Diet-induced obesity impairs AKT signalling in the retina and causes retinal degeneration

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dc.contributor.authorMarçal, Anderson C.
dc.contributor.authorLeonelli, Mauro
dc.contributor.authorFiamoncini, Jarlei
dc.contributor.authorDeschamps, Francisco C.
dc.contributor.authorRodrigues, Maria A.M. [UNESP]
dc.contributor.authorCuri, Rui
dc.contributor.authorCarpinelli, Angelo R.
dc.contributor.authorBritto, Luiz R.G.
dc.contributor.authorCarvalho, Carla R.O.
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionEmpresa de Pesquisa Agropecuária e Extensão Rural de Santa Catarina (EPAGRI)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-27T11:27:26Z
dc.date.available2014-05-27T11:27:26Z
dc.date.issued2013-01-01
dc.description.abstractRetinopathy, a common complication of diabetes, is characterized by an unbalanced production of nitric oxide (NO), a process regulated by nitric oxide synthase (NOS). We hypothesized that retinopathy might stem from changes in the insulin receptor substrate (IRS)/PI3K/AKT pathway and/or expression of NOS isoforms. Thus, we analysed the morphology and apoptosis index in retinas of obese rats in whom insulin resistance had been induced by a high-fat diet (HFD). Immunoblotting analysis revealed that the retinal tissue of HFD rats had lower levels of AKT1, eNOS and nNOS protein than those of samples taken from control animals. Furthermore, immunohistochemical analyses indicated higher levels of iNOS and 4-hydroxynonenal and a larger number of apoptotic nuclei in HFD rats. Finally, both the inner and outer retinal layers of HFD rats were thinner than those in their control counterparts. When considered alongside previous results, these patterns suggest two major ways in which HFD might impact animals: direct activity of ingested fatty acids and/or via insulin-resistance-induced changes in intracellular pathways. We discuss these possibilities in further detail and advocate the use of this animal model for further understanding relationships between retinopathy, metabolic syndrome and type 2 diabetes. © 2012 John Wiley & Sons, Ltd.en
dc.description.affiliationDepartamento de Fisiologia e Biofísica Instituto de Ciências Biomédicas (ICB) Universidade de São Paulo (USP), SP
dc.description.affiliationEmpresa de Pesquisa Agropecuária e Extensão Rural de Santa Catarina (EPAGRI), Itajaí, SC
dc.description.affiliationDepartamento de Patologia Faculdade de Medicina de Botucatu Universidade Estadual Paulista (UNESP), SP
dc.description.affiliationUnespDepartamento de Patologia Faculdade de Medicina de Botucatu Universidade Estadual Paulista (UNESP), SP
dc.format.extent65-74
dc.identifierhttp://dx.doi.org/10.1002/cbf.2861
dc.identifier.citationCell Biochemistry and Function, v. 31, n. 1, p. 65-74, 2013.
dc.identifier.doi10.1002/cbf.2861
dc.identifier.issn0263-6484
dc.identifier.issn1099-0844
dc.identifier.scopus2-s2.0-84872387225
dc.identifier.urihttp://hdl.handle.net/11449/74097
dc.identifier.wosWOS:000313549300010
dc.language.isoeng
dc.relation.ispartofCell Biochemistry and Function
dc.relation.ispartofjcr2.186
dc.relation.ispartofsjr0,520
dc.relation.ispartofsjr0,520
dc.rights.accessRightsAcesso restrito
dc.sourceScopus
dc.subjectAKT
dc.subjectCell death
dc.subjectHigh-fat diet
dc.subjectInsulin resistance
dc.subjectLipid peroxidation
dc.subjectNOS isoforms
dc.subjectObesity
dc.subjectRetina
dc.subject4 hydroxynonenal
dc.subjectendothelial nitric oxide synthase
dc.subjectinducible nitric oxide synthase
dc.subjectinsulin receptor substrate
dc.subjectneuronal nitric oxide synthase
dc.subjectnitric oxide synthase
dc.subjectphosphatidylinositol 3 kinase
dc.subjectprotein kinase B
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectapoptosis
dc.subjectcontrolled study
dc.subjectdiabetic retinopathy
dc.subjectimmunoblotting
dc.subjectimmunohistochemistry
dc.subjectinsulin resistance
dc.subjectintracellular signaling
dc.subjectlipid diet
dc.subjectmale
dc.subjectnonhuman
dc.subjectobesity
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectrat
dc.subjectretina
dc.subjectretina degeneration
dc.subjectAnimals
dc.subjectApoptosis
dc.subjectAstrocytes
dc.subjectBlood Glucose
dc.subjectDiabetic Retinopathy
dc.subjectDietary Fats
dc.subjectDisease Models, Animal
dc.subjectEye Proteins
dc.subjectFatty Acids
dc.subjectInsulin Receptor Substrate Proteins
dc.subjectInsulin Resistance
dc.subjectLipid Peroxidation
dc.subjectLipids
dc.subjectLiver
dc.subjectMale
dc.subjectNitric Oxide Synthase Type I
dc.subjectNitric Oxide Synthase Type III
dc.subjectPhosphatidylinositol 3-Kinases
dc.subjectProto-Oncogene Proteins c-akt
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectRetinal Degeneration
dc.subjectSignal Transduction
dc.subjectAnimalia
dc.subjectRattus
dc.titleDiet-induced obesity impairs AKT signalling in the retina and causes retinal degenerationen
dc.typeArtigo
dcterms.licensehttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
unesp.author.orcid0000-0001-9073-2405[2]
unesp.author.orcid0000-0001-5824-8656[9]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt

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