises SGLT2 protein availability and activity and seems to directly inhibit the SGLT1 activity despite it activating this transporter indirectly. Besides, insulin regulates SGLT2 inhibitor bioavailability, inhibits renal gluconeogenesis, and interferes with Na(+)K(+)ATPase activity impacting on glucose transport. Conclusion. Available data points to an important insulin participation in renal glucose handling, including tubular glucose transport, but human studies with reproducible and comparable method are still neededpt_BR
dc.relation.ispartofJournal of diabetes researchpt_BR
dc.relation.ispartofabbreviationJ. diabetes res.pt_BR
dc.publisher.cityLondonpt_BR
dc.publisher.countryReino Unidopt_BR
dc.publisherHindawipt_BR
dc.date.issued2020-
dc.date.monthofcirculationJan.pt_BR
dc.language.isoengpt_BR
dc.description.volume2020pt_BR
dc.rightsAbertopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn2314-6745pt_BR
dc.identifier.eissn2314-6753pt_BR
dc.identifier.doi10.1155/2020/8492467pt_BR
dc.identifier.urlhttps://www.hindawi.com/journals/jdr/2020/8492467/pt_BR
dc.date.available2020-06-05T15:39:46Z-
dc.date.accessioned2020-06-05T15:39:46Z-
dc.description.provenanceSubmitted by Mariana Aparecida Azevedo (mary1@unicamp.br) on 2020-06-05T15:39:46Z No. of bitstreams: 0. Added 1 bitstream(s) on 2020-08-27T19:17:40Z : No. of bitstreams: 1 000508361700001.pdf: 2046952 bytes, checksum: 1adeeebfb8419b44837c33fdaac53dc5 (MD5)en
dc.description.provenanceMade available in DSpace on 2020-06-05T15:39:46Z (GMT). No. of bitstreams: 0 Previous issue date: 2020en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/342769-
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.identifier.source000508361700001pt_BR
dc.creator.orcid0000-0003-2465-4044pt_BR
dc.creator.orcid0000-0001-6979-3553pt_BR
dc.type.formArtigo de pesquisapt_BR
dc.identifier.articleid8492467pt_BR
Appears in Collections:FCM - Artigos e Outros Documentos

Files in This Item:
File Description SizeFormat 
000508361700001.pdf2 MBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.