Insulin controls clock gene expression in the liver of goldfish probably via Pi3k/Akt pathway

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dc.contributor.authorSaiz Aparicio, Nuria
dc.contributor.authorVelasco, Cristina
dc.contributor.authorPedro Ormeño, Nuria De
dc.contributor.authorSoengas, José Luis
dc.contributor.authorIsorna Alonso, Esther
dc.date.accessioned2024-07-04T18:27:34Z
dc.date.available2024-07-04T18:27:34Z
dc.date.issued2023-07-25
dc.description.abstractThe liver circadian clock plays a pivotal role in driving metabolic rhythms, being primarily entrained by the feeding schedule, although the underlying mechanisms remain elusive. This study aimed to investigate the potential role of insulin as an intake signal mediating liver entrainment in fish. To achieve this, the expression of clock genes, which form the molecular basis of endogenous oscillators, was analyzed in goldfish liver explants treated with insulin. The presence of insulin directly increased the abundance of per1a and per2 transcripts in the liver. The dependency of protein translation for such insulin effects was evaluated using cycloheximide, which revealed that intermediate protein translation is seemingly unnecessary for the observed insulin actions. Furthermore, the putative interaction between insulin and glucocorticoid signaling in the liver was examined, with the results suggesting that both hormones exert their effects by independent mechanisms. Finally, to investigate the specific pathways involved in the insulin effects, inhibitors targeting PI3K/AKT and MEK/ERK were employed. Notably, inhibition of PI3K/AKT pathway prevented the induction of per genes by insulin, supporting its involvement in this process. Together, these findings suggest a role of insulin in fish as a key element of the multifactorial system that entrains the liver clock to the feeding schedule.
dc.description.departmentDepto. de Genética, Fisiología y Microbiología
dc.description.facultyFac. de Ciencias Biológicas
dc.description.refereedTRUE
dc.description.sponsorshipMinisterio de Ciencia e Innovación (España)
dc.description.sponsorshipXunta de Galicia
dc.description.sponsorshipUniversidad Complutense de Madrid
dc.description.statuspub
dc.identifier.citationSaiz N, Velasco C, De Pedro N, Soengas JL, Isorna E. Insulin Controls Clock Gene Expression in the Liver of Goldfish Probably via Pi3k/Akt Pathway. IJMS. 2023;24(15):11897
dc.identifier.doi10.3390/ijms241511897
dc.identifier.essn1422-0067
dc.identifier.issn1661-6596
dc.identifier.officialurlhttps://doi.org/10.3390/ijms241511897
dc.identifier.relatedurlhttps://www.mdpi.com/1422-0067/24/15/11897
dc.identifier.urihttps://hdl.handle.net/20.500.14352/105668
dc.issue.number15
dc.journal.titleInternational Journal of Molecular Sciences
dc.language.isoeng
dc.page.final15
dc.page.initial1
dc.publisherMDPI
dc.relation.projectIDPID2019-103969RB-C32
dc.relation.projectIDPID2019-103969RB-C31
dc.relation.projectIDSUG, ED431B 2022/01
dc.relation.projectIDCT42/18-CT43-18
dc.rightsAttribution 4.0 Internationalen
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subject.cdu576.52
dc.subject.cdu597
dc.subject.keywordCircadian system
dc.subject.keywordFood-entrainable oscillator (FEO)
dc.subject.keywordCarassius auratus
dc.subject.keywordInsulin
dc.subject.keywordLiver
dc.subject.keywordPeriod genes
dc.subject.keywordPhosphatidylinositol 3-kinase (PI3K)
dc.subject.keywordFish
dc.subject.ucmFisiología animal (Biología)
dc.subject.ucmBioquímica (Biología)
dc.subject.ucmPeces
dc.subject.unesco2401.13 Fisiología Animal
dc.subject.unesco2302 Bioquímica
dc.titleInsulin controls clock gene expression in the liver of goldfish probably via Pi3k/Akt pathway
dc.title.alternativeLa insulina controla la expresión del gen del reloj en el hígado de los peces de colores, probablemente a través de la vía Pi3k/Akt
dc.typejournal article
dc.type.hasVersionVoR
dc.volume.number24
dspace.entity.typePublication
relation.isAuthorOfPublication726982f8-731a-4fa2-906e-98119fd02494
relation.isAuthorOfPublication9b7c3c2b-b207-43b8-ad17-add5130a3d2f
relation.isAuthorOfPublication882d1fb3-a920-418a-9f3f-1b8f6b967032
relation.isAuthorOfPublication.latestForDiscovery726982f8-731a-4fa2-906e-98119fd02494
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