Glucose Homeostasis Is Not Affected in a Murine Model of Parkinson's Disease Induced by 6-OHDA

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dc.contributor.authorGames, Felipe Azevedo
dc.contributor.authorFlores, Rafael Appel
dc.contributor.authorBruxel, Maciel Alencar
dc.contributor.authorSllva, Flavia Natividade da
dc.contributor.authorMoreira, Eduardo Luiz Gasnhar
dc.contributor.authorZoccal, Daniel Breseghello [UNESP]
dc.contributor.authorPrediger, Rui Daniel
dc.contributor.authorRafacho, Alex
dc.contributor.institutionUniversidade Federal de Santa Catarina (UFSC)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2019-10-04T12:34:20Z
dc.date.available2019-10-04T12:34:20Z
dc.date.issued2019-01-09
dc.description.abstractThere is a mutual relationship between metabolic and neurodegenerative diseases. However, the causal relationship in this crosstalk is unclear and whether Parkinson's disease (PD) causes a posterior impact on metabolism remains unknown. Considering that, this study aimed to evaluate the appearance of possible changes in metabolic homeostasis due to 6-hydroxydopamine (6-OHDA) administration, a neurotoxin that damage dopaminergic neurons leading to motor impairments that resemble the ones observed in PD. For this, male Wistar rats received bilateral 6-OHDA administration in the dorsolateral striatum, and the motor and metabolic outcomes were assessed at 7, 21, or 35 days post-surgical procedure. Dexamethasone, a diabetogenic glucocorticoid (GC), was intraperitoneally administered in the last 6 days to challenge the metabolism and reveal possible metabolic vulnerabilities caused by 6-OHDA. Controls received only vehicles. The 6-OHDA-treated rats displayed a significant decrease in locomotor activity, exploratory behavior, and motor coordination 7 and 35 days after neurotoxin administration. These motor impairments paralleled with no significant alteration in body mass, food intake, glucose tolerance, insulin sensitivity, and biochemical parameters (plasma insulin, triacylglycerol, and total cholesterol levels) until the end of the experimental protocol on days 35-38 post-6-OHDA administration. Moreover, hepatic glycogen and fat content, as well as the endocrine pancreas mass, were not altered in rats treated with 6-OHDA at the day of euthanasia (38th day after neurotoxin administration). None of the diabetogenic effects caused by dexamethasone were exacerbated in rats previously treated with 6-OHDA. Thus, we conclude that bilateral 6-OHDA administration in the striatum causes motor deficits in rats with no impact on glucose and lipid homeostasis and does not exacerbate the adverse effects caused by excess GC. These observations indicate that neurodegeneration of dopaminergic circuits in the 6-OHDA rats does not affect the metabolic outcomes.en
dc.description.affiliationUniv Fed Santa Catarina, Postgrad Program Pharmacol, Florianopolis, SC, Brazil
dc.description.affiliationUniv Fed Santa Catarina, Multictr Postgrad Program Physiol Sci, Florianopolis, SC, Brazil
dc.description.affiliationUniv Fed Santa Catarina, Dept Physiol Sci, Ctr Biol Sci, Florianopolis, SC, Brazil
dc.description.affiliationSao Paulo State Univ, Dept Physiol & Pathol, Sch Dent, Araraquara, Brazil
dc.description.affiliationUnespSao Paulo State Univ, Dept Physiol & Pathol, Sch Dent, Araraquara, Brazil
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipIdCAPES: 001
dc.description.sponsorshipIdCNPq: 306359/2017-0
dc.description.sponsorshipIdCNPq: 310331/2017-0
dc.description.sponsorshipIdFAPESP: 2013/17.251-6
dc.format.extent18
dc.identifierhttp://dx.doi.org/10.3389/fnins.2018.01020
dc.identifier.citationFrontiers In Neuroscience. Lausanne: Frontiers Media Sa, v. 12, 18 p., 2019.
dc.identifier.doi10.3389/fnins.2018.01020
dc.identifier.issn1662-453X
dc.identifier.urihttp://hdl.handle.net/11449/185297
dc.identifier.wosWOS:000455333600001
dc.language.isoeng
dc.publisherFrontiers Media Sa
dc.relation.ispartofFrontiers In Neuroscience
dc.rights.accessRightsAcesso aberto
dc.sourceWeb of Science
dc.subjectglucocorticoid
dc.subjectglycemia
dc.subjectlipids
dc.subjectliver
dc.subjectpancreatic islets
dc.subjectParkinson's disease
dc.titleGlucose Homeostasis Is Not Affected in a Murine Model of Parkinson's Disease Induced by 6-OHDAen
dc.typeArtigo
dcterms.rightsHolderFrontiers Media Sa
unesp.author.orcid0000-0002-8637-6097[8]

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