Suppression of prolactin secretion partially explains the antidiabetic effect of bromocriptine in ob/ob mice

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dc.contributor.authorFURIGO, ISADORA C.
dc.contributor.authorSUZUKI, MIRIAM F.
dc.contributor.authorOLIVEIRA, JOAO E.
dc.contributor.authorRAMOS-LOBO, ANGELA M.
dc.contributor.authorTEIXEIRA, PRYSCILA D.S.
dc.contributor.authorPEDROSO, JOAO A.
dc.contributor.authorALENCAR, AMANDA de
dc.contributor.authorZAMPIERI, THAIS T.
dc.contributor.authorBUONFIGLIO, DANIELLA C.
dc.contributor.authorQUARESMA, PAULA G.F.
dc.contributor.authorPRADA, PATRICIA O.
dc.contributor.authorBARTOLINI, PAOLO
dc.contributor.authorSOARES, CARLOS R.J.
dc.contributor.authorDONATO JUNIOR, JOSE
dc.coverageInternacionalpt_BR
dc.date.accessioned2018-12-28T10:52:43Z
dc.date.available2018-12-28T10:52:43Z
dc.date.issued2019pt_BR
dc.description.abstractPrevious studies have shown that bromocriptine mesylate (Bromo) lowers blood glucose levels in adults with type 2 diabetes mellitus; however, the mechanism of action of the antidiabetic effects of Bromo is unclear. As a dopamine receptor agonist, Bromo can alter brain dopamine activity affecting glucose control, but it also suppresses prolactin (Prl) secretion, and Prl levels modulate glucose homeostasis. Thus, the objective of the current study was to investigate whether Bromo improves insulin sensitivity via inhibition of Prl secretion. Male and female ob/ob animals (a mouse model of obesity and insulin resistance) were treated with Bromo and/or Prl. Bromo-treated ob/ob mice exhibited lower serum Prl concentration, improved glucose and insulin tolerance, and increased insulin sensitivity in the liver and skeletal muscle compared with vehicle-treated mice. Prl replacement in Bromo-treated mice normalized serum Prl concentration without inducing hyperprolactinemia. Importantly, Prl replacement partially reversed the improvements in glucose homeostasis caused by Bromo treatment. The effects of the Prl receptor antagonist G129R-hPrl on glucose homeostasis were also investigated. We found that central G129R-hPrl infusion increased insulin tolerance of male ob/ob mice. In summary, our findings indicate that part of Bromo effects on glucose homeostasis are associated with decrease in serum Prl levels. Because G129R-hPrl treatment also improved the insulin sensitivity of ob/ob mice, pharmacological compounds that inhibit Prl signaling may represent a promising therapeutic approach to control blood glucose levels in individuals with insulin resistance.pt_BR
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorshipIDFAPESP: 12/24345-4; 15/10992-6; 12/15517-6; 13/21722-4; 13/25032- 2; 14/11752-6; 17/25281-3pt_BR
dc.format.extent193-204pt_BR
dc.identifier.citationFURIGO, ISADORA C.; SUZUKI, MIRIAM F.; OLIVEIRA, JOAO E.; RAMOS-LOBO, ANGELA M.; TEIXEIRA, PRYSCILA D.S.; PEDROSO, JOAO A.; ALENCAR, AMANDA de; ZAMPIERI, THAIS T.; BUONFIGLIO, DANIELLA C.; QUARESMA, PAULA G.F.; PRADA, PATRICIA O.; BARTOLINI, PAOLO; SOARES, CARLOS R.J.; DONATO JUNIOR, JOSE. Suppression of prolactin secretion partially explains the antidiabetic effect of bromocriptine in ob/ob mice. <b>Endocrinology</b>, v. 160, n. 1, p. 193-204, 2019. DOI: <a href="https://dx.doi.org/10.1210/en.2018-00629">10.1210/en.2018-00629</a>. Disponível em: http://repositorio.ipen.br/handle/123456789/29404.
dc.identifier.doi10.1210/en.2018-00629pt_BR
dc.identifier.fasciculo1pt_BR
dc.identifier.issn0013-7227pt_BR
dc.identifier.orcidaguardandopt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-7982-1789
dc.identifier.percentilfi72.378
dc.identifier.percentilfiCiteScore83.00
dc.identifier.urihttp://repositorio.ipen.br/handle/123456789/29404
dc.identifier.vol160pt_BR
dc.relation.ispartofEndocrinologypt_BR
dc.rightsopenAccesspt_BR
dc.subjectendocrine diseases
dc.subjectbromine
dc.subjectglucose
dc.subjectinsulin
dc.subjectdiabetes mellitus
dc.subjecthomeostasis
dc.subjectmice
dc.titleSuppression of prolactin secretion partially explains the antidiabetic effect of bromocriptine in ob/ob micept_BR
dc.typeArtigo de periódicopt_BR
dspace.entity.typePublication
ipen.autorCARLOS ROBERTO JORGE SOARES
ipen.autorPAOLO BARTOLINI
ipen.autorJOAO EZEQUIEL DE OLIVEIRA
ipen.autorMIRIAM FUSSAE SUZUKI
ipen.codigoautor509
ipen.codigoautor1503
ipen.codigoautor425
ipen.codigoautor557
ipen.contributor.ipenauthorCARLOS ROBERTO JORGE SOARES
ipen.contributor.ipenauthorPAOLO BARTOLINI
ipen.contributor.ipenauthorJOAO EZEQUIEL DE OLIVEIRA
ipen.contributor.ipenauthorMIRIAM FUSSAE SUZUKI
ipen.date.recebimento18-12pt_BR
ipen.identifier.fi3.934pt_BR
ipen.identifier.fiCiteScore7.5
ipen.identifier.ipendoc25193pt_BR
ipen.identifier.iwosaguardando WoSpt_BR
ipen.identifier.ods3
ipen.range.fi3.000 - 4.499
ipen.range.percentilfi50.00 - 74.99
ipen.type.genreArtigo
relation.isAuthorOfPublicationd6719ab2-f2e9-4d7c-9cea-a6316fc14c9e
relation.isAuthorOfPublication7d228133-8477-43fb-941d-2cfb6a48c46c
relation.isAuthorOfPublicatione9e6346c-9b8b-4d39-8bdd-505ea6997646
relation.isAuthorOfPublicationda7833cb-421a-4163-9e42-8e06173b3242
relation.isAuthorOfPublication.latestForDiscoveryda7833cb-421a-4163-9e42-8e06173b3242
sigepi.autor.atividadeSUZUKI, MIRIAM F.:557:810:Npt_BR
sigepi.autor.atividadeOLIVEIRA, JOAO E.:425:810:Npt_BR
sigepi.autor.atividadeBARTOLINI, PAOLO:1503:810:Npt_BR
sigepi.autor.atividadeSOARES, CARLOS R.J.:509:810:Npt_BR
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